The Wiley Handbook of Cognitive Behavioral Therapy

PC4-Galliard c001.tex V1 - 07/30/2013 9:59 P.M.
Page xi
Contributors
Jonathan S. Abramowitz, University of North Carolina at Chapel Hill,

United States
Lesley A. Allen, University of Medicine and Dentistry of New Jersey–Robert Wood
Johnson Medical School, United States
Nader Amir, San Diego State University, United States
Martin M. Antony, Ryerson University, Canada
Bruce A. Arnow, Stanford University School of Medicine, United States
Lauren D. Asarnow, University of California, Berkeley, United States
Gordon J. G. Asmundson, University of Regina, Canada
Donald H. Baucom, University of North Carolina at Chapel Hill, United States
Aaron T. Beck, University of Pennsylvania, United States
Emily Becker-Weidman, Center for Family Development and New York University,
Child Study Center, United States
Shadi Beshai, University of Calgary, Canada
Niels Birbaumer, University of Tübingen, Germany, and Ospedale San Camillo,
Venice, Italy
Aaron J. Blashill, Massachusetts General Hospital and Harvard Medical School,
United States
Ellen J. Bluett, Utah State University, United States
Lori A. Brotto, University of British Columbia, Canada
Laura C. Bruce, Adult Anxiety Clinic of Temple University, Philadelphia,
United States
Shannon A. Byrne, University of Connecticut Health Center, United States
PC4-Galliard c001.tex V1 - 07/30/2013 9:59 P.M. Page xii
xii Contributors
Matthew R. Capriotti, University of Wisconsin-Milwaukee, United States

Kathleen M. Carroll, Yale School of Medicine, United States
Trudie Chalder, King’s College London, United Kingdom
Priscilla T. Chan, Boston University, United States
Candice Chow, Boston University, United States
David A. Clark, University of New Brunswick, Canada
Xavier Clayton, La Trobe University, Australia
Shauna L. Clen, Kent State University, United States
Adam R. Cobb, Laboratory for the Study of Anxiety Disorders, The University of
Texas at Austin, United States
Sara Conley, San Diego State University, United States
Kathleen M. Corcoran, Stanford University School of Medicine, United States
Amy Cummins, La Trobe University, Australia
Frank M. Dattilio, Harvard Medical School, United States
Melissa A. Day, University of Alabama, United States
Rachele Diliberto, University of Nevada, United States
Keith S. Dobson, University of Calgary, Canada
Christopher Donahue, University of Minnesota, United States
Norman B. Epstein, University of Maryland, United States
Flint M. Espil, University of Wisconsin-Milwaukee, United States
Joshua C. Eyer, University of Alabama, United States
Melanie S. Fischer, University of North Carolina at Chapel Hill, United States
Evan M. Forman, Drexel University, United States
Andrea Fortunato, New School for Social Research, United States
Marci G. Fox, Academy of Cognitive Therapy, United States
Rachel D. Freed, Boston University, United States
Arthur Freeman, Midwestern University, United States
David M. Fresco, Kent State University, United States
Maryrose Gerardi, Emory University School of Medicine, United States
Miguelina Germán, Montefiore Medical Center/Albert Einstein College
of Medicine, United States
Susan Gingerich, Philadelphia, United States
PC4-Galliard c001.tex V1 - 07/30/2013 9:59 P.M. Page xiii
Contributors xiii
Jennifer D. Gottlieb, Boston University, United States

Jon E. Grant, University of Chicago, United States
Jennifer L. Greenberg, Massachusetts General Hospital and Harvard Medical School,
United States
Kurt Hahlweg, Technische Universität Braunschweig, Germany
Nailah O. Harrell, University of Maryland, United States
Allison G. Harvey, University of California, Berkeley, United States
Richard G. Heimberg, Adult Anxiety Clinic of Temple University, Philadelphia,
United States
Scott W. Henggeler, Medical University of South Carolina, United States
James D. Herbert, Drexel University, United States
Stephen P. Hinshaw, University of California, Berkeley, United States
Devon E. Hinton, Massachusetts General Hospital, Harvard Medical School, and
Arbour Counseling Services, Lowell, United States
Robin B. Jarrett, University of Texas Southwestern Medical Center, United States
Nikolaos Kazantzis, La Trobe University, Australia
Christopher A. Kearney, University of Nevada, United States
Meghan E. Keough, University of Washington, United States
Brian D. Kiluk, Yale School of Medicine, United States
Laura E. Knouse, University of Richmond, United States
Kristina J. Korte, Florida State University, United States
David A. Langer, Boston University, United States
Cynthia L. Lancaster, Laboratory for the Study of Anxiety Disorders, The University
of Texas at Austin, United States
Martin La Roche, Children’s Hospital/Martha Eliot Health Center and Harvard
Medical School, United States
Carl W. Lejuez, University of Maryland, United States
Tania Lincoln, University of Hamburg, Germany
Marsha M. Linehan, University of Washington, United States
Laura MacPherson, University of Maryland, United States
Brittain L. Mahaffey, University of North Carolina at Chapel Hill, United States
L.E. Marshall, Rockwood Psychological Services, Kingston, Canada
William. L. Marshall, Rockwood Psychological Services, Kingston, Canada
PC4-Galliard c001.tex V1 - 07/30/2013 9:59 P.M. Page xiv
xiv Contributors
Michael R. McCart, Medical University of South Carolina, United States

Daniel S. McGrath, Mount Allison University, Canada
Douglas S. Mennin, Hunter College, City University of New York, United States
Alec L. Miller, Montefiore Medical Center/Albert Einstein College of Medicine,
United States
Stephen J. Morley, University of Leeds, United Kingdom
Kate L. Morrison, Utah State University, United States
Samantha J. Moshier, Boston University, United States
Kim T. Mueser, Boston University, United States
Simone Munsch, Fribourg University, Switzerland
Lindsay D. Nelson, Florida State University, United States
Leorra Newman, Ryerson University, Canada
Michelle G. Newman, Pennsylvania State University, United States
Arthur M. Nezu, Drexel University, United States
Christine Maguth Nezu, Drexel University, United States
Pedro Nobre, Universidade do Porto, Portugal
Aaron M. Norr, Florida State University, United States
Matilda E. Nowakowski, Ryerson University, Canada
Brian L. Odlaug, University of Copenhagen, Denmark
Michael W. Otto, Boston University, United States
Christopher J. Patrick, Florida State University, United States
Paola Pedrelli, Massachusetts General Hospital and Harvard Medical School,
United States
Daniel L. Peluso, University of Regina, Canada
Nancy M. Petry, University of Connecticut Health Center, United States
Linda J. Pfiffner, University of California, San Francisco, United States
Donna B. Pincus, Boston University, United States
Jessica Rasmussen, Massachusetts General Hospital and Harvard Medical School,
United States
Jenny Rogojanski, Ryerson University, Canada
Barbara O. Rothbaum, Emory University School of Medicine, United States
PC4-Galliard c001.tex V1 - 07/30/2013 9:59 P.M. Page xv
Contributors xv
Steven A. Safren, Massachusetts General Hospital and Harvard Medical School,

United States
Cindy Schaeffer, Medical University of South Carolina, United States
Stefan K. Schmertz, Red Sox Foundation and Massachusetts General Hospital,
Harvard Medical School, United States
Norman B. Schmidt, Florida State University, United States
Michael Simons, RWTH Aachen University, Germany
Leslie Sokol, Academy of Cognitive Therapy, United States
Gail Steketee, Boston University, United States
Sherry H. Stewart, Dalhousie University, Canada
Jennifer Svaldi, University of Freiburg, Germany
Lauren E. Szkodny, Pennsylvania State University, United States
Steven Taylor, University of British Columbia, Canada
Michael J. Telch, Laboratory for the Study of Anxiety Disorders, The University of
Texas at Austin, United States
Michael E. Thase, Perelman School of Medicine of the University of Pennsylvania
and Philadelphia Veterans Affairs Medical Center, United States
Michel A. Thibodeau, University of Regina, Canada
Beverly E. Thorn, University of Alabama, United States
Martha C. Tompson, Boston University, United States
Brunna Tuschen-Caffier, University of Freiburg, Germany
Michael P. Twohig, Utah State University, United States
Miguel T. Villodas, University of California, San Francisco, United States
Jeffrey R. Vittengl, Truman State University, United States
Johan W.S. Vlaeyen, University of Leuven, Belgium, and Maastricht University,
The Netherlands
Valerie Vorstenbosch, Ryerson University, Canada
Erin F. Ward-Ciesielski, University of Washington, United States
Adrian Wells, University of Manchester, United Kingdom, and NTNU, Norway
Henny A. Westra, York University, Canada
Sabine Wilhelm, Massachusetts General Hospital and Harvard Medical School,
United States
Michelle R. Woidneck, Utah State University, United States
PC4-Galliard c001.tex V1 - 07/30/2013 9:59 P.M. Page xvi
xvi Contributors
Douglas W. Woods, University of Wisconsin-Milwaukee, United States

Sheila Woody, University of British Columbia, Canada
Robert L. Woolfolk, Rutgers University and Princeton University, United States
Sarah Wyckoff, University of Tübingen and International Max Planck Research
School, Germany
Morag A. Yule, University of British Columbia, Canada
1
The Therapeutic Relationship
Arthur Freeman
Midwestern University, United States
My position is not that technique is irrelevant to outcome. Rather I maintain that,

as developed in the text, the success of all techniques depends on the patient’s sense of
alliance with an actual or symbolic healer.
Frank, 1991, p. xiv
The Merriam-Webster Dictionary (2010) offers several definitions of the term “rela-
tion,” all of which address (i.e., relate to) the focus of this chapter. The first definition
involves “the act of telling or recounting,” which is one of the basic psychotherapeutic
techniques, across all models of treatment. The second involves “an aspect or quality
(as resemblance) that connects two or more things or parts as being or belonging
or working together or as being of the same kind.” A third definition involves “a
person connected by consanguinity or affinity.” Fourth, it is defined as “the attitude
or stance which two or more persons or groups assume toward one another,” and
finally, “the state of being mutually or reciprocally interested.” The importance of
the therapeutic relationship was a major focus for all of the therapeutic pioneers,
Freud, Adler, Jung, and Horney. For psychoanalysts the relationship, in the form of
the processes of transference and countertransference, was the vehicle by which the
treatment progressed. Among the early pioneers, it was Harry Stack Sullivan who
placed the greatest emphasis on the relational experience of human interactions and
defined building and enhancing the individual’s interactive experience as a major goal
for therapy (Sullivan, 1953). The effective outcome of Sullivan’s interpersonal psychi-
atry was enhanced interpersonal functioning. Sullivan posited that individuals develop
assumptions about others and create and maintain schemata that serve as templates
for understanding the interpersonal world. Some of these templates are used to define
and understand the self and others and the multiple interactions between the two.
The Wiley Handbook of Cognitive Behavioral Therapy, First Edition.

Edited by Stefan G. Hofmann. Volume I edited by David J.A. Dozois.
© 2014 John Wiley & Sons, Ltd. Published 2014 by John Wiley & Sons, Ltd.
DOI: 10.1002/9781118528563.wbcbt01
4 General Strategies
A common criticism of cognitive behavioral therapy (CBT) is that by its very name
it would seem to exclude the obvious and essential human components of emotion
and of attending to a systemic focus, that is, one’s social and cultural world. The
na ı̈ve idea about the content and process of CBT is that it is a simple procedure
that involves the therapist actively challenging, arguing, and disputing the patient’s
irrational or dysfunctional thoughts. This view of CBT is that the goal of therapy
is for the patient to develop these same disputational skills and bring them to bear
on the ongoing negative percepts and ideas. After all, those individuals who have
negative thoughts will be depressed, and those with fearful thoughts will be anxious.
This view of CBT has the required grain of truth. The content and style of one’s
thoughts, percepts, ideas, attributions, and philosophies have a powerful influence on
how one feels and acts. Gilbert and Leahy (2009) collected a number of papers on the
therapeutic connection that address the role of the relationship in specific therapies
(e.g., dialectical behavior therapy, acceptance and commitment therapy, and a social
cognitive model).
Where, then, is the therapeutic influence of the therapist in the treatment mix?
Can one treat a number of self-identified psychological problems via self-help books,
DVDs, or online therapy? There is, as in most things, a broad spectrum of opinion.
There are those who posit that techniques are not the change agent in psychotherapy,
but rather the therapeutic context—that is, the relationship—that is curative. On
the other hand, there are those who advise that the relationship between patient and
therapist is unnecessary.
Ellis (1995) stated:
Lots of people call me abrasive or sharp. But I just call a spade a spade, and show
people pretty quickly what they are saying to themselves to upset themselves, so they
call that abrasive. I have one thing that I got over, my sickness, which I think that most
psychotherapists still have, the dire need to be approved of by their colleagues, clients,
etc. So I don’t have any of that nonsense. If my clients love me, that’s great. Most do
because I help them. But if they don’t I don’t care that much.
‘Personal communication’
Interestingly, Ellis’s practice belied his words. A careful viewing of his many
videotaped interviews demonstrates clearly that rather than ignore the relationship
issue, Ellis was able in a very short time (sometimes mere minutes) to establish
a connection with a patient and to establish an effective and useful therapeutic
communication and relationship. Undoubtedly, there were patients who did not like
his direct and often confrontational style, and never came back for a second session.
That, however, was probably true for Freud’s patients, who may have found his
distant and nonresponsive therapeutic stance too isolating and difficult to accept.
Assuming a position quite opposed to Ellis was Carl Rogers. Rogers, in his book On
becoming a person (1961), credits Stanley Standal with coining the term unconditional
positive regard (UPR), a term that has, in fact, become firmly attached to Rogers.
Rogers defined this construct as:
Unconditional Positive Regard, in general use, is knowing the other person, and accepting
all the faults, traits, and beliefs, without saying anything against it. This helps the
The Therapeutic Relationship 5
relationship to get stronger and keeps from breaking due to minor differences. However,
this is possible only if the sufferer does not cause harm to the people (p. 283).
This last point becomes something of a sticking point for many therapists inasmuch
as most therapists learn of UPR without Rogers’s caveat regarding harming others.
The basic issue is that if the therapist can accept the patient with all of the patient’s
eccentricities, flaws, faults, weaknesses, imperfections, defects, shortcomings, errors
of thought and deed, and blemishes (visible and hidden), then the patient would (or
could) learn to accept him- or herself in the shadow of his or her imperfect feelings,
thoughts, and behaviors. Within the aura generated by the therapist’s acceptance,
the patient could deal with the myriad and complex life issues which were the basis
of seeking therapy. By providing UPR, therapists seek to help their patients accept
and take responsibility for themselves. By providing the patient with UPR and the
resulting acceptance, the Rogerian (or Humanistic) therapist believes that he or she
is providing the client with the best possible conditions for personal growth. The
goal of the strategy was for the therapist to suspend judgment regarding the patient’s
actions, thoughts, and feelings, and to listen to that person with the attitude that
the patient has within him- or herself the ability to change what he or she does,
without actually changing who he or she is. One wonders, if the patient causes
harm to others (as broadly defined), should he or she receive the same UPR that
is accorded to the individual who does not cause harm to others? In contrast to
Rogers’s UPR is Ellis’s notion of the patient learning unconditional self-acceptance
(USA). According to this idea, the goal is for patients to learn that they have the
right to accept themselves. This is an idea that many individuals fail to internalize in
their early years in their family of origin, school, and religious experience. A more
common idea is that an individual has value mainly in the eyes of others, that is,
through the compliments, trophies, grades, or promotions that are garnered through
the years.
The Therapeutic Relationship
Hardy, Cahill, and Barkham (2009) have chosen to use the terms “therapeutic rela-
tionship,” “working relationship,” “alliance,” “working alliance,” and “therapeutic
bond” interchangeably. Bordin (1979) defined the therapeutic alliance as encom-
passing (a) an agreement on the goals of the therapy, (b) a designation of what
the tasks and goals of the therapy shall be, and (c) the development of “bonds” or
partnership that can be developed by the therapist and the patient as co-scientists
in the therapeutic experiments. Lack of clarity in the definition of problems and the
related goals, lack of precision, clarity, and explication in the definition of the tasks
of treatment, as well as confusion about the division of labor in treatment and the
failure to establish a collaborative, goal-directed relationship, can severely limit the
effectiveness of treatment.
The therapeutic bond is often seen as a subset of the therapeutic alliance. In
discussing the value of the therapeutic bond in the treatment of depressed patients,
Krupnick et al. (1998) found that the therapeutic bond formed between therapist
and patient was a leading influence on the patient’s recovery regardless of the type of
treatment used. This was among the earliest empirical studies that compared the ther-
apeutic alliance established between therapist and patient and its effect on improving
the patient’s depressive symptoms not only in different types of psychotherapy but
also in pharmacotherapy. This study also used the terms interchangeably. To permit a
fuller exposition of the issue in this chapter, these two constructs are treated separately
and will be discussed as they fit into a CBT emphasis. My goal in this chapter is to
describe the therapeutic connection or relationship in terms of the two elements, the
therapeutic bond and the therapeutic alliance, not as synonymous and interchangeable
but as discrete components. Each of these elements is specific to a particular thera-
peutic goal and can be used by the therapist in terms of identifiable techniques that
help to realize the overall and limited therapeutic goals. To illustrate the elements of
the therapeutic relationship, descriptions of the therapeutic interactions are provided
to elucidate the relational elements.
The Therapeutic Bond
In this chapter I use the term therapeutic bond as a shorthand term for the therapeutic
relationship. It is the interpersonal exchange between patient and therapist, and
is governed by many of the same rules as are relationships outside the context of
therapy. These general rules involve civility, appropriateness, boundary setting, respect
for the space and boundaries of others, adherence to basic codes of ethics, etiquette,
interaction, bidirectional influence, and conflict resolution skills. In addition to their
acquired interpersonal skills, as part of their training in psychotherapy, therapists
develop skills of empathy and skills of therapy that are designed to establish and
enrich the relationship/bond so that the therapeutic endeavor can proceed more
easily. Effective clinical training, regardless of the discipline, requires that the therapist
develop these therapy-enhancing techniques. These include the development of
rapport and the ability to demonstrate that the therapist is understanding of the
patient’s life experience, cognitive style, and vulnerabilities, and is developing a
conceptual framework for the understanding of the patient’s personal life journey.
This conceptual framework will guide the therapy and clarify for patients why they do
what they do, and why they have done what they have done, and will help them plan
for the future.
The Therapeutic Alliance
In this chapter I use the term therapeutic alliance to describe the contract or agreement
between patient and therapist as to the focus, goals, aims, purposes, and objectives of
therapy. The particular mix of bond and alliance will differ, depending on the patient’s
life situation, strengths and skills, needs, aspirations, available time, and motivation.
It will also be influenced by the therapist’s experience, goals, available time, and
setting. Of course, for both patient and therapist, the therapeutic context and what
is happening within the therapeutic collaboration at that time will further influence
the mix and use of bond and alliance. For example, in times of crisis, the therapist
may need to take a far more directive position that emphasizes the alliance. While
we can recognize the importance of the relationship, in times of crisis the focus may
need to be more active, instructive, and directed. The approach may be high alliance
and low bond so that the therapeutic “contract” is the major focus of the therapy. If
a patient is suicidal, the contract would be for the patient to be helped to stay alive
until the many issues that are negatively impacting the patient can be ameliorated.
If the presenting problem is a recent death, divorce, job loss, or financial problem,
the patient needs the therapist to be more directive to help ease the pressure while
skill-building and reducing both internal and external pressures until the patient’s
resources can be brought to bear on the crisis.
A second possible mix is what we might term “coaching.” This is especially useful
in short-term, non-crisis, directive interactions and needs both high alliance and high
bond. The patient–therapist relationship becomes important to maintain motivation
where the agreement of therapeutic goals is explicit and agreed upon. For example, if
the patient is experiencing job-related or relationship-related problems, the therapist
can be the objective individual who listens to the patient with great attention. The
bond makes the use of the Socratic dialogue even more effective because of the
elements that are bond-related, such as trust, confidence, and perceived support.
These can then provide a platform for the development of therapeutic skills and
problem solutions.
A third focus is what is typically labeled as “supportive therapy.” This approach is
most helpful when the patient has developed a direction and focus for treatment and
has identified targets and strategies for change as well as an emphasis for his or her
therapy work. What patients need at this point is emotional support, encouragement,
feedback on progress, and, at times, a cheering squad to help keep them moving
in their chosen direction. In some cases, the supportive work can be likened to
the function of a cast for a broken or stressed limb. The support is necessary to
allow the proper setting and healing of a bone. Once the bone is well healed, the
support can be removed. In the case of a sprain, a support is necessary to maintain
movement. In the case of chronic weakness, a support may always be necessary
to allow optimal movement. Supportive therapy may encompass guidance, reality
testing, environmental manipulation (e.g., referral for testing, vocational evaluation,
or training), reassurance, persuasion, redirection of goals, helping the patient to
understand patterns of culture, or helping with referrals for the patient or family
member to an institution, agency, school, or specific treatment setting. Given that
the contract for treatment is set, this approach requires low alliance, but a high bond.
A question commonly asked by novice cognitive therapists is whether they can do
supportive therapy or whether that is a different model that would be antithetical to
CBT. In fact, supportive work can be a key ingredient in helping the patient during
crises and relapses, and when coming to a particularly large “speed-bump.” There are
times, when the patient’s motivation wanes, or for any of a variety of reasons, that a
supportive stance can help fill the gap and keep the treatment moving.
The final combination of the bond and alliance is used most often at the conclusion
of therapy. As the therapy approaches the point of termination, it is important for the
therapist to taper off the bond to prepare the patient for independent function, and
to review and emphasize the progress that the patient has made in achieving his or
her therapeutic goals. This involves frequent reviews of what the patient has gained
from therapy and of his or her plans for meeting near- and far-end goals. This will be
discussed in greater detail later in the chapter.
Wolberg (1954) identified a number of factors that went into the therapeutic work,
some bond, and some alliance. For patients these included:
• the need to depend on an authority, or to seek support from a credible and strong
figure, the therapist;
• the need for empathy and understanding of his or her position and problems;
• the need to unburden themselves from anxiety, depression, guilt, responsibility,
fault, or blame (part of this need may be the desire to “get it off their chest” and
be able to experience catharsis and a consequential short-term relief of pent-up
emotion);
• the need to reality test their percepts and experience; and
• the need for a nonjudgmental and wholesome relationship that may be a far cry
from what they experienced in their family of origin.
For the therapist, Wolberg (1954) identified the following therapeutic elements:
• taking and accepting the role as a helping authority;

• being willing to be a fair, unbiased, nonjudgmental, and caring person;
• being willing to accept the slings and arrows of the displaced anger that the patient
may have developed toward others;
• being a representative of both the good and the bad that the patient experiences;
• having the ability to be a cooperative partner in the therapeutic endeavor;
• maintaining the canons of ethics at the highest level; and
• establishing and maintaining the requisite skills for treating particular types of
patients and specific disorders.
Resistances and Impediments to the Working Relationship
When the therapeutic relationship goes askew, several factors can be noted. As an
extension of Bordin’s work, Freeman and McCloskey (2004) identify four major areas
that negatively impact the therapy relationship, none of which are mutually exclusive.
The sources of the difficulty to the therapy alliance and bond can come from the
patient, the therapist, the environment, or the disorder.
Patient Factors
These are cognitive, affective, or behavioral aspects of the client, and may even be
seen as emblematic of his or her style. These characteristics may be clear, obvious, and
overt, and not easily missed. On the other hand, these characteristics may be far more
limited and evident only under stress, or when the individual experiences threat. They
may include the following:
• The client lacks skills to comply with the therapeutic requirements or tasks, thereby
negatively impacting the alliance.
• Previous treatment experience, often of failure, has produced negative
expectations or cynicism. This may negatively impact both the bond and the
alliance.
• The client fears that others will be hurt or impacted in a negative way by the
changes produced in therapy. This may negatively impact both the bond and the
alliance.
• There is secondary gain from maintaining symptoms, for the client or significant
others. This may, more likely, impact the bond.
• The client lacks compelling reasons to change. This may negatively impact both
the bond and the alliance.
• The client has a generally negative set toward therapy. This may negatively impact
both the bond and the alliance.
• The client has limited ability for the self-monitoring of thoughts, feelings, and
behavior.
• The client has limited or poor ability to monitor the responses and reactions
of others. This may impact the bond inasmuch as he or she may misread or
misunderstand the therapist’s actions, words, or ideas.
• The client has a demanding or self-centered interpersonal style with a low tolerance
for frustration and expects progress to be effortless and rapid. This almost always
will impact the bond.
• The client perceives being in therapy as a loss of social status and feels stigmatized.
This can negatively impact both the bond and the alliance.
Therapist Factors
As an active participant, the therapist brings his or her own values, skills, and
motivation(s) to the treatment endeavor. However, all therapists, no matter how
many years of experience or training they have, can potentially contribute to the
therapeutic roadblocks. The therapist’s contributions to the impediments include the
following:
• The therapist lacks either interpersonal skills or therapeutic skills.

• The patient and therapist maintain congruent distortions.
• The patient has been poorly socialized by the therapist to the expectations of the
therapy or of a particular treatment model.
• The therapist is unable to build or communicate an active working alliance. The
therapy goals are unstated, unrealistic, or vague. Essentially, the therapist has not
obtained informed consent and agreement with therapy goals.
• The therapist and the patient are attempting to operate from an impaired or
limited database.
• The therapist has therapeutic narcissism.
• The therapist’s timing of interventions is poor.
• The therapist has limited skills and/or lacks experience.
• The therapist is unable to build and maintain the therapeutic bond.
• The therapist has a lack of understanding of the norms and of the developmental
process.
• The therapist has unrealistic expectations of the client.
Environmental Factors
We all live within a subgroup, a group, and a society. Each of those entities has
expectations and demands for conformity, for allegiance, and for contribution from
the client. Sometimes these demands will be in conflict; at other times they may be in
direct opposition to one another. The patient’s difficulty may come from the delicate
balancing act of trying to meet the demands of many masters, and not being able to
do it. These psychosocial stressors could include:
• environmental stressors that preclude change;

• significant others who foil or sabotage therapy;
• agency or institutional reinforcement of pathology and illness through compensa-
tion and benefits;
• cultural opposition to help-seeking;
• maintenance of system homeostasis;
• gross family pathology;
• unrealistic demands on the client by self and family members;
• unrealistic demands on the client by institutions;
• financial factors that limit the opportunities for change; and
• lack of resources or support from the environment.
Problem or Pathology Factors

Some factors that cause difficulties could be related to the patient’s personal style as
listed above or are indicative or diagnostic of the patient’s problems and pathology.
These factors could include:
• rigid cognitive style;

• significant medical or physiological problems;
• trust impairments;
• impulsivity and poor executive control;
• cognitive impairment, confusion, or limited cognitive ability;
• social isolation or alienation;
• symptom profusion;
• extreme dependence;
• ongoing self-devaluation;
• limited energy for change; and
• substance misuse.
Understanding Schemas
As in all aspects of CBT, schemas are the central points for understanding past behav-
ior, making sense of present behavior, and predicting future behavior. If a patient
comes to therapy with complaints about how the world has treated him or her badly
and how others take advantage, and regales the therapist with examples of how he or
she is being subjected to the demands of others less intelligent, less accomplished, and
inferior in just about every way, the therapist should take note. It might be projected
that the therapeutic relationship will likely be subject to the same issues and schemas
that have influenced life relationships. On the other hand, if a patient seeks help in a
more consultative manner, for example, for overcoming sleep problems, the therapist
can use the alliance to help the patient to change what he or she does that might inter-
fere with sleep, or relaxation more generally. Therapists must be equally aware of their
own schemas regarding various patient problems, patient types, and patient reactions.
Building and Enhancing the Working Relationship
The building blocks for the therapy work include the therapist’s ability to communicate
and his or her understanding of the problem. The simple aura of being sought for
help imbues the therapeutic relationship with certain magical powers. The use of
restatement and questioning the patient to ascertain that what the therapist heard was
indeed what the patient said, and, even more, what he or she meant, is important.
Taking the position of fallibility can, in fact, help nurture the relationship. The range
of therapeutic positioning by the therapist can run the range from being Sherlock
Holmes to being more concrete and simple-minded. For example, the individual who
presents him- or herself at 221B Baker Street might experience the Holmesian style
as identifying some small aspect of the individual and immediately having Holmes
build a hypothetical structure of the individual based on his or her dress, posture,
skin tone, speech, or any other observable aspect of his or her being. Another,
more contemporary detective was Columbo, who had “just one more question.” The
following therapeutic examples illustrate these themes:
THERAPIST: I can tell from the way in which you describe your boss that you are
enraged. That would account for the rumination, sleep difficulty, and your use of sleep
medications and alcohol to treat your problem.
THERAPIST: Let me stop you here and tell you what I am understanding of your
problem. Are you saying that everyone in your life has abandoned you?
THERAPIST: That seems really important. I want to write that down so as to not forget
or lose the importance of your point. We can come back to that again.
THERAPIST: Go over that again. Say that again so we can both hear it. I want to be sure
that I am tuned in to what you have experienced.
The dangerous temptation for the therapist is simply to nod and grunt, seeming
to indicate that what the patient has said has been understood. The typical pattern of
agenda setting and of the review at the end of the session can also be a building block
for the working relationship. Careful agenda setting enhances the therapeutic relation-
ship in that it asks the patient to help to establish a session focus and to help to design
and establish goals for the therapy and for the individual sessions. The end of session
review is relationship-enhancing in that it asks the patient what he or she is taking
home from the session. Asking patients what they are taking home and what they have
derived from the session places the therapist in a far more collaborative position. The
therapist is not simply assuming what the patient gained in the session (if anything),
nor is the therapist sure of the understanding that the patient has developed of the ses-
sion content. For example, a 29-year-old man was referred by his wife because of what
appeared to be paranoid ideas related to his constant comments to her that his cowork-
ers at the law firm where he was employed were trying to poison him through the use
of aerosol sprays. He reported to the therapist that he could see the “after image” of
a hand and a spray can being withdrawn from the doorway to his office, and then his
smelling a chemical smell. He would then become lightheaded for a brief time. At the
pleading of his wife he told the office manager of his experience and asked if there were
any efforts being made to exterminate vermin in the office suite. Her response was that
there was no such activity, and that any cleaning would be carried out after work hours.
In the first session, after having the man describe his experience, the therapist asked him
if he knew or had heard of any such aerosol poisons. The therapist further questioned
the young man about who in the law firm might want to kill him. Finally, the therapist
asked if the young attorney was using the idea of gathering evidence that was a basic
technique in litigation. The young man looked up and said brightly, “You’re right. I
have no evidence. Thank you doctor, you have saved my life.” The therapist was proud
of how he had helped this man in only one session. The therapist never asked for a
review of the session. What exactly was the patient taking home? They set a second
appointment for one week hence. When the patient approached his wife in the waiting
room, he said, “Honey, things are going to be okay … The doctor has helped me to see
my distorted thinking and everything will be okay now at work.” His wife cried tears
of relief and they both thanked the therapist and they left. That night, at about 2 a.m.,
the therapist received an emergency call through the office answering service from the
patient’s wife. She was distraught and kept asking, “What did you tell him? What did
you tell him?” The therapist, roused from his sleep, tried to calm her, asking, “What did
he say?” She responded that when they got home her husband described the session
and that the therapist suggested that what was needed was evidence so he was going to
go into the office in the middle of the night and search everyone’s office for the poison.
A second building block strategy involves the use of homework. This extends the
therapeutic work outside the consulting room. The strategy involves making sure
that any homework that was done is reviewed in the next session. If it is not put
on the agenda and the agenda is not followed, it may model a pattern of either
disorganization or a lack of concern or caring.
Third, it is essential that the therapist communicate interest in the patient not
simply as a “patient” but as a vulnerable, fallible, and important individual. By paying
attention and noting what the patient states are his or her likes and dislikes, goals,
ambitions, and experiences, the therapist communicates that the patient is perceived
as a significant and important individual. Remembering small facts about the patient’s
life (where he or she went to school, or his or her favorite football team) can be a
part of the connection-building. If the therapist forgets some piece of information
about the patient or something discussed in a previous session it is better to ask
about it rather than trying to fake it. Therapists are also fallible. There are times when
they may, because of their own life pressures, be more muted, more down (even
depressed), upset, dull, or inactive in the session. At other times they may be inspired,
active, alert, and positive. No matter what the therapist’s personal reactions, it is
essential to convey interest in patients and what they are doing. For example, Maria, a
42-year-old woman, related an experience that she had with a previous therapist. The
therapist fell asleep during the session. Maria did not know what to do. She waited
until her time was up and then cleared her throat loudly and woke the therapist. The
therapist interpreted Maria’s behavior as hostile by (a) not waking him sooner, and
(b) speaking in a low and lulling voice that put him to sleep. It was the last session
that Maria had with that therapist. She pointed out to her present therapist that as a
child she was blamed for most of the things that went wrong in her home. The idea
that the therapist blamed her for his “nap” was intolerable.
It is important to realize that patients may be troubled, but not stupid. It would
be far better to admit any kernel of truth in the patient’s reaction rather than to try
to interpret one’s way out of it. For example, the therapist could have said to Maria
at the start of the session, “I am having a bad allergy day today and just took some
medication. If I appear tired, it is the medication.”
A fourth factor is therapists’ ability to communicate tolerance, in a nonpunitive,
objective, and impartial way. The fine line for the therapist to navigate is to accept
the patient’s perception while helping him or her to identify and posit alternative
possibilities. Rather than arguing and engaging in confrontational disputes, the ther-
apist can use the Socratic dialogue to help the patient to feel heard while encouraged
to change without simply yielding to the therapist’s views and possible biases.
A fifth factor involves communicating empathy. The use of empathy not only builds
the working relationship, but also models an interpersonal skill for the patient. This
may involve verbalizing how upset a patient might feel, elaborating on some unspoken
or unrecognized conflict, trying to take into account the patient’s perspective, or
accepting nonjudgmentally what the patient has done.
The therapist’s empathic skill will never be more needed than when the patient
exhibits anger or hostility, especially if it is toward the therapist. If the therapist has
difficulty accepting the patient’s anger, then the therapist can ask the patient to explore
how he or she feels, what he or she gains from the expressions of anger, and whether
the patient understands that the therapist may not like being the target of anger and
hostility. If the extent of the anger overwhelms the therapist, then a referral to another
therapist may be essential rather than trying to “tough it out.” In addition, if this is
a frequent experience, then the therapist might seek consultation and even therapy.
Sixth, therapists should avoid exclamations of shock and surprise. Patients may
experience many people, places, and things that are beyond the experience of the
therapist. The therapist needs to take a step back and not respond in a way that
might convey a negative perception, perspective, or bias. The therapist can ask for
clarification. Using Rogers’s point, if there are activities that are harmful to self or
others, the therapist must act quickly and directly to intervene.
A seventh factor is avoiding making promises that may not (or cannot) be kept.
Promises of “cure,” “never having problems,” or “a perfect effect of therapy” must
be avoided. Focusing on the problem list and using homework experiments to try out
new skills and perfect others can help to avoid making promises in the first place.
Giving in to therapeutic narcissism is the eighth therapeutic relationship-buster. It
can be very tempting to accept the patient’s positive comments about how wonderful
the therapy has been and how the therapist should be nominated for psychological
sainthood (as in the case of the “poisoned lawyer” above). Therapeutic narcissism
involves therapists believing that (a) they are smarter than they are, (b) they are more
skilled than they are, (c) charisma is an adequate substitute for skill, (d) theoretical
grounding is unnecessary, (e) comments or interpretations to the patient must be
totally accepted by the patient or they are then interpreted as resistant, (f) their model
cannot or should not be challenged, (g) their model must be accepted as applicable
to all patients without question or modification, (h) calls for empirical support of
their therapeutic model must be resisted as unnecessary, (i) they have some “priestly”
function, and (j) whatever therapy they practice is the only true religion.
Ninth, therapists should avoid confrontation, debate, or sarcasm. Confrontational
statements may, with some patients, at some points be necessary, but should only be
used when the therapist’s countertransference is under control. Countertransference,
the therapist’s reaction to the patient’s reactions and responses, must also be used
for the good of the therapy and the patient and not become a source or rationale
for punishment. Countertransference can be viewed as several different responses.
There is a countertransference reaction which is a brief and transient experience in the
session; for example, the patient makes what might be seen as a thoughtless remark
that is not repeated and is not part of the patient’s usual style. Countertransference
stress involves a reaction to the patient that is longer-lived. The therapist might
be thinking about the patient’s comment(s) after the session. The phenomenon
of countertransference structure involves the therapist maintaining either ongoing
negative or positive reactions; for example, the therapist is informed that a particular
patient has canceled an appointment for the day and the therapist’s negative reactions
may be relief or joy. Alternately, if the patient is a favorite of the therapist, the reaction
might be disappointment. In the circumstances of countertransference neurosis, the
therapist steps over the bounds of ethical practice. Finally, there is what we term
the “reasonable person hypothesis.” This involves a reaction to a patient and his or
her behavior that would probably be one with which most reasonable persons would
agree; for example, that pedophilia can in no circumstances be acceptable.
Altering the Working Alliance
Alteration of the goals and foci of treatment requires a strong working knowledge
of the components (criteria) for various disorders, whether from the Diagnostic and
Statistical Manual of Mental Disorders (4th ed., text rev.; DSM-IV-TR; American
Psychiatric Association, 2000) or the International Statistical Classification of Diseases
(10th ed.; ICD-10; World Health Organization, 1992). For example, an individual
with a paranoid personality disorder would be reluctant or even find it impossible
to establish and maintain a relationship with the therapist inasmuch as his or her
typical schema includes ideas regarding the lack of trustworthiness of others, potential
damage or insult, or even death. Similarly, the individual with an avoidant style might
very much want a relationship but would be reluctant to move in the direction of a
relationship without unconditional guarantees of acceptance. Without a complete and
careful understanding of the multiple criteria which become the building blocks of a
diagnosis, the therapist may lose out on opportunities for structuring and enhancing
the therapeutic work. For example, a 38-year-old woman was referred by a colleague
who, because of time constraints, had to limit her practice. In the transfer phone
call, the former therapist described the woman as “very borderline.” When the new
therapist saw the patient for the first session he engaged her in a dialogue that
focused on those characteristics that are most typical (according to DSM-IV-TR). For
example, “Do you often feel yourself losing, or close to losing control of what you
say or do?” The patient agreed that that was a frequent experience. The therapist
followed that with, “I would think that that would sometimes cause you difficulty
or problems. Am I hearing you accurately?” At the end of the session, the patient
commented in her review of the session that she felt very comfortable with the new
therapist. “Why was that?” inquired the therapist. “Well,” she replied, “you seemed
to understand me really well. You were familiar with my type of problem and you
kept asking if what you thought was accurate. That felt really good.”
Conversely, the patient with a dependent personality disorder may seek (or even
demand) a stronger relationship because of his or her schema regarding the need for
a strong “other” person upon whom he or she can lean and depend. The patient
with a narcissistic personality may be best served by maintaining a stronger alliance.
The patient may seek to build a personal relationship rather than be focused on the
therapeutic work. For example, a patient may invite the therapist out for a drink or for
dinner, even offering his home as a venue for the therapy. With both of these patient
types the therapist must establish and maintain firm ground rules and boundaries. It
is best that these are established early in the therapy so that the boundaries and/or
limits are not seen as punitive. Therapists are sometimes reluctant to set and maintain
limits because of the fear that limit-setting will injure the therapeutic relationship. To
the contrary, patients are most comfortable when they know the parameters and rules
of the therapeutic engagement. They may not like the rules or agree with them, but
they know what will be expected of them. For example, Karen, a 38-year-old woman,
arrived at her first therapy session and informed the therapist that what she needed
was “reparenting.” She had seen this on television and researched it on the Internet.
She needed, she said, to be held and cuddled by the therapist to make up for the
lack of physical contact from her parents. There was, she said, “Nothing sexual for
the therapist to worry about.” When the therapist set out some basic rules of therapy
that emphasized that the medium for the therapy was talk, not touching, the patient
reacted explosively. She left her chair and walked around the office shouting, “This is
what I need. You are supposed to give me what I need. I don’t care who hears me.
The whole clinic can hear what a terrible therapist you are.” The therapist was able
to calm her down by using the rules that were just set: talking, not yelling; working
together by talking rather than threats; no touching.
After about a year of weekly sessions (during which there were infrequent outbursts)
Karen decided to change careers. She decided to become a social worker and help
others by doing therapy to ease their pain. The therapy work focused on Karen’s
negative view that no school of social work would accept her, she was unfit to be a
helper, she was too crazy to be a help to anyone, and so on. Karen was helped to
use her basic therapy tools to respond to these negative ideas. She applied to two
local schools and was awaiting their response. One day the therapist went to get
Karen from the waiting room for her session. She was very excited and said, “Guess
what? I was accepted to the social work school here at the university.” The therapist
extended his hand and congratulated her. She shook his hand and thanked him. At
the beginning of the session Karen was upset and was yelling at the therapist: “When I
needed touching you said that touching was out. Touching was forbidden in therapy.
When I needed it you wouldn’t do it. Now I don’t need it and now you are initiating
touching.” The therapist did, indeed, break his own rule without any renegotiation.
He apologized. While the reader may see this as minor, the reader does not view the
situation through the eyes and experience of Karen. She was right. The boundary was
not maintained by the therapist.
Process and Content of Therapy
One of the hallmarks of the cognitive behavioral models of therapy is that the therapy
must be crafted and customized for each patient. One size does not fit all. It is
essential for the therapist to work collaboratively with the patient to identify and
choose targets for therapeutic work and possible change. The therapist must be aware
that the therapeutic alliance subsumes both the process of therapy and the content
of therapy, which may differ. The goals of the therapy (process or content), though
related, must be conceptualized and addressed separately. The process of therapy
would include the structure of the therapy, the interaction between therapist and
patient, and the acquisition of particular and specific therapy-enhancing skills. The
content of therapy involves dealing with the reasons for the patient seeking therapy,
the application of skills and insights to the patient’s life, and the amelioration of
dysfunction or maladaptive behavior.
The elements of the therapeutic relationship involve the therapist being able to
nurture the interpersonal connection (rapport), as needed. This will involve setting
a stage for emotional exploration within a safe and accepting frame. A treatment
intervention may be far more available and usable if it is aimed toward a point of
emotional relevance—that is, toward what the patient is experiencing at the moment,
not what the patient experienced in the last session, at some time in his or her previous
life experience, or outside of the session. Not every patient needs, is interested in, or
wants to deal with emotional issues inasmuch as he or she is unskilled in coping with
emotions, or may be frightened by the breadth, content, and unfamiliarity of his or
her emotions. To help the patient increase his or her emotional vocabulary therapists
sometimes employ a chart that has on it a number of faces, each purporting to express
a different emotion. Some charts contain 50 or more faces. While the goal is to
help the patient (and the therapist) to identify felt emotions, these extensive charts
are more often confusing. In establishing the relationship, the use of happy, angry,
fearful, sad, or neutral may offer to the patient a context for expressing emotion.
These basic emotions can then be further specified in the therapy. For patients with
powerful anxiety disorders, the fear is often connected to imminent death. It is in this
vein that creativity, inspiration, and artistry abound.
For example, the obsessive patient may appear to be distanced from his or her
emotions. Such patients seem to live beside life as observers rather than acting in it,
and use language to fend off or avoid feelings rather than to express them. For this
patient, the use of emotionally laden imagery offers a wake-up call and introduction
to his or her emotional reactions. Consistent with the creativity of the therapist, the
therapeutic stance within the session will involve the therapist playing different roles.
For the frightened patient, a calm voice and clear boundaries may help the patient to
feel safer. For the patient with emotional dyscontrol, the therapist may also need to
be a patient-whisperer; that is, to be able to maintain boundaries and offer a safe and
calm setting where thoughts can be explored, feelings expressed, and systemic change
and behavioral control discussed. For the patient who is in need of more color and
verve, the use of metaphorical language that is sensory-rich, along with a varying of
voice quality, can provide life and color to the therapy.
Both depression and anxiety can be contagious. The therapist must take care not to
“catch” the disorder from the patient. In trying to mirror the patient’s affective state,
the therapist may find him- or herself feeling demoralized and thinking that possibly
the patient is right. Things are, indeed, as hopeless as the patient has described them,
and solutions, if any can be found, will likely not work. While feeling the patient’s
pain, the therapist has to be clear that one does not have to be Pollyanna or Mary
Poppins to work to move the patient from a depressive view toward a less depressive
view. Within the therapeutic work the therapist can try using a lighter tone with
care not to be interpreted by the patient as making light of his or her suffering. The
therapist must be willing to describe the patient’s depressive behavior and affect. This
may give feedback that the patient may not be able to obtain elsewhere and limit his
or her need to be even more depressed so as to “prove” how badly off he or she is.
When the emotion appears to be bottled up with a reluctance or an inability to
express negative emotion, the therapist may make affect-laden statements (e.g., “You
must be furious”). In this way the therapist is able to voice the patient’s anger or
rage, vicariously. For example, Jane, a 43-year-old woman, had responded rather
minimally in therapy. Her responses were monosyllabic and she did not follow up on
any statements that she made. She remained emotionally neutral, to that point. She
reacted to the therapist expressing the anger that she had toward a former boyfriend
by crying. When asked by the therapist what she was thinking and feeling, she spoke
of being scared of her anger, of thinking that once she acknowledged her anger she
would become out of control and be angry all of the time, that her anger would
bring even worse consequences upon her than her depression, and that anger was
considered as “bad behavior.” This response opened the therapy work to discuss
Jane’s thoughts and schemas about anger, expressions of anger, fear of anger, and
consequential thinking. She could identify her mother’s words and tone as that which
she used on herself. In this way, the therapeutic bond demonstrated empathy. The
therapist could feel what the patient left unsaid and became the patient’s voice,
loaning the patient the words and affect. The therapist cannot simply debate and
dismiss the schema.
For isolated and depressed patients, the therapist must walk a very fine line between
trespassing on the patient’s solitude (not necessarily his or her loneliness) and trying
to have the patient cross the line to be willing to interact with others. For some
patients the therapist may choose to use broader statements that are more general
to people rather than to this person (e.g., “Many people see this as … ”), or even
be somewhat tentative (e.g., “Some folks may view this as … ”). In all of this, the
therapist must be aware of his or her personal values. With acting-out patients, the
results of their actions are usually so loud and can be so all-consuming that they
drown out the reflective part of their psyche. Such patients do not see or understand
the potential consequences of their actions nor can they see the situation in which
they find themselves. Therefore, explanations are often not effective, inasmuch as the
patient cannot “hear” them. With these patients a more confrontational style may be
needed. Confrontation must only be used when countertransference is under control.
The therapist must be able to be aware of and attuned to his or her own anger or
negative reactions to the patient’s behavior.
This is often seen in treating individuals with narcissistic personality disorder. These
individuals become the patients that therapists love to hate. When therapists get
together in social situations and talk about their case loads, the narcissistic patient
is often the source of many shared clinical experiences. For example, Sid was a 45-
year-old accountant who came to therapy at the request of his “poor, addled wife.”
When Sid entered the therapist’s office for his first session he ran his fingertips over
a credenza as if looking for dust. He surveyed the office and said, “This office is
furnished so poorly. Doesn’t the university care how it looks? For what I am paying
you I would expect a far nicer office. I could give you the name of my office decorator
but I don’t think that that would help.” All of this was said before sitting down for
the initial session. How does the therapist respond? Does the therapist express his or
her reactions? “That was a totally inappropriate thing to say”; or “Why would you say
that?”; or “If you don’t like the way this office is furnished, you can just leave now”;
or “Yeah. The offices are all furnished with university cheapo furniture”; or simply
smile and say “Uh huh”? The therapist’s initial reaction to what must be viewed as
a test of the therapeutic relationship, “How far can this person be pushed?” may set
the stage for the therapeutic relationship and for the therapy.
One of the first steps in establishing a therapeutic collaboration is the task of
agreeing on goals for therapy. Since the narcissistic patient is not likely to present
“becoming less narcissistic” or even “getting along better with others” as goals for
therapy, it is important for the therapist to focus on clarifying and operationalizing the
patient’s goals rather than on trying to convince the patient to work to change his or
her narcissism. After the initial assessment, the building of a collaborative relationship
that focuses on the alliance is essential since participation in psychotherapy requires
that the narcissistic client be asked to do things which he or she has had great difficulty
doing, or has never had to do, or has never learned to do. These tasks might include
tolerating frustration, enduring anxiety without the usually employed strategies such
as avoidance, alcohol or drug abuse, or abusive behavior toward others, and instead
choosing to talk out rather than act out ideas, thoughts, and feelings. Collaboration
can be difficult both because of the characteristics of the patient and the reactions the
patient elicits from the therapist. Within the therapeutic alliance, the therapist must be
willing and able to draw a “line in the sand” that cannot be crossed. By virtue of the
diagnosis, narcissistic individuals may need special handling or grooming to motivate
them for treatment. The therapist must be sensitive to the patient’s “hot-buttons” and
tread very carefully to avoid an empathic (bond) or therapeutic (alliance) rupture. The
therapist must be able to bring the patient’s grandiosity to the fore without insulting
or humiliating the patient. This may be criticized as too “supportive” and not reality-
based; that is, some people may think it is better to make them change, because
what they are doing is wrong/bad/improper. Intervention is difficult inasmuch as the
behavior and style are ego-syntonic. Probably the easiest approach is to inquire of the
patient what would be in his or her best interest, presently, near-term, and long-term.
The therapeutic alliance with these patients is focused on helping them get more of
what they want but without hurting themselves or others in the process. Once the
schemas are identified, this must be followed by a re-constructive (or constructive)
strategy that is built into the working alliance. We must recognize that the therapeutic
collaboration is never evenly balanced, that is, 50/50. For some patients and in some
patient therapeutic interactions that collaboration may be 80/20, or 20/80. The old
saying about the therapist not working harder in therapy than the patient was posited
by a therapist who did not see many difficult patients (or any adolescents).
Imagery can be used to avoid therapy ruptures where the patient may leave therapy
or become so resistant to the process or persona of the therapist that there can be little
or no progress. Using what Hammer (1990) terms the poetic style, the use of imagery
offers an economy of words, a directness of meaning, a basic pictorial presentation,
high affective valence, and density of affect. Images and metaphors can come from
fairy tales and myths, or from everyday experience. Images must be simple and easily
understood at a concrete operational level. Images can be multisensory, and culturally
related images may be of special value. For example, Karl, aged 30, was working to
maintain his sobriety after many years of alcohol and heroin. He went to Alcoholics
Anonymous meetings three times a week, but had frequent slips and returned to using
heroin. When asked why this occurred, Karl said that he had friends who came over
to his apartment and would offer him a “taste” of the latest import. This would get
him using once again. After several therapeutic and systemic interventions (calls to
his sponsor) went either unused or were unsuccessful, Karl was feeling and expressing
hopelessness about his ever being able to be sober. The therapist used the story of the
three pigs. The first built a house of straw because straw was light and easy to use, and
the house could be built quickly. The house was, of course, blown down by the Big
Bad Wolf. The second pig built a house of sticks because sticks were light and easy to
use, and the house could be built quickly. Again, the Big Bad Wolf huffed and puffed
and blew the house down. The third pig built a house of brick and stone which was
a much harder job, and took more time and effort. The huffing and puffing of the
wolf had no effect on the brick and stone house. The therapist then asked Karl what
was the moral of the story. At first he did not understand the question. The therapist
explained that Karl’s sobriety was, up to that point, one of straw or sticks. At that
point Karl interjected that to be safe, he had to build a sobriety of bricks and stone.
Both the alliance and the bond were advanced in that Karl saw that the therapist
understood the problem and offered a solution. The caveat is that the patient must
understand the therapeutic references and metaphors.
Humor can add to the therapeutic relationship in several ways. It can be used
for evaluating and testing the patient’s “mirth” response. In the case of depressed
patients there may appear to be little life behind their eyes. Humor can be used to
bypass emotional or intellectual stricture, to make a point, or to ease the patient’s
anxiety or discomfort. Freud wrote on the use of humor and warned about the need
for a judicious hand in using humor as a therapeutic tool. Key for Freud was to make
sure that the therapist has his or her countertransference under control so that the
humor is not negative, insulting, or mocking. A danger is that the therapist may
be discomforted by the tone and climate of the therapy and use humor as a form
of tension relief for him- or herself. At some times, for some patients, maintaining
tension allows it to be explored and tolerated.
Humor is, in many ways, a parallel to a therapeutic intervention. First, the setting
must be explicated. Second, the basic premise must be clarified. Third, the characters
or characterizations are presented. Fourth, an event or series of circumstances occurs.
Fifth, there is an inherent tension to the situation. Sixth, there is a “punch line” that
feeds off the tension and serves a relief. Seventh, there are truths or a moral to the
story. The stories or humor must be well within the cultural mores of the patient,
of sufficient value to use valuable session time, and serve as a shortcut to insight and
understanding. To avoid having the patient see him- or herself as the butt of a joke
it is far better for the therapist to place him- or herself as the pivot person in the
joke. For example, Ellen, aged 52, kept waiting for the opportune time to end her
marriage of 30 years. She had wanted to leave the marriage for the past 20 years but
had maintained that life events had precluded her leaving. Her husband was verbally
abusive, at times had been sexually abusive, had had several affairs, and refused to
let her work, making her totally dependent on him for money. Her therapist told
her the following story: “A couple came in to see me for marital counseling. They
wanted a divorce. This, in and of itself, was not unusual. I see many couples wanting
to end a marriage. What was notable was that the man was 92 and his wife was 90.
They had been married for 70 years. They described a marriage very much like yours.
When I asked them why they had waited so long to seek a divorce they said that
there were always life events that intervened. They were waiting until the children
died so that they would not hurt the children by a divorce.” Ellen began to laugh
and then began to cry. After several minutes Ellen said to the therapist that she
was now ready to talk about a divorce. She would not have to wait for the children
to die.
Linehan (1994) trains therapists to use humor, believing that humor can help
the therapist deal with the difficult patients with whom she has specialized. Ellis
(1977a, 1977b, 1995) used humor as a relationship-building tool. He believed that
many patients took themselves too seriously so he wrote hundreds of songs to help
patients see the humor in their life situations. However, the use of humor requires
the ability to tell and understand a joke. Not all people are equally equipped to use
humor.
Termination
A basic tenet of CBT is that termination begins with the first session. The therapist
and the patient have their view of the endgame in therapy. What is it that patients
want to accomplish? What general and specific goals are identified? What are the
skills necessary to accomplish the goals? What is the time frame for meeting the
goals? What benchmarks will be used for short-term, mid-term, and long-term goal
accomplishment? Davis (2008) describes the basic and advanced issues related to
termination. Termination must be viewed in two respects, bringing closure both to
the therapeutic alliance and to the therapeutic bond. Both must be addressed. Reik
(1965), in his classic Listening with the third ear, described his emotional leave-taking
from Freud who had been Reik’s teacher, mentor, and friend. Both knew that they
would likely never see each other again. To ease the moment, Freud said, “People
do not have to stay together to be together.” It was on this note that Reik left. The
goal of therapy and the role of the therapist is to equip the patient with the skills and
motivation to deal with the range of life problems.
Regarding the alliance, patients often experience the internalization of the thera-
pist’s voice along with other voices that they have acquired over their life experience.
The question they must ask is, What would my therapist say? How would he or she
react to my present dilemma? What tools can I bring to bear on these problems?
How can I best solve this? In some cases, a follow-up visit, a scheduled tune-up, or
a periodic review is helpful. The bond is, for some patients, much harder to end.
The therapist may be the first person in their lives who has truly “heard” them.
The therapist may have been their support or major source of encouragement when
discouragement was their main experience. Similarly, the bond may be difficult for
the therapist to end. Therapists have made the decision, by choosing this career, to
be a supporter, a port in the storm, and a voice of reason, when necessary. Therapists
cannot do this without an investment of their own. It is not unlike parents who may
have strong reactions to helping their child pack the car and leave for college, knowing
that the interaction within the family will never be the same as it was prior to that
moment (phones, texting, and Skype notwithstanding). The danger for the therapist
is to avoid termination more for the therapist’s needs than for the patient’s. Therapists
continue to think of their former patients and enter them into the scrapbook of their
professional career, whether the patient represented the good, the bad, or the ugly.
Summary
Unlike the negative characterization of the na ı̈ve or critic, CBT is firmly based in
the idea that the therapeutic relationship is an important element in successful and
effective treatment. The nature, quality, process, and content of the relationship will
differ for each patient, and is based on patient need, the goals of the therapy, the
skills of the patient, the skills of the therapist, the time frame for the therapy, and
the venue of the therapy. The therapeutic relationship can be broken down to the
elements of the therapeutic bond which is the emotional connection between patient
and therapist, and the therapeutic alliance which is the contract and goals for therapy.
It is essential that the therapist master the basics of rapport and relationship building,
and to use the goal-setting strategies that are among the major strengths of the CBT
model.
References
American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders
(4th ed., text rev.). Washington, DC: Author.
Bordin, E. S. (1979). The generalizability of the psychoanalytic concept of the working alliance.
Psychotherapy: Theory, Research, & Practice, 16, 252–260.
Davis, D. D. (2008). Terminating therapy: A professional guide to ending on a positive note.
Hoboken, NJ: John Wiley & Sons, Inc.
Ellis, A. (1977a). Fun as psychotherapy. Rational Living, 12, 2–6.
Ellis, A. (1977b). A garland of rational songs. New York, NY: Albert Ellis Institute.
Ellis, A. (1995). AABT Archive Series Interview. New York, NY: Association for Advancement
of Behavior Therapy.
Frank, J. (1991). Persuasion and healing (3rd ed.). Baltimore, MD: Johns Hopkins University
Press.
Freeman, A., & McCloskey, R. D. (2003). Impediments to psychotherapy. In R. L. Leahy (Ed.),
Roadblocks in cognitive-behavioral therapy: Transforming challenges into opportunities for
change (pp. 24–48). New York, NY: Guilford Press.
Gilbert, P., & Leahy, R. L. (Eds.). (2009). The therapeutic relationship in the cognitive
behavioural therapies. London, England: Routledge.
Hammer, E. F. (1990). Reaching the affect: Style in the psychodynamic therapies. Northvale, NJ:
Jason Aronson.
Hardy, G., Cahill, J., & Barkham, M. (2009). Active ingredients of the therapeutic relationship
that promote client change. In P. Gilbert and R. L. Leahy (Eds.), The therapeutic rela-
tionship in the cognitive behavioural therapies (pp. 24–42). London, England: Routledge.
Krupnick, J. L., Stotsky, S. M., Simmens, S., Moyer, J., Watkins, J., Elkin, I., & Pilkonis, P.
A. (1998). The role of the therapeutic alliance in psychotherapy and pharmacotherapy
outcome: Findings in the National Institute of Mental Health Treatment of Depression
Collaborative Research Program. Journal of Consulting and Clinical Psychology, 64,
532–539.
Linehan, M. (1994). Cognitive behavioral treatment of borderline personality disorder. New
York, NY: Guilford Press.
Merriam-Webster Dictionary. (2010). www.merriam-webster.com
Reik, T. (1965). Listening with the third ear. New York, NY: Doubleday Anchor.
Rogers, C. (1961). On becoming a person. London, England: Constable & Robinson.
Sullivan, H. S. (1953). The collected works of Harry Stack Sullivan. New York, NY: W.W.
Norton & Co.
Wolberg, L. R. (1954). The technique of psychotherapy. New York, NY: Grune & Stratton.
World Health Organization. (1992). International statistical classification of diseases and related
health problems (10th ed.). Geneva, Switzerland: Author.
2
Cognitive Restructuring
David A. Clark
University of New Brunswick, Canada
A. T. Beck’s cognitive therapy (CT) has made a substantial contribution to current

evidence-based cognitive behavioral therapy (CBT) for a variety of psychiatric dis-
orders, most notably depression, anxiety, personality disorders, and, more recently,
psychosis. A. T. Beck’s (1987, 1996) cognitive model postulates that biased self-
relevant thoughts, evaluations, and beliefs are key contributors to the development
and persistence of psychopathological states. The biased thoughts and appraisals that
characterize psychopathology are derived from maladaptive mental representations
of reality stored in memory structures called schemas. Schematic content or beliefs
organize and guide the selection, encoding, and retrieval of information. Given their
central role as progenitors of a biased and maladaptive information processing appa-
ratus, the cognitive model considers schematic change essential for significant and
enduring symptom reduction (A. T. Beck, Rush, Shaw, & Emery, 1979; D. A. Clark,
Beck, & Alford, 1999).
The term cognitive restructuring has been used to describe the schematic change
mechanism articulated in CT. It refers to a structured, collaborative therapeutic
approach in which distressed individuals are taught how to identify, evaluate, and
modify the faulty thoughts, evaluations, and beliefs that are considered responsible
for their psychological disturbance (Burns & Beck, 1978; Dobson & Dozois, 2010;
Hollon & Dimidjian, 2009). In their first seminal treatment manual, Beck and
associates emphasized thought self-monitoring, reality testing, external reattribution,
evidence gathering, examining consequences, cost/benefit analysis, generating alter-
natives, and behavioral assignments as key interventions for inducing cognitive change
(A. T. Beck et al., 1979). However, A. T. Beck did not refer to this suite of interven-
tions as cognitive restructuring until the publication of his second treatment manual
for anxiety disorders (A. T. Beck & Emery, 1985). Since then, various descriptions of

Edited by Stefan G. Hofmann. Volume I edited by David Dozois.
DOI: 10.1002/9781118528563.wbcbt02
CT have referred to the cognitive interventions utilized to achieve schematic change

as cognitive restructuring (e.g., D. A. Clark & Beck, 2010; Dobson & Dobson, 2009).
In this chapter, cognitive restructuring (CR) is defined as structured, goal-directed,
and collaborative intervention strategies that focus on the exploration, evaluation,
and substitution of the maladaptive thoughts, appraisals, and beliefs that maintain
psychological disturbance. Within this definition both cognitive and experiential or
behavioral interventions are considered CR as long as the intention is cognitive or
schematic change. The remainder of the chapter provides an in-depth examination of
CR. I begin with a conceptual analysis of schemas and the three key components of
CR. This is followed by a review of empirical research that has attempted to isolate
the specific therapeutic efficacy of CR. The chapter concludes with a discussion of
critical research issues pertinent to CR.
The Nature of Cognitive Restructuring
Defining Schematic Change

Since CR is defined in terms of schematic change, a conceptualization of CR is rooted
in the definition of schemas. In A. T. Beck’s cognitive model schemas are meaning-
making constructions of the cognitive organization that have content, structure, and
function (A. T. Beck, 1964). They embody top-down processing in which schema-
driven processes select, organize, and prioritize human cognition. In essence schemas
have an executive function, directing information-processing resources so that
schema-congruent information has priority over schema-incongruent information.
In depression, for example, negative self-referent schemas of loss, failure, rejection,
and hopelessness predominate. As a result the cognitive apparatus of the person
with clinical depression is oriented toward processing schema-congruent negative
self-referent information.
A key goal of CR, then, is to reverse this maladaptive schema-congruent pro-
cessing bias by questioning the automatic acceptance of negative schema-congruent
information and encouraging assimilation of more adaptive schema-incongruent data.
Traditionally, a change in belief ratings is considered a measure of the client’s shift
from maladaptive schematic processing to more normal, adaptive schema activation
(A. T. Beck et al., 1979). Thus a depressed client, in the course of therapy, demon-
strates a reversal in depressotypic schema-congruent processing bias when he or she
professes diminished belief in the view “I am a complete loser who will never amount
to anything,” and greater belief in the idea “I have had some failures in my life but
also many successes; this means I can learn from my failures and forge a brighter
future for myself.” However, it is not clear how well this indicator of change applies to
CR more generally. Belief ratings may be a less sensitive indicator of cognitive change
for some disorders, such as anxiety, and reversal of the dominance of maladaptive
schema-congruent processing is far from a monotonic, linear decline in absolute
influence, as any practitioner can attest. Rather, clients often exhibit a more fluctuat-
ing pattern of shifting schematic processing that is influenced by circumstances and
even mood state, with symptom improvement associated with an eventual dominance
Cognitive Restructuring 3
of adaptive schematic processing over the maladaptive disorder-related schemas. It

must also be recognized that long-term dominance of maladaptive schema-congruent
processing in distressed individuals poses special challenges for CR because these
beliefs will always seem more intuitive and inherently plausible to the individual. The
more entrenched the maladaptive schematic organization, the less responsive they are
to initial CR efforts.
As well as executive function, schemas also have structural characteristics. A. T.
Beck (1967) noted that maladaptive schemas are inflexible, closed, impermeable, and
relatively concrete systems. Most often they are rooted in negative, or even adverse,
early childhood experiences and are subsequently reinforced and strengthened by
congruent life events in adolescence and adulthood. For example, the person with an
obsessive-compulsive personality disorder will have experiences that appear to confirm
his or her belief that “It is critical that I pay close attention to detail in all that I do
in order to avoid making mistakes.” With repeated activation and reconfirmation, the
maladaptive schemas attain a higher degree of interrelatedness so they gain greater
capability of dominating the information processing system (Segal, 1988). Various
studies have investigated schematic structure in depression. Using a grid task to assess
schematic structure, Dozois and Dobson (2001) found that a clinically depressed
group had more interconnectedness for negative self-referent adjectives and less
interconnectedness for positive adjectives than nonpsychiatric controls, although the
anxious and depressed groups differed primarily in their organization of positive,
rather than negative, schemas. In a later study, Dozois (2007) found that clinically
depressed individuals may exhibit more interrelatedness of negative interpersonal but
not achievement schemas that endures even with remission of the depressive state.
The very structure of psychopathological schemas and their inherent prepotent
nature makes schematic change especially difficult to achieve. In the course of con-
ducting CR, most clients will have great difficulty recognizing schema-incongruent
information, questioning their intuitively based maladaptive schemas, and accepting
more adaptive beliefs. For the individual with health anxiety, the automatic maladap-
tive interpretation “What if the red spot on my arm is cancerous?” will feel more
intuitively plausible because of underlying rigid, highly interrelated, and generalized
dysfunctional schemas about death, disease, and vulnerability. Cognitive therapists
using CR, then, must build into their intervention plan recognition of the relative
impermeability of psychopathological schemas.
It is schematic content that is the primary focus of CR. The content or proposi-
tional elements of maladaptive schemas consist of negative idiosyncratic generalized
attitudes, beliefs, and assumptions about the self, personal world, future, achievement,
and interpersonal relations (Dozois & Beck, 2008; Ingram & Kendall, 1986). A. T.
Beck (1976, 1987) proposed that different psychopathological conditions, as well as
normal emotion states, are characterized by their own unique belief content. Known
as the content-specificity hypothesis (D. A. Clark et al., 1999), the cognitive model
proposes that depression is characterized by themes of loss and deprivation, anxiety by
threat and vulnerability, each of the personality disorders by disorder-specific content,
and psychosis by misinterpretation of subjective experience. This disorder-specific
schematic content will be easily accessed by a wide range of triggering cues and readily
available to guide information processing. Thus, the goal of CR is to modify schematic
organization or interconnectedness, reduce the accessibility or activation threshold of

maladaptive schematic content, and strengthen access to competing, more adaptive
beliefs and assumptions.
In sum, the schematic change achieved by CR involves two fundamental processes.
After identifying the key disorder-relevant schemas, the cognitive behavioral therapist
utilizes a series of cognitive interventions to reduce the activation threshold, accessibil-
ity, and availability of the maladaptive schemas. Over time and with repeated effortful
evaluation, the processing priority and interconnectedness of the maladaptive schemas
are weakened and schema-congruent processing becomes less automatic. Second, CR
also involves the process of learning to substitute more normal, adaptive schemas
about the self, world, and future. Lowering the activation threshold and strength-
ening the accessibility and acceptance of competing adaptive schemas that counter
disorder-related beliefs are critical objectives of CR. In the end, CR seeks to elevate
normal adaptive schematic processing through evidence-based thinking so it comes
to predominate the information processing system. It is through this process that CR
achieves enduring symptomatic change and remission of the psychopathological state.
Key Components of Cognitive Restructuring

In order to achieve schematic change, an effective CR program has three critical
components. Each of these components is necessary for the success of CR. If any
component is missing, the intervention would not constitute CR but some other
form of intervention. Each component may consist of various intervention strategies,
but together collaborative empiricism, verbal intervention, and empirical hypothesis-
testing constitute the therapeutic process involved in CR. The following provides an
explanation and illustration of these three central elements of CR.
Collaborative empiricism. A. T. Beck and colleagues (A. T. Beck et al., 1979; A. T.

Beck & Emery, 1985) introduced the term “collaborative empiricism” to describe the
therapeutic relationship adopted in CR. The concept has been refined and elaborated
by subsequent clinical researchers and is now considered a critical element in the
effectiveness of CT or CBT (J. S. Beck, 2011; Kuyken, Padesky, & Dudley, 2009;
Tee & Kazantzis, 2011). In essence, collaborative empiricism involves the client and
therapist sharing their respective expertise in order to describe, explain, and help
resolve the client’s problems. In recognizing their respective contributions to the
therapeutic enterprise, the therapist as an expert in the human change process, and
the client as having the lived experience of the problem, work together on formulating
treatment goals, setting the session agenda, and negotiating homework assignments.
Therapist and client share equal responsibility for the direction of therapy, in which
the therapist frequently seeks feedback and ensures understanding from the client.
A strong therapeutic alliance and client engagement in the therapy process is a
necessary but not sufficient feature of effective CR. To achieve a collaborative atmo-
sphere, the therapist (a) educates the client on the CT model to establish an agreed
rationale for achieving change, (b) involves the client in identifying and prioritizing
treatment goals, (c) collaborates on setting the session agenda, (d) asks questions
and requests client feedback throughout the session, and (e) negotiates homework
assignments. This strong emphasis on mutual responsibility and joint involvement

in the therapeutic process ensures that CR does not become dictatorial, with the
therapist imposing ideas and direction on the client. An authoritarian, overly didactic,
and uncompromising therapist style will quickly undermine the effectiveness of CR.
Empiricism is another central feature of the therapeutic process in CR. The thera-
pist encourages the client to take an investigative, questioning approach to long-held
beliefs and attitudes. Throughout treatment, an emphasis is placed on observa-
tion, experiential evaluation, and learning (Kuyken et al., 2009). The therapist uses
Socratic questioning of the client’s past personal experiences to evaluate the validity of
maladaptive beliefs and to introduce the possibility of a more adaptive alternative per-
spective. In addition, experientially based exercises are formulated that can empirically
verify the veracity of the alternative belief and challenge the validity of maladaptive
schemas. The cognitive therapist frequently encourages the client to “test this with
your experience,” or “collect some evidence and see what can be learned.” Through-
out each session the therapist places a strong emphasis on empiricism to achieve
schematic change. Tee and Kazantzis (2011) argue that effective collaborative empiri-
cism will encourage clients more readily to attribute behavioral change to their own
efforts rather than external forces or the skills of the therapist. This self-determined
attribution should result in better and more persistent treatment outcomes.
The importance of collaborative empiricism is especially acute when a therapeutic
impasse arises. This can often happen in the treatment of the anxiety disorders,
for example. Most clients seeking CBT for anxiety desire immediate relief from
their heightened subjective anxiety. For them the goal of treatment is quite clear;
the elimination of anxious feelings. However, CBT for anxiety involves exposure to
anxious situations, intentional elevation of subjective anxiety, and a greater acceptance
or tolerance of anxiety. In this case the client’s and therapist’s treatment objectives may
collide. A strong emphasis on collaborative empiricism will be critical for overcoming
these differences by helping the client identify and evaluate schemas that might
threaten the effectiveness of CR (D. A. Clark, in press).
Verbal interventions. Over the years cognitive behavioral researchers and practitioners
have proposed a number of verbal intervention strategies that can be used by therapists
directly to modify maladaptive schematic content. These strategies, which in many
respects are the essence of CR, are summarized in Table 2.1.
The first four strategies are the most common verbal interventions used in CR, first
introduced by A. T. Beck et al. (1979; A. T. Beck & Emery, 1985) in the original
CT treatment manuals and then later refined and elaborated by other cognitive
therapists (e.g., J. S. Beck, 2011; D. A. Clark & Beck, 2010, 2012; Dobson &
Dobson, 2009; Greenberger & Padesky, 1995; Wells, 1997; Wright & McCray,
2012). Evidence gathering, cost/benefit analysis, identifying cognitive errors, and
generating alternative explanations are such an integral part of CR that implementing
these verbal interventions is what most therapists think of as cognitive restructuring.
They are robust and versatile interventions that can be used in most clinical disorders.
Since these strategies are well described in the sources cited, I will confine my
comments to a few general observations.
Table 2.1 Verbal Intervention Strategies Employed in Cognitive Restructuring
Intervention strategy Description
1. Evidence Obtaining schema-congruent and -incongruent evidence from

gathering the client’s past and current experience that enables a more
balanced evaluation of schematic content.
2. Consequential Examining the immediate and long-term costs and benefits of
analysis continued acceptance of the maladaptive belief.
3. Cognitive bias Training clients in greater awareness of the cognitive biases
identification that operate when processing schema-relevant information
(e.g., dichotomous thinking, catastrophizing, mind reading,
magnification/minimization, etc.).
4. Generate Formulating a more adaptive conceptualization of the self or
alternative some aspect of personal experience that more accurately
represents external contingencies and that enhances the
client’s functional adaptation.
5. Normalization Reconceptualizing unwanted thoughts, feelings, and behavior
as deviations of normal human experience in order to
encourage greater acceptance and confidence in dealing with
schema-related subjective experience.
6. Decatastrophizing Developing a hypothetical account of a worst-case scenario,
evaluating its realistic and probable effects on quality of life,
and formulating a coping plan to deal with the catastrophe.
7. Problem solving Specifying a real-life problem, delineating the pros and cons of
various responses to the problem, selecting a course of
action, and evaluating the outcome.
8. Imaginal exposure Guiding the client in repeatedly and systematically generating
a schema-related unwanted intrusive thought, image, or
emotion in order to enhance client self-efficacy in dealing
with unacceptable emotions.
9. Distancing Teaching clients to take a “third party” or observer stance to
their unwanted thoughts and emotions; to react to their
subjective experience as if it belonged to another person.
10. Reframing or Focusing on current experience as a moment in time and
perspective situating it within a longer lifespan time frame or the totality
taking of one’s life experience.
11. Reattribution Identifying the external or situational causes of the client’s
difficulties in order to address exaggerated internal
attributions and self-blame.
12. Positivity Refocusing the client on positive, adaptive personal coping
reorientation experiences that provide schema-incongruent information.
In order to utilize any of these verbal interventions, clients must be willing to engage
in an evaluative process. That is, they must be willing at least to consider the possibility
that their maladaptive schematic thinking might be inaccurate, counterproductive, and
unrealistic. Of course, clients will be considerably invested in retaining their schematic
view of themselves and current circumstances, but there has to be a willingness at
least to consider alternative perspectives. Clients who insist that their maladaptive
beliefs are immutable facts will not be amenable to CR. Second, the therapist always
begins by inviting clients simply to examine and evaluate their thoughts and beliefs in
the light of empirical evidence, that is, their own personal experience. The therapist
refrains from cajoling, debating, or trying to convince the client of a more adaptive
alternative belief instead of clinging to the maladaptive schematic perspective. Rather,
clients are encouraged to generate an alternative view that provides the best fit with
“objective” external experience and would be associated with an improvement in
their emotional functioning. Third, effective CR will ensure an equal emphasis on
questioning the veracity of the maladaptive beliefs and evaluating the relevance of
a more adaptive alternative viewpoint. The objective of CR is to raise doubts in
the client’s mind about long-held maladaptive beliefs (e.g., “People will notice I’m
anxious and think there is something wrong with me”) and to consider the accuracy
and utility of an alternative perspective (e.g., “People might notice I’m a little anxious
but consider it unimportant”).
The remaining verbal interventions in Table 2.1 are more specific to particular
clinical disorders or client situations. Normalization, for example, is used frequently
in CR for anxiety in which clients are taught to view their distress as an extreme variant
of normal emotion rather than as a distinct and disconnected experience. A client with
health anxiety, for example, could be asked to describe other nonhealth situations in
which he or she felt anxious and yet coped with the emotion very well (e.g., a job
interview). The client could then be encouraged to think of his or her high anxiety
associated with an unexpected physical pain in the same way that he or she thought
of heightened anxiety during the job interview. In other words, the health anxiety
experience is normalized rather than being considered a unique human experience.
Likewise, distancing encourages the client to consider his or her thoughts and
beliefs from the perspective of another person, a third-party observer, such as a friend
or work colleague. The therapist can ask the client to talk about his or her thoughts
“as if they were the product of someone else’s mind.” For example, a cognitive
therapist might say to a client, “Imagine for a moment that your conviction, ‘I’ll be
alone and miserable the rest of my life’, is a belief expressed by a close friend. What
would you think about her perspective on life? What would you say to her as an
alternative way to view being single?” The goal of distancing is to teach the client to
take a more external, observer orientation to disturbing thoughts and beliefs.
Reframing or perspective taking encourages clients to consider their emotional
experience as a single moment in time and to view their current emotional state from
a longer time perspective. This not only helps clients to “live in the moment” rather
than the past or future, as emphasized in mindfulness cognitive therapy, but to view
the present as one moment in a longer lifespan continuum. For example, a client
with panic disorder who becomes completely immersed in his or her heightened
anxiety while in a supermarket is encouraged to view this experience as one instance
of hundreds of experiences that comprise a typical week. A person with social phobia
is asked to consider his or her current speech anxiety and fear of negative evaluation in
terms of the long-term consequences of this single anxious event, say, 10 years later.
Reattribution is an important verbal intervention for clients with excessive self-
blame and guilt, or what Abramson, Metalsky, and Alloy (1989) call hopelessness
depression. These individuals exhibit a negative inferential style in which they tend to
make global, stable, and negative self-referent attributions for the cause of distressing
life events. Findings from the Cognitive Vulnerability to Depression (CVD) Project
indicate that a negative inferential style and endorsement of dysfunctional beliefs
confers vulnerability to depression onset (Alloy, Abramson, Safford, & Gibb, 2006).
Given its prominence as a cognitive vulnerability factor, it is important that the
cognitive therapist helps clients become aware of their biased inferential style and
teaches them how to shift their focus onto external circumstances that may have
contributed to the negative life experience. A responsibility pie chart can be used to
teach the client how to distribute responsibility for a bad outcome among several causes
rather than narrowly attributing all blame to the self (see Greenberger & Padesky,
1995). Reattribution is an important verbal intervention in CT for depression and
was first described by A. T. Beck et al. (1979) in the depression treatment manual.
The final verbal strategy listed in Table 2.1 is positivity reorientation. This is a term
that refers to teaching clients more deeply to encode positive, adaptive experiences and
information that indicates the client is able to cope with strong unwanted feelings. In
most cases more positive, schema-incongruent information is not well processed and
so an important goal of CR is to teach clients intentionally and effortfully to select,
encode, and retrieve positive experiences. This therapeutic work is critical for reversing
the heightened sense of personal vulnerability and helplessness that is commonly seen
in the emotional disorders. A person with generalized anxiety disorder (GAD), for
example, would be taught to process past experiences when his or her worries did
not come true or when he or she successfully coped with a negative experience. The
later sessions in any trial of CBT should shift from a focus on refuting maladaptive
schemas to the processing of a positive orientation to self, world, and future. This will
strengthen the resourcefulness of clients and prepare them for treatment termination.
Empirical hypothesis-testing. CT has always taken a strong behavioral view from its
very inception and so empirical hypothesis-testing is a critical component of CR.
A. T. Beck et al. (1979) described the use of activity scheduling, mastery and pleasure
techniques, grade task assignment, behavioral rehearsal, assertiveness training, and
role playing in CT for depression. The use of these therapeutic strategies has been well
explained in the original treatment manual and numerous subsequent descriptions
of CT (e.g., J. S. Beck, 2011; Dobson & Dobson, 2009; Fennell, Bennett-Levy, &
Westbrook, 2004; Leahy, 2010; Wright & McCray, 2012). For the anxiety disorders,
behavioral experiments mainly take the form of systematic, graded exposure to
fear triggers along with prevention of escape, avoidance and safety, or compulsive
responses (A. T. Beck & Emery, 1985; D. A. Clark & Beck, 2010). Behavioral
interventions in CR for personality disorders often involve observations about the
real-life effects of long-held and exaggerated beliefs about the self or others, which
may be supplemented with experiential techniques such as reliving childhood events
and imagery (A. T. Beck, Freeman, Davis, & Associates, 2004). CR for psychosis again
involves setting up behavioral experiments that test the accuracy of clients’ erroneous
interpretations of reality and help them adopt more effective coping responses to
hallucinations, delusions, and thought disorder (A. T. Beck, Rector, Stolar, & Grant,
2009; Kingdon & Turkington, 2005).
Empirical hypothesis-testing can be defined as “planned experiential activities,

based on experimentation or observation, which are undertaken by patients in or
between cognitive therapy sessions” (Bennett-Levy et al., 2004, p. 8). The authors
note that behavioral experiments are derived from the cognitive case formulation and
are designed to test the validity of disorder-related schematic beliefs and contribute to
the construction of more adaptive schemas. The critical difference between traditional
behavior therapy and CT lies in the purpose of the behavioral intervention. In
standard behavior therapy the focus remains on behavior change, whereas CT utilizes
behavioral experiences as a means to achieve schematic restructuring. For this reason,
behavioral experimentation or empirical hypothesis-testing is a key element of CR.
When using behavioral experimentation in CR, there are seven steps that the ther-
apist follows in order to achieve schematic change (D. A. Clark & Beck, 2010; Rouf,
Fennell, Westbrook, Cooper, & Bennett-Levy, 2004). First, a rationale or purpose of
the behavioral experiment must be discussed with the client. The experiment will be
derived from the case formulation and is introduced as a way of testing a maladaptive
belief that contributes to the persistence of the disorder. For example, a student
with pathological worry may believe that worry about “failing an exam” is helpful
because it strengthens her motivation for studying. A behavioral experiment would
be introduced as a means of testing out the positive and negative consequences of
exam worry. The second step involves a clear statement of the maladaptive belief
and its alternative. In our case example, the therapist would record the maladaptive
belief as “worrying about my exams is actually helpful because I’ll study more” and
an alternative belief as “worrying about my exams is more detrimental than good
because it distracts me from studying.”
In the third step the therapist and client collaborate in designing the experiment.
It is important that clients feel invested in devising the experiment. Noncompliance
is likely higher when clients do not understand the rationale for the experiment or do
not feel responsible for its design and implementation. In the current experiment, the
client and therapist decided that the best way to test out the utility of the “exam worry
belief” was to pick two midterm exam courses. For one she would purposefully worry
about her performance for at least one hour per day, and for the other course she let
her worries come and go with the intention that less time would be spent worrying.
Specific details about the time, place, and responses associated with the exercise were
elaborated and recorded for the client’s benefit.
The fourth step involves a clear statement of the experimental hypothesis. In the
present example the client was to record study hours associated with both courses and
to rate her level of motivation to study. If worry facilitated study behavior, the client
would record more study time for the “worry course,” whereas if worry interfered
with study, the client would record more study time for the “nonworry course.”
In the fifth step, the client conducts the experiment, usually as a between-session
homework assignment, and records the outcome. It is important that the therapist
write out details of where, when, and how to carry out the experiment so there
is no misunderstanding on what outcome constitutes evidence for or against the
maladaptive belief. It is often helpful to have clients predict beforehand the outcome
they expect from the behavioral activity. In addition, it is important that a written
record of the outcome is made so the therapist is able to review the outcome at the
next therapy session.
The sixth step involves consolidation of the results of the empirical hypothesis-
testing experiment at the subsequent session. The therapist explores with clients their
thoughts and feelings while conducting the experiment, and whether their experience
confirms the maladaptive belief or its alternative. In the present example the client
discovered that the more she worried about her course the less time she spent studying
that evening. On the other hand, letting go of her worries resulted in less worry time
and, surprisingly, more time spent studying the course material. The therapist was
able to use this experience to challenge the client’s belief that “worry motivates me
to study more.”
The final phase is to summarize the findings from the experiment and to draw out
the broader implications. It is important to emphasize how a maladaptive schema
can be modified in light of the findings from the behavioral experiment and how
schematic change will lead to treatment goals and ultimately symptom reduction. As
well, the outcome of a behavioral experiment should lead to further planning for the
next empirical hypothesis-testing experiment (Rouf et al., 2004). In this way each
behavioral experiment plays an important role in moving the client toward schematic
change and achieving significant symptom improvement.
Empirical Evidence for Cognitive Restructuring
Over the years there has been considerable interest in empirically testing the effective-
ness of CR in achieving symptom improvement. Many of these studies have attempted
to contrast “purely” behavioral interventions with “purely” cognitive interventions.
Unfortunately such comparisons are misleading because it can be difficult to ensure
external validity of the treatment conditions (Rodebaugh, Holaway, & Heimberg,
2004) and, as previously discussed, behavioral experiments are a key component of
CR. Stripping CR of its behavioral elements would be tantamount to testing the
effectiveness of fear hierarchies with some proxy to actual hierarchy exposure in real
life. Nevertheless, it is reasonable to ask whether an intervention that emphasizes
schematic change (i.e., CR) is more or less effective than an intervention that omits
reference to schemas (i.e., behavioral activation or exposure alone).
There are two types of psychotherapy process studies that bear on the effectiveness
of CR. The first is component analysis in which CR is compared with a non-
CR intervention. This design represented some of the earliest dismantling studies
that examined the incremental contribution of CR to symptom reduction. The
second is mediation analysis which examines whether cognitive or schema change
precedes symptom reduction. If CR is an effective intervention, one would expect that
schematic change should be a key mechanism in symptom improvement. Most studies
on cognitive mediation have examined changes across baseline, posttreatment, and
follow-up intervals, although a few studies have conducted a more refined analysis of
session-by-session changes in cognitions and symptoms. Another question addressed
by mediation research is whether cognitive change is specific to cognitive interventions
such as CR, or whether it is also evident in noncognitive treatments such as exposure

alone or pharmacotherapy.
Component Analysis
One of the earliest component studies compared behavioral activation (BA), automatic
thought modification (AT), and full CT in 152 individuals with major depression
randomly assigned to 12–20 sessions of treatment (Jacobson, Dobson, Truax, Addis,
& Koerner, 1996). CT was the only condition to focus specifically on identification
and modification of core beliefs, whereas BA primarily focused on behavioral change.
Analysis of outcome measures at posttreatment and 6-month follow-up revealed
no significant differences between treatment conditions. Moreover, none of the
treatments had a significant differential effect on specific cognitive or behavioral change
variables. That is, CT did not produce significantly more change in depressogenic
schemas nor did BA result in a significantly greater increase in mastery or pleasure
activities. The authors concluded that BA alone was equally effective to the full CT
treatment protocol. Given equivalence across treatment conditions, Jacobson and
colleagues questioned whether verbal interventions (i.e., CR) were necessary in the
treatment of depression and whether schematic change was as critical to depressive
symptom remission as proposed by Beck’s model.
A subsequent 2-year follow-up revealed that all three treatment conditions were
equally effective in preventing depressive relapse (Gortner, Gollan, Dobson, &
Jacobson, 1998). Again the authors concluded that their findings raised questions
about the validity of the cognitive model and more specifically the clinical utility
of verbal interventions such as CR. In other words, it would appear that schematic
change is not necessary for long-term depressive symptom remission and prevention
of relapse. However, a significant limitation is the one-sided evaluation of the additive
effects of CR without also testing the additive effects of BA. In other words, the
finding indicated that CR may not add significantly beyond the therapeutic benefits
of BA, but we do not know whether BA would have incremental benefits beyond a
“purely” cognitive intervention. It is possible that the treatments are equally effica-
cious and their combination confers no added benefit. Nevertheless, the results do
suggest that one therapy (i.e., BA) is just as effective as another therapy (i.e., CT),
and the findings call into question the necessity of CR in the treatment of depression.
A more recent randomized controlled trial (RCT) based on the Jacobson studies
compared an expanded version of BA to standard CT, paroxetine alone, and an
8-week pill placebo condition in 241 adults with major depression (Dimidjian et al.,
2006). Cognitive interventions were excluded from the BA condition but the CT
condition presented the full range of CT interventions including CR and behavioral
activity scheduling. At posttreatment all three active treatments were equally effective
for depression in the mild to moderate range of severity, but BA and medication were
both significantly more effective in treating those with severe major depression than
was CT. However, a 2-year follow-up revealed that CT may have a more enduring
effect than BA, and both treatments were at least as efficacious over the long term as
maintaining individuals on antidepressant medication (Dobson et al., 2008).
What then can be concluded about the role of CR in the treatment of depression?
The dismantling studies have shown that CR is effective in the treatment of depression
but it is clearly not necessary for achieving immediate symptom improvement.
However, there is more recent evidence that CR might contribute to improved
endurance of depressive remission. Thus in terms of depression, CR is effective
but not superior to other “noncognitive” interventions, and it appears not to be
a necessary treatment component for effective psychotherapy of the acute phase of
major depression.
Several studies have compared the effectiveness of cognitive interventions and
exposure in the treatment of anxiety disorders. In studies of panic disorder, CR
alone can lead to a significant reduction in panic symptoms (Bouchard et al., 1996;
Margraf & Schneider, 1991; see Gould, Otto, & Pollack, 1995), although exposure
alone appears to be as effective as exposure plus CR (Bouchard et al., 1996; Öst,
Thulin, & Ramnerö, 2004; van den Hout, Arntz, & Hoekstra, 1994). However for
social anxiety, CR may play a more critical therapeutic role. In their RCT for social
anxiety, D. M. Clark et al. (2006) found that CT was more effective than exposure plus
applied relaxation at posttreatment and 3-month and 6-month follow-up. In an earlier
study, Mattick and Peters (1988) found that therapist-assisted exposure plus CR was
more effective than therapist-assisted exposure alone, although this finding was not
replicated in a later study (Feske & Chambless, 1995). Hofmann (2004) randomly
assigned 90 individuals with social anxiety to group CBT, exposure without cognitive
restructuring, or a wait list control. Although both active treatments produced similar
symptom improvement at posttreatment, only the CBT group exhibited continued
symptom improvement after treatment termination. Thus CR, with its focus on
the identification and modification of maladaptive beliefs, may be a key treatment
ingredient for social anxiety disorder.
Numerous studies have compared exposure and response prevention (ERP) with
a combination of ERP and CR in the treatment of obsessive-compulsive disorder
(OCD). Like other anxiety disorders, a CBT approach to treatment of obsessions and
compulsions that includes a strong CR component does lead to significant immediate
and long-term symptom reduction (e.g., Freeston et al., 1997; McLean et al., 2001;
van Oppen et al., 1995; Whittal, Robichaud, Thordarson, & McLean, 2008; Whittal,
Thordarson, & McLean, 2005). Furthermore, it is apparent that CR alone can have a
significant treatment effect even in the absence of systematic, intensive ERP (Cottraux
et al., 2001; Whittal et al., 2005; Wilson & Chambless, 2005). Although some
studies have found CBT equivalent to ERP (Cottraux et al., 2001; Whittal et al.,
2005), others reported that intensive ERP alone is more effective than CBT (McLean
et al., 2001) or that adding CR to ERP did not significantly improve treatment
outcome (O’Connor et al., 2005). Moreover, Whittal, Woody, McLean, Rachman,
and Robichaud (2010) found that CBT and stress management were equally effective
in treating individuals who experienced obsessions without overt compulsions. This
finding has led to the conclusion that cognitive strategies alone are less effective than
ERP alone and that adding CR to ERP does not boost the effectiveness of treatment
for OCD (Abramowitz, Taylor, & McKay, 2005).
Component analysis of CR, per se, has not been conducted with GAD. However,
outcome studies comparing CBT with applied relaxation or pharmacotherapy alone
have concluded that CBT has equivalent or superior treatment effectiveness (see
Fisher, 2006; Mitte, 2005). In posttraumatic stress disorder (PTSD) there has
been considerable research on whether CR adds any treatment effectiveness beyond
prolonged trauma exposure. Several meta-analyses have concluded that individual
trauma-focused CBT that includes exposure to an individual’s memory of the trauma
and its personal meaning is an effective treatment for PTSD (e.g., Bisson & Andrew,
2009; Seidler & Wagner, 2006; see also discussion by Ehlers et al., 2010). However,
there is considerable controversy over whether CR of trauma-related thoughts and
beliefs adds any therapeutic effectiveness over prolonged imaginal exposure to the
trauma memory. In their systematic review, Ponniah and Hollon (2009) concluded
that trauma-focused CBT that included exposure and/or CR was an efficacious
treatment for PTSD. However, other researchers have concluded that cognitive
interventions may be unnecessary in the treatment of anxiety disorders including
PTSD (Longmore & Worrell, 2007).
Recently, Hassija and Gray (2010) conducted a thorough review of component
studies comparing CR and prolonged exposure in PTSD. These researchers found
sufficient evidence that CR is an effective intervention for PTSD and that the
effects are generally comparable to prolonged exposure. Moreover, CR may produce
more enduring effects than does imaginal exposure alone (Tarrier & Sommerfield,
2004) and may differentially affect associated features of PTSD such as detachment,
catastrophic cognitions, and guilt (Hassija & Gray, 2010). Outcome and dismantling
studies of cognitive processing therapy (CPT), which involves intense CR of beliefs
and negative cognitions, indicate that the therapy is as effective as prolonged exposure
in the immediate and longer term (Resick, Nishith, Weaver, Astin, & Feuer, 2002;
Resick, Williams, Suvak, Monson, & Gradus, 2012). In addition, CPT may have
some superiority over trauma-focused exposure alone in treatment of chronic PTSD
in military samples (Alvarez et al., 2011). Recent CPT dismantling studies indicate
that CR may be the more potent component of the treatment package (Resick et al.,
2008; Stein, Dickstein, Schuster, Litz, & Resick, 2012). At this point the most
parsimonious conclusion is that the CR component of CPT and prolonged exposure
produce similar changes in PTSD so that the average person with PTSD can benefit
from either treatment (Stein et al., 2012).
Before concluding this review of component studies, it is worth considering the
most recent meta-analysis on the efficacy of exposure and CT in treatment of anxiety
disorders. Ougrin (2011) identified 20 RCTs that directly compared CT and exposure
alone. Studies of CT versus CT plus exposure, or the reverse, were excluded. Analysis
revealed equivalent short- and long-term effect sizes for PTSD, OCD, and panic
disorder. However, there was a statistically significant difference in effect size favoring
CT for immediate and long-term outcomes for social anxiety disorder.
In summary, the component studies clearly indicate that CR is an effective treatment
intervention for anxiety and depression, and in some cases may convey a distinct ther-
apeutic advantage. This is very different from the conclusion reached by Longmore
and Worrell (2007) in their review of CBT component analysis studies for anxiety and
depression, in which they stated that “for a range of clinical problems, specifically cog-
nitive interventions do not produce superior outcomes to the behavioral components
of CBT” (p. 180). The failure of cognitive interventions to add significant therapeutic
value beyond exposure or behavioral activation alone was a significant factor in leading
the authors to question whether challenging negative thoughts was necessary in CBT.
The present review considers this a misguided conclusion, although it is true that the
general finding of equivalence of cognitive and behavioral interventions provides little
practical guidance for the clinician who must decide how much emphasis should be
placed on CR when treating an individual client with anxiety or depression.
Mediation Analysis
Cognitive mediation is a fundamental hallmark of CT and CBT (D. A. Clark et al.,
1999; Garratt, Ingram, Rand, & Sawalani, 2007; Maxwell & Tappolet, 2012).
It is the assertion that symptom improvement and recovery from a disorder is
the result of change in underlying maladaptive thoughts and beliefs, and biased
information processing. It is change in the functioning of the cognitive apparatus
that mediates symptom amelioration. Although CT acknowledges that modification
in physical processes, emotions, behavior, and experiences can result in cognitive
change, it is assumed that CR provides a more direct means to modify the faulty
information processing apparatus. Thus, there are two fundamental questions in
cognitive mediation. Is schematic change a significant causal mechanism of symptom
improvement, and is CR unique in its ability to produce change in schematic
content (Garrett et al., 2007; Hofmann, 2008)? I turn now to the initial question of
mechanisms of therapeutic change.
Longmore and Worrell (2007) reviewed a select number of early CBT treatment
process studies and concluded that there is limited evidence that cognitive variables
mediate therapeutic change in CBT. Hofmann (2008), however, was critical of the
Longmore and Worrell (2007) discussion of cognitive mediation, noting that several
recent CBT process studies that employed more rigorous data analytic procedures in
support of cognitive mediation were missing from their review. Interestingly Garrett
et al. (2007) arrived at a different conclusion in their review of cognitive mediation
in treatment of depression. They stated that in CT, change in cognition does predict
changes in depressive symptoms, although it appears that studies are divided on
whether cognitive change is specific to CT or also evident in other psychosocial
treatments or even pharmacotherapy.
There have been several rigorous tests of cognitive mediation in CBT for the
anxiety disorders. Hofmann (2004) found that group CBT, and exposure alone,
produced equivalent improvements in social anxiety disorder at posttreatment, but
at 6-month follow-up only CBT was associated with continued symptom reduction.
Using linear regression analyses, he demonstrated that change in the estimated
social cost associated with 20 hypothetical negative social events predicted pre-post
difference scores in self-reported social anxiety symptoms, especially for the CBT
group at 6-month follow-up. Smits, Rosenfield, Telch, and McDonald (2006) found
evidence of cognitive mediation for exposure-based treatment of social anxiety using
growth modeling analysis and a cross-lagged panel design. Change in probability
judgmental bias predicted later self-rated fear during exposure, although the reverse
relationship was also found and judgments of cost bias did not predict fear.
Based on an RCT comparing CBT and pharmacotherapy for panic disorder,

Hofmann et al. (2007) used multilevel modeling to show that change in catastrophic
cognitions was a significant mediator of change in panic symptoms for those receiving
CBT but not for participants in the imipramine alone condition. A recent study
of one session exposure versus CBT-based exposure for spider phobia revealed that
change in maladaptive cognitions mediated posttreatment and follow-up reductions
in self-report phobic symptoms (Raes, Koster, Loeys, & De Raedt, 2011). Finally, a
systematic review of CBT studies of anxiety disorders concluded that change in threat
reappraisal has a causal effect on reduction in anxious symptoms, although it was not
possible to support the stronger position that threat reappraisal is responsible for the
efficacy of CBT (Smits, Julian, Rosenfield, & Powers, 2012).
Several studies have examined session-by-session change in cognitions and symp-
toms in order to investigate temporal precedence. Tang and DeRubeis (1999) found
that CT sessions involving sudden gains (i.e., large depressive symptom reduction
during a single between-session interval) were associated with cognitive changes in
the previous session. A subsequent reanalysis of the Jacobson et al. (1996) data set
again confirmed that significantly more cognitive change occurred in the pregain than
control sessions (Tang, DeRubeis, Beberman, & Pham, 2005). However, another
study using multivariate hierarchical linear modeling of session-by-session changes
in Beck Depression Inventory symptoms found similar trajectories of change for
cognitive and vegetative symptoms for depressed outpatients randomly assigned to
CT or pharmacotherapy (Bhar et al., 2008).
In a stringent test of cognitive mediation in CBT for obsessions, Woody, Whittal,
and McLean (2011) found that maladaptive appraisals of the primary obsession
significantly accounted for improvement in obsessive symptoms. Although this finding
supported the cognitive mediation hypothesis, a session-by-session analysis using
latent change modeling revealed that prior obsession severity led to subsequent
change in appraisals for both CBT and stress management treatment conditions. In
this study, then, symptom change had temporal precedence over cognitive change.
However, a multivariate time series analysis of session-by-session data for CR versus
exposure treatment for panic disorder indicated that changes in dysfunctional beliefs
and self-efficacy preceded change in panic apprehension (Bouchard et al., 2007).
Overall the research on temporal precedence presents a mixed picture, with some
studies showing cognitive change is a cause of symptom change, others cognitive
change is a consequence of symptom change, and still others a co-occurring change
with bidirectional effects.
Before concluding this review on cognitive mediation, it is worth considering
several lines of research that demonstrated that a specific focus on cognitive change
does have an impact on symptom remission. For example, Segal and colleagues found
that depressed participants treated with CT were less cognitively reactive during sad
mood induction at posttreatment than those treated with medication alone, and
this in turn predicted probability of relapse (Segal, Gemar, & Williams, 1999; Segal
et al., 2006). Furthermore, a study of CT plus medication versus medication alone
for major depression found that both treatments produced a significant reduction
in depressive symptoms and negative cognitions, but only the CT plus medication
group evidenced increased organization of positive schema content and reduced
interconnectedness for negative schema content (Dozois et al., 2009). The specific
type of automatic thought targeted during group CBT for social anxiety also appears
to influence treatment outcome (Hope, Burns, Hayes, Herbert, & Warner, 2010).
Finally, patients’ competence in acquiring CR skills in CT predicted lower 1-year
relapse in one study (Strunk, DeRubeis, Chiu, & Alvarez, 2007), although the
evidence is mixed on whether therapist adherence to or competence in the CT
protocol is significantly related to outcome (Strunk, Brotman, DeRubeis, & Hollon,
2010; Webb, DeRubeis, & Barber, 2010). Overall, then, considerable progress has
been made in understanding the mechanisms of change in CBT. It is clear that the
quality of the cognitive intervention, its focus, and the degree of subsequent cognitive
change does have a significant impact on treatment outcome.
Concluding Remarks
CR is a multifaceted therapeutic intervention that seeks symptom reduction by

modifying the maladaptive schematic content considered crucial in the etiology and
maintenance of psychological disorders. Since its first conceptualization by A. T. Beck
and colleagues in the 1970s (A. T. Beck et al., 1979), considerable progress has been
made in elaborating, refining, and applying CR to a variety of psychiatric disorders.
Psychotherapy process research has indicated that CR is an effective intervention for
anxiety and depression, and that CR’s most significant contribution might be in
conferring more enduring treatment effects or mediating change in specific disorder
symptoms. However, it is also clear that CR is at best equivalent to, and at worst
less effective than, “noncognitive” interventions such as exposure or behavioral
activation, at least in terms of short-term symptom reduction. Although there is
substantial evidence in support of cognitive mediation in symptom improvement, the
direction of causality is still a matter of debate and it is evident that cognitive change
is not specific to CR.
There are several issues that remain unresolved about the effectiveness and mech-
anism of change in CR. At the schematic level, the effects of CR remain relatively
unknown. Does CR alter existing maladaptive schema content or does it introduce
more adaptive schemas that compete with or inhibit activation of disorder-related
schemas? There have been no dismantling studies of CR itself to indicate the rel-
ative importance of collaborative empiricism, verbal interventions, and empirical
hypothesis-testing to determine the effectiveness of the intervention. Most of the
component and mediation research has relied on symptom measures taken at limited
time intervals throughout treatment (i.e., baseline, posttreatment, follow-up). What
is needed are more session-by-session studies that use specific cognitive and symp-
tom measures employing multilevel modeling techniques to chart the trajectories of
cognitive and symptom change. It is also unclear which clinical, client, and therapist
variables might moderate the effectiveness of CR, and we are only just beginning to
learn the role that therapist competence and client acquisition of CT skills might play
in the effectiveness of CR. Unfortunately the treatment process research has not yet
matured to the point where it can provide guidelines to clinicians on when to use
CR, when to combine it with other interventions, or when to refrain from its use.
Until then, clinicians can consider CR an effective intervention that should hold a
prominent place in their treatment armamentarium.
References
Abramowitz, J. S., Taylor, S., & McKay, D. (2005). Potentials and limitations of cognitive
treatments for obsessive-compulsive disorder. Cognitive Behaviour Therapy, 34, 140–147.
Abramson, L. Y., Metalsky, G. I., & Alloy, L. B. (1989). Hopelessness depression: A theory-
based subtype of depression. Psychological Review, 96, 358–372.
Alloy, L. B., Abramson, L. Y., Safford, S. M., & Gibb, B. E. (2006). The Cognitive Vulnerability
to Depression (CVD) Project: Current findings and future directions. In L. B. Alloy & J.
H. Riskind (Eds.), Cognitive vulnerability to emotional disorders (pp. 33–61). Mahwah,
NJ: Erlbaum.
Alvarez, J., McLean, C., Rosen, C. S., Ruzek, J. I., Harris, A. H. S., & Kimerling, R. (2011).
The comparative effectiveness of cognitive processing therapy for male veterans treated
in a VHA posttraumatic stress disorder residential rehabilitation program. Journal of
Consulting and Clinical Psychology, 79, 590–599.
Beck, A. T. (1964). Thinking and depression. II. Theory and therapy. Archives of General
Psychiatry, 10, 561–571.
Beck, A. T. (1967). Depression: Causes and treatment. Philadelphia, PA: University of Pennsyl-
vania Press.
Beck, A. T. (1976). Cognitive therapy of the emotional disorders. New York, NY: New American
Library.
Beck, A. T. (1987). Cognitive models of depression. Journal of Cognitive Psychotherapy: An
International Quarterly, 1, 5–37.
Beck, A. T. (1996). Beyond belief: A theory of modes, personality, and psychopathology. In
P. M. Salkovskis (Ed.), Frontiers of cognitive therapy (pp. 1–25). New York, NY: Guilford
Press.
Beck, A. T., & Emery, G. (with Greenberg, R.) (1985). Anxiety disorders and phobias: A
cognitive perspective. New York, NY: Basic Books.
Beck, A. T., Freeman, A., Davis, D. D., & Associates (2004). Cognitive therapy of personality
disorders (2nd ed.). New York, NY: Guilford Press.
Beck, A. T., Rector, N. A., Stolar, N., & Grant, P. (2009). Schizophrenia: Cognitive theory,
research, and therapy. New York, NY: Guilford Press.
Beck, A. T., Rush, A. J., Shaw, B. F., & Emery, G. (1979). Cognitive therapy of depression.
New York, NY: Guilford Press.
Beck, J. S. (2011). Cognitive behavior therapy: Basics and beyond (2nd ed.). New York, NY:
Guilford Press.
Bennett-Levy, J., Westbrook, D., Fennell, M., Cooper, M., Rouf, K., & Hackmann, A. (2004).
Behavioural experiments: Historical and conceptual underpinnings. In J. Bennett-Levy,
G. Butler, M. Fennell, A. Hackmann, M. Mueller, & D. Westbrook (Eds.), Oxford guide
to behavioural experiments in cognitive therapy (pp. 1–20). Oxford, England: Oxford
University Press.
Bhar, S. S., Gelfand, L. A., Schmid, S. P., Gallop, R., DeRubeis, R. J., Hollon, S. D., … Beck,
A. T. (2008). Sequence of improvement in depressive symptoms across cognitive therapy
and pharmacotherapy. Journal of Affective Disorders, 110, 161–166.
Bisson, J., & Andrew, M. (2009). Psychological treatment of post-traumatic stress disorder
(PTSD) (Review). The Cochrane Library, 2009 (1). www.thecochranelibrary.com
Bouchard, S., Gauthier, J., Laberge, B., French, D., Pelletier, M. H., & Godbout, C.
(1996). Exposure versus cognitive restructuring in the treatment of panic disorder with
agoraphobia. Behaviour Research and Therapy, 34, 213–224.
Bouchard, S., Gauthier, J., Nouwen, A., Ivers, H., Vallières, A., Simard, S., & Fournier,
T. (2007). Temporal relationship between dysfunctional beliefs, self-efficacy and panic
apprehension in the treatment of panic disorder with agoraphobia. Journal of Behavior
Therapy and Experimental Psychiatry, 38, 275–292.
Burns, D. D., & Beck, A. T. (1978). Cognitive behavior modification of mood disorders. In
J. P. Foreyt & D. P. Rathjen (Eds.), Cognitive behavior therapy: Research and application
(pp. 109–134). New York, NY: Plenum Press.
Clark, D. A. (in press). Collaborative empiricism: A cognitive response to exposure reluctance
and low distress tolerance. Cognitive and Behavioral Practice.
Clark, D. A., & Beck, A. T. (2010). Cognitive therapy of anxiety disorders: Science and practice.
Clark, D. A., & Beck, A. T. (2012). The anxiety and worry workbook: The cognitive behavioral
solution. New York, NY: Guilford Press.
Clark, D. A., Beck, A. T., & Alford, B. A. (1999). Scientific foundations of cognitive theory and
therapy of depression. New York, NY: John Wiley & Sons, Inc.
Clark, D. M., Ehlers, A., Hackmann, A., McManus, F., Fennell, M., Grey, N., … Wild, J.
(2006). Cognitive therapy versus exposure and applied relaxation in social phobia: A
randomized controlled trial. Journal of Consulting and Clinical Psychology, 74, 568–578.
Cottraux, J., Note, I., Yao, S. N., Lafont, S., Note, B., Mollard, E., … Dartiques, J. F. (2001).
A randomized controlled trial of cognitive therapy versus intensive behavior therapy in
obsessive compulsive disorder. Psychotherapy and Psychosomatics, 70, 288–297.
Dimidjian, S., Hollon, S. D., Dobson, K. S., Schmaling, K. B., Kohlenberg, R. J., Addis,
M. E., … Jacobson, N. S. (2006). Randomized trial of behavioral activation, cognitive
therapy, and antidepressant medication in the acute treatment of adults with major
depression. Journal of Consulting and Clinical Psychology, 74, 658–670.
Dobson, D., & Dobson, K. S. (2009). Evidence-based practice of cognitive-behavioral therapy.
Dobson, K. S., & Dozois, D. J. A. (2010). Historical and philosophical bases of the cognitive-
behavioral therapies. In K. S. Dobson (Ed.), Handbook of cognitive-behavioral therapies
(3rd ed., pp. 3–38). New York, NY: Guilford Press.
Dobson, K. S., Hollon, S. D., Dimidjian, S., Schmaling, K. B., Kohlenberg, R. J., Gallop,
R. J., … Jacobson, N. S. (2008). Randomized trial of behavioral activation, cognitive
therapy, and antidepressant medication in the prevention of relapse and recurrence in
major depression. Journal of Consulting and Clinical Psychology, 76, 468–477.
Dozois, D. J. A. (2007). Stability of self-structures: A longitudinal comparison of depressed,
remitted, and nonpsychiatric controls. Journal of Clinical Psychology, 63, 319–338.
Dozois, D. J. A., & Beck, A. T. (2008). Cognitive schemas, beliefs and assumptions. In K.
S. Dobson & D. J. A. Dozois (Eds.), Risk factors in depression (pp. 121–143). Oxford,
England: Elsevier/Academic Press.
Dozois, D. J. A., Bieling, P. J., Patelis-Siotis, I., Hoar, L., Chudzik, S., McCabe, K., & Westra,
H. A. (2009). Changes in self-schema structure in cognitive therapy for major depressive
disorder: A randomized clinical trial. Journal of Consulting and Clinical Psychology, 77 ,
1078–1088.
Dozois, D. J. A., & Dobson, K. S. (2001). Information processing and cognitive organization
in unipolar depression: Specificity and comorbidity issues. Journal of Abnormal Psychology,
110, 236–246.
Ehlers, A., Bisson, J., Clark, D. M., Creamer, M., Pilling, S., Richards, D., … Yule, W. (2010).
Do all psychological treatments really work the same in posttraumatic stress disorder?
Clinical Psychology Review, 30, 269–276.
Fennell, M., Bennett-Levy, J., & Westbrook, D. (2004). Depression. In J. Bennett-Levy, G.
Butler, M. Fennell, A. Hackmann, M. Mueller, & D. Westbrook (Eds.), Oxford guide
to behavioural experiments in cognitive therapy (pp. 205–222). Oxford, England: Oxford
University Press.
Feske, U., & Chambless, D. L. (1995). Cognitive behavioral versus exposure only treatment
for social phobia: A meta-analysis. Behavior Therapy, 26, 695–720.
Fisher, P. L. (2006). The efficacy of psychological treatments for generalized anxiety disorder.
In G. C. L. Davey & A. Wells (Eds.), Worry and its psychological disorders: Theory,
assessment and treatment (pp. 359–377). Chichester, England: John Wiley & Sons.
Freeston, M. H., Ladouceur, R., Gagnon, F., Thibodeau, N., Rhéaume, J., Letarte, H., &
Bujold, A. (1997). Cognitive-behavioral treatment of obsessive thoughts: A controlled
study. Journal of Consulting and Clinical Psychology, 65, 405–413.
Garratt, G., Ingram, R. E., Rand, K. L., & Sawalani, G. (2007). Cognitive processes in
cognitive therapy: Evaluation of the mechanisms of change in the treatment of depression.
Clinical Psychology: Science and Practice, 14, 224–239.
Gortner, E. T., Gollan, J. K., Dobson, K. S., & Jacobson, N. S. (1998). Cognitive-behavioral
treatment for depression: Relapse prevention. Journal of Consulting and Clinical Psychol-
ogy, 66, 377–384.
Gould, R. A., Otto, M. W., & Pollack, M. H. (1995). A meta-analysis of treatment outcome
for panic disorder. Clinical Psychology Review, 15, 819–844.
Gould, R. A., Otto, M. W., Pollack, M. H., & Yap, L. (1997). Cognitive behavioral and
pharmacological treatment of generalized anxiety disorder: A preliminary meta-analysis.
Behavior Therapy, 28, 285–305.
Greenberger, D., & Padesky, C. A. (1995). Mind over mood: Change how you feel by changing
the way you think. New York, NY: Guilford Press.
Hassija, C. M., & Gray, M. J. (2010). Are cognitive techniques and interventions necessary? A
case for the utility of cognitive approaches in the treatment of PTSD. Clinical Psychology:
Science and Practice, 17 , 112–127.
Hofmann, S. G. (2004). Cognitive mediation of treatment change in social phobia. Journal of
Hofmann, S. G. (2008). Common misconceptions about cognitive mediation of treatment
change: A commentary to Longmore and Worrell (2007). Journal of Consulting and
Clinical Psychology, 28, 67–70.
Hofmann, S. G., Meuret, A. E., Rosenfield, D., Suvak, M. K., Barlow, D. H., Gorman, J. M., …
Woods, S. W. (2007). Preliminary evidence for cognitive mediation during cognitive-
behavioral therapy of panic disorder. Journal of Consulting and Clinical Psychology, 75,
374–379.
Hollon, D. S., & Dimidjian, S. (2009). Cognitive and behavioral treatment of depression. In
I. H. Gotlib & C. L. Hammen (Eds.), Handbook of depression (2nd ed., pp. 586–603).
Hope, D. A., Burns, J. A., Hayes, S. A., Herbert, J. D., & Warner, M. D. (2010). Automatic
thoughts and cognitive restructuring in cognitive therapy behavioral group therapy for
social anxiety disorder. Cognitive Therapy and Research, 34, 1–12.
Ingram, R. E., & Kendall, P. C. (1986). Cognitive clinical psychology: Implications of
an information processing perspective. In R. E. Ingram (Ed.), Information processing
approaches to clinical psychology (pp. 3–21). Orlando, FL: Academic Press.
Jacobson, N. S., Dobson, K. S., Truax, P. A., Addis, M. E., & Koerner, K. (1996). A component
analysis of cognitive-behavioral treatment of depression. Journal of Consulting and Clinical
Psychology, 64, 295–304.
Kingdon, D. G., & Turkington, D. (2005). Cognitive therapy of schizophrenia. New York, NY:
Guilford Press.
Kuyken, W., Padesky, C. A., & Dudley, R. (2009). Collaborative case conceptualization:
Working effectively with clients in cognitive-behavioral therapy. New York, NY: Guilford
Press.
Leahy, R. L. (2010). Beat the blues before they beat you: How to overcome depression. Carlsbad,
CA: Hay House.
Longmore, R. J., & Worrell, M. (2007). Do we need to challenge thoughts in cognitive
behavior therapy? Clinical Psychology Review, 27 , 173–187.
Margraf, J., & Schneider, S. (1991, November). Outcome and active ingredients of cognitive-
behavioral treatments for panic disorder. Paper presented at the 25th Annual Meeting of
the Association for the Advancement of Behavior Therapy, New York.
Mattick, R. P., & Peters, L. (1988). Treatment of severe social phobia: Effects of guided
exposure with and without cognitive restructuring. Journal of Consulting and Clinical
Maxwell, B., & Tappolet, C. (2012). Rethinking cognitive mediation: Cognitive-behavioral
therapy and the perceptual theory of emotion. Philosophy, Psychiatry, & Psychology, 19,
1–12.
McLean, P. D., Whittal, M. L., Thordarson, D. S., Taylor, S., Sochting, I., Koch, W. J., …
Anderson, K. W. (2001). Cognitive versus behavior therapy in the group treatment
of obsessive-compulsive disorder. Journal of Consulting and Clinical Psychology, 69,
205–214.
Mitte, K. (2005). Meta-analysis of cognitive-behavioral treatments for generalized anxiety
disorder: A comparison with pharmacotherapy. Psychological Bulletin, 131, 785–795.
O’Connor, K. P., Aardema, F., Bouthillier, D., Fournier, S., Guay, S., Robillard, S., … Pitre,
D. (2005). Evaluation of an inference-based approach to treating obsessive-compulsive
disorder. Cognitive Behaviour Therapy, 34, 148–163.
Öst, L.-G., Thulin, U., & Ramnerö, J. (2004). Cognitive behavior therapy vs exposure in vivo
in the treatment of panic disorder with agoraphobia. Behaviour Research and Therapy, 42,
1105–1127.
Ougrin, D. (2011). Efficacy of exposure versus cognitive therapy in anxiety disor-
ders: Systematic review and meta-analysis. BMC Psychiatry, 11. Retrieved from
http://www.medscape.com/viewarticle/763501
Ponniah, K., & Hollon, S. D. (2009). Empirically supported psychological treatments for adult
acute stress disorder and posttraumatic stress disorder: A review. Depression and Anxiety,
26, 1086–1109.
Raes, A. K., Koster, E. H. W., Loeys, T., & De Raedt, R. (2011). Pathways to change in
one-session exposure with and without cognitive intervention: An exploratory study in
spider phobia. Journal of Anxiety Disorders, 25, 964–971.
Resick, P. A., Galovski, T. E., Uhlmansiek, M. O., Scher, C. D., Clum, G. A., & Young-Xu,
Y. (2008). A randomized clinical trial to dismantle components of cognitive processing
therapy for posttraumatic stress disorder in female victims of interpersonal violence.
Journal of Consulting and Clinical Psychology, 76, 243–258.
Resick, P. A., Nishith, P., Weaver, T. L., Astin, M. C., & Feuer, C. A. (2002). A comparison
of cognitive-processing therapy with prolonged exposure and a waiting condition for
the treatment of chronic posttraumatic stress disorder in female rape victims. Journal of
Resick, P. A., Williams, L. F., Suvak, M. K., Monson, C. M., & Gradus, J. L. (2012). Long-
term outcomes of cognitive-behavioral treatments for posttraumatic stress disorder among
female rape survivors. Journal of Consulting and Clinical Psychology, 80, 201–210.
Rodebaugh, T. L., Holaway, R. M., & Heimberg, R. G. (2004). The treatment of social
anxiety disorder. Clinical Psychology Review, 24, 883–908.
Rouf, K., Fennell, M., Westbrook, D., Cooper, M., & Bennett-Levy, J. (2004). Devising effec-
tive behavioural experiments. In J. Bennett-Levy, G. Butler, M. Fennell, A. Hackmann,
M. Mueller, & D. Westbrook (Eds.), Oxford guide to behavioural experiments in cognitive
therapy (pp. 21–58). Oxford, England: Oxford University Press.
Segal, Z. V. (1988). Appraisal of the self-schema construct in cognitive models of depression.
Psychological Bulletin, 103, 147–162.
Segal, Z. V., Gemar, M., & Williams, S. (1999). Differential cognitive response to a mood chal-
lenge following successful cognitive therapy or pharmacotherapy for unipolar depression.
Journal of Abnormal Psychology, 108, 3–10.
Segal, Z. V., Kennedy, S., Gemar, M., Hood, K., Pedersen, R., & Buis, T. (2006). Cognitive
reactivity to sad mood provocation and the prediction of depressive relapse. Archives of
General Psychiatry, 63, 749–755.
Seidler, G. H., & Wagner, F. E. (2006). Comparing the efficacy of EMDR and trauma-
focused cognitive-behavioral therapy in the treatment of PTSD: A meta-analytic study.
Psychological Medicine, 36, 1515–1522.
Smits, J. A. J., Julian, K., Rosenfield, D., & Powers, M. B. (in press). Threat reappraisal as
a mediator of symptom change in cognitive-behavioral treatment of anxiety disorders: A
systematic review. Journal of Consulting and Clinical Psychology, 80, 624–635.
Smits, J. A. J., Rosenfield, D., Telch, M. J., & McDonald, R. (2006). Cognitive mechanisms
of social anxiety reduction: An examination of specificity and temporality. Journal of
Stein, N. R., Dickstein, B. D., Schuster, J., Litz, B. T., & Resick, P. A. (2012). Trajecto-
ries of response to treatment for posttraumatic stress disorder. Behavior Therapy, 43,
790–800.
Strunk, D. R., Brotman, M. A., DeRubeis, R. J., & Hollon, S. D. (2010). Therapist competence
in cognitive therapy for depression: Predicting subsequent symptom change. Journal of
Strunk, D. R., DeRubeis, R. J., Chiu, A. W., & Alvarez, J. (2007). Patients’ competence in and
performance of cognitive therapy skills: Relation to the reduction of relapse risk following
treatment. Journal of Consulting and Clinical Psychology, 75, 523–530.
Tang, T. Z., & DeRubeis, R. J. (1999). Sudden gains and critical sessions in cognitive-
behavioral therapy for depression. Journal of Consulting and Clinical Psychology, 67 ,
894–904.
Tang, T. Z., DeRubeis, R. J., Beberman, R., & Pham, T. (2005). Cognitive changes, critical
sessions, and sudden gains in cognitive-behavioral therapy for depression. Journal of
Tarrier, N., & Sommerfield, C. (2004). Treatment of chronic PTSD by cognitive therapy and
exposure: 5-year follow-up. Behavior Therapy, 35, 231–246.
Tee, J., & Kazantzis, N. (2011). Collaborative empiricism in cognitive therapy: A definition
and theory for the relationship construct. Clinical Psychology: Science and Practice, 18,
47–61.
van de Hout, M., Arntz, A., & Hoekstra, R. (1994). Exposure reduced agoraphobia but not
panic, and cognitive therapy reduced panic but not agoraphobia. Behaviour Research and
Therapy, 32, 447–451.
van Oppen, P., de Haan, E., van Balkom, A. J. L. M., Spinhoven, P., Hoogduin, K., & van
Dyck, R. (1995). Cognitive therapy and exposure in vivo in the treatment of obsessive
compulsive disorder. Behaviour Research and Therapy, 33, 379–390.
Webb, C. A., DeRubeis, R. J., & Barber, J. P. (2010). Therapist adherence/competence and
treatment outcome: A meta-analytic review. Journal of Consulting and Clinical Psychology,
78, 200–211.
Wells, A. (1997). Cognitive therapy of anxiety disorders: A practice manual and conceptual
guide. Chichester, England: John Wiley & Sons, Inc.
Whittal, M. L., Robichaud, M., Thordarson, D. S., & McLean, P. D. (2008). Group
and individual treatment of obsessive-compulsive disorder using cognitive therapy and
exposure plus response prevention: A 2-year follow-up of two randomized trials. Journal
of Consulting and Clinical Psychology, 76, 1003–1014.
Whittal, M. L., Thordarson, D. S., & McLean, P. D. (2005). Treatment of obsessive-compulsive
disorder: Cognitive behavior therapy vs. exposure and response prevention. Behaviour
Research and Therapy, 43, 1559–1576.
Whittal, M. L., Woody, S. R., McLean, P. D., Rachman, S. J., & Robichaud, M. (2010).
Treatment of obsessions: A randomized controlled trial. Behaviour Research and Therapy,
48, 295–303.
Wilson, K. A., & Chambless, D. L. (2005). Cognitive therapy for obsessive-compulsive
disorder. Behaviour Research and Therapy, 43, 1645–1654.
Woody, S. R., Whittal, M. L., & McLean, P. D. (2011). Mechanisms of symptom reduction in
treatment for obsessions. Journal of Consulting and Clinical Psychology, 79, 653–664.
Wright, J. H., & McCray, L. W. (2012). Breaking free from depression: Pathways to wellness.
3
Exposure Techniques
Valerie Vorstenbosch, Leorra Newman,
and Martin M. Antony
Ryerson University, Canada
Exposure refers to the systematic and controlled confrontation of feared objects

and situations. Current evidence suggests that exposure is an essential component
of many psychological treatments. Specifically, many exposure-based treatments for
anxiety disorders are considered well established, according to the American Psycho-
logical Association’s review of evidence-based treatments (American Psychological
Association Presidential Task Force on Evidence-Based Practice, 2006). Despite the
extant research on the efficacy of exposure therapy, a number of questions remain
regarding the process of fear reduction during exposure therapy.
Historical Roots of Exposure Therapy
Although early psychoanalytic theorists such as Freud (1950) and Janet (1925)
speculated about the possible benefits of exposure for reducing fear and anxiety,
large-scale interest in exposure therapy grew out of the application of learning theory
to treatment of clinical disorders; thus, the laboratory work of Ivan Pavlov, Clark
Hull, B. F. Skinner, Edward Thorndike, and John Watson in developing principles
of classical and operant conditioning was particularly influential. For example, Mary
Cover Jones, a student of Watson, reported successful treatment of a young boy’s fear
of rabbits in one of the earliest descriptions of graduated exposure techniques (Jones,
1924). The application of learning theory to psychopathology blossomed in the 1950s
and 1960s, aided by the convergence of the work of clinical researchers in South
Africa, England, and the United States, such as Hans Eysenck, Cyril Franks, Arnold
Lazarus, Isaac Marks, S. Rachman, G. Terence Wilson, and Joseph Wolpe. Behavior
therapy, with its emphasis on exposure techniques and other laboratory-derived
principles of learning, quickly became established as a legitimate psychotherapeutic

DOI: 10.1002/9781118528563.wbcbt03
approach during this era. For example, exposure techniques, in which patients were
exposed to anxiety-provoking stimuli and prevented from engaging in compulsive
rituals, were first reported by Meyer (1966) in case studies of obsessive-compulsive
disorder (OCD). Other notable precursors to contemporary exposure therapy include
systematic desensitization and flooding.
Systematic Desensitization
Systematic desensitization, developed by Wolpe (1958) for the treatment of phobias,
is based on the principles of classical conditioning. In systematic desensitization,
the patient and therapist work collaboratively to develop a hierarchy of feared
stimuli or situations. The patient is subsequently taught progressive muscle relaxation
(Jacobson, 1938), which is then combined with systematic and gradual exposure
in imagination. The goal of systematic desensitization is for the patient to be
relaxed in the presence of feared stimuli. Wolpe (1958) described this process as
reciprocal inhibition, and hypothesized that practicing relaxation techniques during
exposure would inhibit a fear response, thereby weakening the association between
the feared stimulus and the phobic response. While certain aspects of systematic
desensitization are still included in contemporary exposure-based treatments, today’s
exposure therapy for phobic disorders is more likely to emphasize in vivo exposure
(versus imaginal exposure), consistent with early research showing that in vivo
exposure is more effective (e.g., Emmelkamp & Wessels, 1975). Furthermore, given
that exposure reduces fear regardless of whether relaxation training is included (Kazdin
& Wilson, 1978), relaxation is typically not included in contemporary exposure-based
treatments.
Flooding
In contrast to the graduated approach in systematic desensitization, flooding refers
to a high intensity approach in which patients rapidly confront their most feared
stimuli and stay in the situation until their fear decreases. Implosive therapy is a
variant of flooding that involves exposing patients to their fears in imagination. These
imaginal exposures are often exaggerated to produce maximum anxiety and frequently
incorporate psychodynamic themes (Stampfl & Levis, 1967). When compared with
systematic desensitization, flooding has been shown to be as effective in reducing
fear (e.g., Marks, Boulougouris, & Marset, 1971), although improvements following
systematic desensitization may be longer-lasting than those resulting from flooding
(De Moor, 1970).
Contemporary Exposure Methods
In Vivo Exposure
In vivo exposure, sometimes referred to as “situational exposure,” refers to intentional
real-life confrontation of a feared situation. For example, an individual who fears large
dogs might practice being in a room with a dog, and work up eventually to touching
Exposure Techniques 47
it. In vivo exposure is the most studied and best supported treatment for specific
phobia and is commonly a component of treatments for all of the anxiety disorders.
In vivo exposure practices are often conducted during therapy sessions (both in
the therapist’s office and in naturalistic settings, such as driving, crowded places, or
heights), and may include behavioral role plays, as well as modeling of approach
behaviors by the therapist. In addition, patients are typically encouraged to practice
in vivo exposures on their own, between sessions. Although therapist-directed in
vivo exposure is often more effective than self-directed in vivo exposure (e.g., Öst,
Salkovskis, & Hellström, 1991), self-directed in vivo exposure is frequently assigned
as homework to supplement therapist-directed exposure during treatment sessions.
Imaginal Exposure
Exposure in imagination may be indicated when patients are fearful of their own mental
experiences (e.g., thoughts, images, impulses, or memories). In addition, imaginal
exposure may provide opportunities to practice encountering a feared situation that
might otherwise be unsafe (e.g., military combat) or that is difficult to create in
real life (e.g., storms). Abramowitz (2006) described three additional ways in which
therapists can use imaginal exposure: primary imaginal exposure, secondary imaginal
exposure, and preliminary imaginal exposure. Primary imaginal exposure involves
directly confronting thoughts or images that are associated with anxiety, distress, or
avoidance. Examples include confronting memories of a traumatic event, unwanted
obsessive thoughts, or distressing images. Secondary imaginal exposure is used as an
adjunct to in vivo exposure, when the situational exposure evokes fears of catastrophic
outcomes that are themselves distressing to the patient. For example, a patient with
contamination obsessions in the context of OCD might practice in vivo exposure
to dirty surfaces, followed by imaginal exposure to thoughts or images of a feared
catastrophic illness. Preliminary imaginal exposure may be used as a stepping-stone
toward in vivo exposure. For example, a patient with a phobia of dogs might practice
imagining encountering a large dog in preparation for this exposure in real life.
The overall goal of imaginal exposure is for the patient continuously to confront
the feared mental stimuli as vividly as possible, without distraction or attempts to
neutralize the distressing thoughts or images. The procedure often involves writing
scripts containing the distressing material, which are then read aloud in a therapy
session (either by the patient or therapist), or recorded and listened to repeatedly. Fear
typically decreases both within and across exposure practices (Abramowitz, Deacon,
& Whiteside, 2011).
For certain disorders (e.g., OCD), the addition of imaginal exposure has been
found to improve outcomes beyond those provided by in vivo exposure alone
(Abramowitz, 1996). Taken separately, in vivo exposure alone is generally considered
to be more effective than imaginal exposure alone, though the advantage of the
former at posttreatment may not endure at follow-up (Wolitzky-Taylor, Horowitz,
Powers, & Telch, 2008), and some studies have found equivalent outcomes when
comparing in vivo to imaginal exposure (e.g., Foa, Steketee, & Grayson, 1985).
Virtual Reality Exposure

Virtual reality (VR) exposure makes use of computer-generated three-dimensional
virtual environments to recreate feared scenarios and facilitate emotion provocation.
Immersion is a key element in VR exposure because patients need to be able to
explore their virtual surroundings or interact with the virtual environment just as
they might in real life. In VR, this is typically accomplished via body-tracking devices
and sensory input devices that integrate patients’ movements with real-time computer
graphics that are viewed on a head-mounted display. While these systems were initially
prohibitively expensive, they have become more affordable and accessible as research
on VR exposure continues to accumulate.
A meta-analysis of VR exposure studies indicated that VR exposure therapy is
effective in reducing fear across anxiety disorders (Parsons & Rizzo, 2008). Further
evidence suggests that VR exposure may be more effective than imaginal expo-
sure (Wiederhold, Gevirtz, & Spira, 2001), and there is evidence that patients
with specific phobias may consider VR to be more attractive than in vivo expo-
sure (Garcia-Palacios, Botella, Hoffman, & Fabregat, 2007). Although VR exposure
is not intended to replace in vivo exposure, it may be indicated when repeated
exposures are difficult to orchestrate (e.g., in phobias of storms or flying, or in
processing of trauma memories) or when patients refuse to attempt in vivo exposure.
In general, VR exposure affords therapists the opportunity to customize expo-
sures for their patients’ idiographic requirements and to manipulate aspects of the
virtual environment for smoother transitions between graded exposure hierarchy
items.
Interoceptive Exposure
Interoceptive exposure focuses on experiencing feared physical arousal sensations. This
technique was first suggested by Goldstein and Chambless (1978) in their classic “fear
of fear” model of agoraphobia and was further developed by Barlow, Craske, Cerny,
and Klosko (1989) as a component of treatment for panic disorder. Interoceptive
exposure is also sometimes used in other disorders in which individuals fear physical
symptoms (e.g., fear of sweating in social anxiety disorder, fear of dizziness in height
phobias).
In interoceptive exposure, feared bodily sensations are intentionally recreated. For
example, patients may breathe through a straw to induce breathlessness, hyperventilate
to bring on symptoms of lightheadedness, spin in a chair to evoke symptoms of
dizziness, or exercise to raise their heart rate (Antony, Ledley, Liss, & Swinson,
2006). Additional hierarchy items in interoceptive exposure may include engaging
in activities that the patient has otherwise avoided due to fear of unwanted physical
sensations. The goal of interoceptive exposure is to help patients learn that their
physical sensations are not dangerous and that they will not “spiral out of control”
(Abramowitz et al., 2011). Interoceptive exposure has been established as efficacious
in reducing panic disorder symptoms, both as part of a broader treatment package
(Barlow, Gorman, Shear, & Woods, 2000) and on its own (Craske, Rowe, Lewin, &
Noriega-Dimitri, 1997).
Mechanisms Underlying Exposure
Fear reduction is a central feature of any effective exposure treatment, whether in

vivo, imaginal, or interoceptive. Our understanding of how and why fear reduction
occurs has evolved over time. For example, early attempts to understand the processes
by which fear reduction occurs were based on Mowrer’s (1939, 1960) two-factor
learning theory of fear acquisition and maintenance, whereas more recent accounts
have been based on emotional processing theory (e.g., Foa & Kozak, 1986).
Mowrer’s Two-Factor Theory

Although Mowrer’s (1939, 1960) two-factor theory was not developed to explain
how exposure therapy works, it was one of the first theories used to explain the
mechanism of fear reduction during exposure therapy. Briefly, Mowrer’s theory
proposes that fears develop when a previously neutral stimulus (e.g., a dog) is paired
with an aversive stimulus (e.g., being bitten) and a conditioned fear response develops
to that neutral stimulus (e.g., fear that one will be bitten by any dog). In addition,
this theory proposes that fears are maintained through operant conditioning (i.e.,
individuals learn that their conditioned fear response can be reduced by escaping or
avoiding their feared stimulus). Thus, according to Mowrer’s theory, exposure may
work because it reduces a patient’s avoidance behavior which, in turn, leads to the
extinction of his or her fear response. More specifically, Mowrer’s theory suggests
that a patient’s conditioned fear response decreases because the previously neutral
stimulus (e.g., a dog) was continuously presented in the absence of the aversive
stimulus (e.g., no biting). While Mowrer’s two-factor theory has been influential in
helping us understand the role of avoidance in the maintenance of fear, it has also
received a great deal of criticism (for a review, see Rachman, 1976). For instance,
traumatic conditioning experiences cannot explain the development of all fears; nor is
there always a causal relationship between fear and avoidance (e.g., some individuals
report traumatic conditioning experiences and learned fear responses but no avoidance
behavior).
Extinction Learning
Although the term “habituation” is frequently cited as a mechanism underly-
ing exposure therapy, research and clinical observation suggest that extinction
learning, rather than habituation, provides a better explanation of how exposure
works. Habituation (i.e., a decrement in response as a result of repeated sensory
stimulation) includes a number of well-established characteristics (e.g., reduced
responding during exposure to a stimulus, followed by a reinstatement of the
response following a brief delay), all of which must be present before concluding
that habituation has occurred (for a review, see Moscovitch, Antony, & Swinson,
2009; Tryon, 2005). Unlike extinction, habituation does not actually involve any new
learning.
In exposure therapy, extinction learning refers to the decrease in fear respond-
ing that occurs as a result of a feared stimulus being repeatedly presented in the
absence of a feared consequence. Although it was previously believed that extinction

learning involved “unlearning” of the association between the feared stimulus and
consequence, recent evidence suggests that the process of extinction learning actually
involves the formation of new associations in which the individual begins to attribute
a neutral meaning to the feared stimulus (e.g., Rescorla, 2001).
Emotional Processing Theory

Extending earlier work by Lang (1977, 1979) and Rachman (1980), Foa and Kozak
(1986) developed their emotional processing theory, which proposes that extinction
learning occurs through the modification of one’s underlying fear structure. Foa and
Kozak (1986) described the fear structure as a program for avoiding threat, and
theorized that it is represented by a memory structure that contains a network of
associations about one’s feared stimulus, escape or avoidance responses, and meaning
of the feared stimulus and response.
In order for exposure to reduce a patient’s fear, Foa and Kozak (1986) suggested
that the following two conditions need to occur. First, the patient’s fear structure needs
to be activated by the exposure stimulus. Activation can be measured by increases in
a patient’s subjective and physiological fear that occur in response to being presented
with the feared stimulus. Second, the new information that is encoded during the
patient’s exposure practice must be incompatible with the previous information that
was stored in the fear structure. The best indicators for predicting who will be able to
encode new information during exposures include the experiencing of (a) heightened
subjective and physiological fear during the exposure practice, (b) within-session
reduction in subjective and physiological fear, and (c) between-session reduction in
subjective and physiological fear (Foa & Kozak, 1986).
Additionally, the following conditions have been proposed as necessary for acti-
vating one’s fear structure and promoting the encoding of new information. First,
the contents of the exposure need to match the information that is represented in
the patient’s fear structure. Matching can include information that is related to the
patient’s feared stimuli, escape or avoidance behaviors, or the meaning they have
given the feared stimuli. Second, the medium of exposure (i.e., in vivo, imaginal, VR)
must be able to access the fear structure. Third, the duration of the exposure must be
long enough for the patient to experience decreases in subjective and physiological
fear. Fourth, the information presented during an exposure needs to be sufficiently
attended to so that the patient’s fear structure can be activated and subsequently
modified (Foa & Kozak, 1986).
According to emotional processing theory, there are several processes through
which fear reduction during exposure occurs. First, it has been proposed that exposure
promotes within-session reduction in physiological fear, which, in turn, generates
information that is incompatible with one’s fear structure. As a result, the pre-existing
association between the feared stimulus and the conditioned fear response weakens
(Foa & Kozak, 1986). Second, it has also been proposed that exposure works by
changing the meaning that individuals make about their feared stimulus. Specifically,
Foa and Kozak (1986) proposed that exposure may reduce probability estimations
related to the likelihood of being harmed, as well as the negativity of valence.
Foa and Kozak’s (1986) emotional processing theory has been updated twice
(Foa & McNally, 1996; Foa, Huppert, & Cahill, 2006). First, Foa and McNally
(1996) revised the emotional processing theory to take into account Bouton’s (1988)
findings, suggesting that fear reduction may involve the formation of new associations,
rather than the weakening of old associations. As a result, the theory now states that
“successful exposure therapy may not involve the abolition of existing pathological
associations, but rather the establishment of new, nonpathological ones” (Foa &
McNally, 1996, p. 339). Second, Foa et al. (2006) reviewed research investigating
the association between within-session fear reduction and treatment outcome, and
concluded that within-session fear reduction may not actually be a necessary condition
for exposure therapy to be effective.
Exposure Practices within Cognitive

Behavioral Therapy Protocols
Exposure therapy is often included as a component of broader cognitive behav-

ioral therapy (CBT) protocols (e.g., Craske & Barlow, 2007) that typically include
various combinations of exposure, cognitive strategies (e.g., cognitive restructuring),
relaxation-based strategies (e.g., progressive muscle relaxation), and other techniques.
Although exposure-based therapies have been found to be efficacious for many psy-
chological disorders (for a review, see Abramowitz et al., 2011), the relative efficacy
of exposure therapy alone versus exposure therapy in combination with additional
components (e.g., cognitive strategies and/or relaxation strategies) has yielded mixed
results. For instance, some studies investigating the efficacy of psychological treat-
ments for social anxiety disorder have found that adding cognitive restructuring to
exposure therapy provides additional benefits, when compared with exposure therapy
alone (for a review, see Antony & Rowa, 2008).
Given these equivocal findings, there currently remains some debate in the literature
as to whether the combination of exposure therapy with additional strategies (e.g.,
cognitive or relaxation strategies) is more efficacious than exposure therapy alone
(Epp, Dobson, & Cottraux, 2009). As various researchers have discussed (e.g.,
Abramowitz et al., 2011; Epp et al., 2009), there are many barriers that make it
difficult to disentangle the relative efficacy of these different treatment components.
First, the issue of treatment labeling (i.e., the inconsistency in how treatments that
include the same procedures are labeled) is a significant concern that makes it difficult
to compare the relative efficacy of exposure therapy alone versus the combination
of exposure therapy and cognitive strategies (Abramowitz et al., 2011; Epp et al.,
2009). In addition, the relative efficacy of cognitive therapy alone has been evaluated
much less frequently than the relative efficacy of exposure therapy alone; thus, future
randomized controlled trials that directly compare behavioral and cognitive strategies
could greatly inform this debate (Deacon & Abramowitz, 2004).
Although current research is mixed regarding the efficacy of combining exposure
therapy with cognitive strategies, there are a number of potential benefits of incor-
porating cognitive restructuring with exposure therapy. Specifically, previous research
has found that the combination of exposure therapy and cognitive strategies was less
aversive for patients (Hunt et al., 2006) and resulted in fewer treatment dropouts
(Vogel, Stiles, & Götestam, 2004), when compared with exposure therapy alone. In
addition, the inclusion of cognitive strategies may help patients to better engage in
exposure-based strategies (Bryant et al., 2008).
Generating Exposure Practices
Constructing a Hierarchy
A hierarchy is an individually tailored list of situations that a patient fears or avoids,
rank ordered with the least anxiety-provoking situations at the bottom and the
most anxiety-provoking situations at the top. Exposure hierarchies typically consist
of about 10–15 items. A hierarchy is used to guide a patient’s exposure practices
and can also be used as a measure of therapeutic change (e.g., Katerelos, Hawley,
Antony, & McCabe, 2008). Before creating an exposure hierarchy, a therapist should
complete a thorough assessment of the patient’s fear. That is, the therapist and patient
should work collaboratively to understand the patient’s (a) feared stimuli, (b) feared
consequences, (c) fear-related safety behaviors, and (d) fear triggers and contexts (for
a review, see Moscovitch et al., 2009).
Once the assessment is complete, the therapist and patient should be able to
identify specific situations that will allow the patient to confront feared stimuli, test
out feared consequences, and eliminate safety behaviors that may interfere with new
learning (Moscovitch et al., 2009). As a general rule, it is recommended that a
patient’s hierarchy include items that directly map onto the specific feared situations,
cognitions, and physiological reactions (Abramowitz et al., 2011). In addition, items
should be as detailed as possible, specifying variables that may influence fear (e.g.,
duration of the practice, who is present during the practice; Antony & Swinson, 2000).
Effect of Context
When constructing a hierarchy with a patient, it is important to keep in mind that
extinction learning has been found to be highly dependent on the context of expo-
sure practices. For example, extinction learning has been found to be dependent
on external cues (e.g., the physical environment, background stimuli, etc.), internal
cues (e.g., drugs, hormones, etc.), and the passage of time (Bouton, 2000, 2002).
Findings from both animal (e.g., Gunther, Denniston, & Miller, 1998) and human
(Bouton, Kenney, & Rosengard, 1990; Mystkowski, Mineka, Vernon, & Zinbarg,
2003; Rodriguez, Craske, Mineka, & Hladek, 1999) studies suggest that the context
in which exposure occurs affects outcomes. In light of these findings, several investiga-
tors (e.g., Bouton, 2000, 2002; Powers, Smits, Leyro, & Otto, 2007) have suggested
specific recommendations for maximizing the durability and generalizability of expo-
sure practices. First, exposures should be conducted across several different contexts
throughout treatment so that the number of cues for recall of extinction learning
is maximized (Bouton, 2002). Furthermore, in order for the effects of exposure
practices to generalize to the patient’s daily life, exposures should be conducted in
situations in which the patient’s fear is most likely to be problematic (Bouton, 2002).
Third, it is important that patients’ learning be independent of contexts that will

not be present in the future (e.g., the therapist, medication; Powers et al., 2007).
Finally, introducing retrieval cues that are associated with extinction learning and
then training the patient to recall these cues when confronted with a feared situation
at a later date may help to prevent relapse (Bouton, 2002; Powers et al., 2007). For
example, Mystkowski, Craske, Echiverri, and Labus (2006) found that participants
with a fear of spiders who were instructed to recall the extinction-learning environ-
ment just before being exposed to a spider in a new environment reported less return
of fear than did participants who were not instructed to recall the extinction-learning
environment.
Guidelines for Conducting Effective Exposure Practices
Although the benefits of exposure therapy have been well documented, less is known
about the optimal conditions under which exposure may work. Given that a number of
variables may moderate (i.e., enhance or interfere with) extinction learning, it is impor-
tant to pay attention to factors that may influence the efficacy of exposure therapy.
Predictability and Perceived Control

Maximizing predictability and a patient’s perception of control over exposures are
two factors that have been found to influence the outcome of exposure practices. In
a study of predictability in participants with snake fears, Lopatka (1989) found that
the completion of predictable exposures led to less avoidance than did unpredictable
exposures. Studies investigating the importance of perceived controllability, however,
have yielded mixed results. For example, some studies have found that participants
experience a greater treatment response when they are able to control the intensity of
their exposure practices (e.g., McGlynn, Rose, & Lazarte, 1994; Rose, McGlynn, &
Lazarte, 1995), whereas other studies found that one’s perceived control over the
intensity of exposure practices does not influence treatment response (e.g., Craske,
Bunt, Rapee, & Barlow, 1991; McGlynn, Rose, & Jacobson, 1995).
Despite the potential benefits of predictability and perceived control, there are
some exposure practices for which the outcome may be inherently unpredictable or
uncontrollable (e.g., asking someone out on a date). Thus, when a patient is ready to
begin unpredictable or uncontrollable exposure practices, it may be useful to consider
a range of possible outcomes and ways to cope with each outcome before the exposure
practice begins. Although the final outcome will still be unknown, at least the patient
will be prepared for various outcomes, both positive and negative.
Frequency of Exposure Practices

Past research investigating the optimal duration and spacing of exposure practices
has yielded mixed results. Some studies have found that massed exposure practices
are more effective than spaced exposure practices (e.g., Dua, 1972; Foa, Jameson,
Turner, & Payne, 1980), whereas others have found that spaced exposure practices
are slightly more effective than massed exposure practices (e.g., Ramsay, Barends,
Breuker, & Kruseman, 1966). In addition, some studies have found no significant dif-
ferences between massed and spaced exposure practices (e.g., Chambless, 1990; Grey,
Rachman, & Sartory, 1981). However, these studies relied on different methodologies
and samples; thus, it is difficult to make a direct comparison of their results.
In addition, treatment studies investigating the short- and long-term effects of
massed exposure practices versus spaced exposure practices have yielded mixed results
(e.g., Abramowitz, Foa, & Franklin, 2003; Bohni, Spindler, Arendt, Hougaard, &
Rosenberg, 2009). Abramowitz et al. (2003) compared a massed treatment schedule
(15 sessions of exposure and response prevention [ERP] delivered over 3 weeks)
to a spaced treatment schedule (15 sessions of ERP delivered twice weekly over 8
weeks) with a sample of individuals with OCD. Results of this study found that the
massed treatment schedule was more effective than the spaced treatment schedule at
posttreatment; however, no significant differences were found at 3-month follow-up
because participants in the massed condition experienced some reduction in their
treatment gains.
In another randomized controlled trial of individuals with panic disorder, Bohni
et al. (2009) found no significant differences between their massed CBT program
(daily 4-hour sessions for the first week, two 2-hour sessions for the second week, and
one 2-hour session for the third week) and spaced CBT program (one 2-hour session
per week for 13 weeks) at posttreatment or follow-up. Thus, given that the massed
treatment program appeared to be as effective as the standard, spaced CBT program,
these results suggest that patients can complete either a massed or spaced schedule,
depending on the preference of the patient or therapist.
Duration of Exposure Practices

Generally, it is recommended that an exposure session last until a patient’s fear has
decreased to a mild or moderate level, or until the patient has learned that the situation
is manageable and safe (Craske & Mystkowski, 2006). If a patient has to discontinue
an exposure practice before the fear has decreased, then it is recommended that the
patient return to the feared situation after a short break.
Although early research considered prolonged exposure practices to be more effec-
tive than briefer exposure practices, because they led to greater within-session fear
reduction (e.g., Chaplin & Levine, 1981; Stern & Marks, 1973), recent evidence
suggests that it may not be necessary for a patient to experience within-session fear
reduction to have improvements across exposure practices (Craske & Mystkowski,
2006). van Minnen and Foa (2006) found that 60-minute imaginal exposure prac-
tices led to significantly greater within-session fear reduction than did 30-minute
imaginal exposure practices for individuals with posttraumatic stress disorder (PTSD);
however, no significant group differences were found for between-session fear reduc-
tion or improvement in PTSD symptoms. Moreover, given that between-session fear
reduction was associated with treatment outcome and within-session fear reduction
was not, results of this study support the notion that within-session fear reduction may
not be necessary for an exposure practice to be effective. Thus, practices in which fear
does not decrease may still be sufficient for a patient to learn that feared consequences
are unlikely to occur, and that the anxiety, although still high, is manageable.
Intensity of Exposure Practices

As previously mentioned, exposure therapy typically includes a hierarchy, beginning
with less fear-provoking practices and moving on to more fear-provoking practices.
Although research suggests that starting with less fear-provoking tasks, rather than
more fear-provoking tasks, will not affect treatment outcome (Gelder et al., 1973),
the effects of an exposure practice that is very low in intensity may not generalize
to other more fear-provoking situations. On the other hand, if the intensity of the
exposure practice is too high, then patients may stop their practice prematurely or
discontinue treatment. In addition, given that inducing horror does not appear to lead
to an improved treatment response when compared to more moderately frightening
practices (Foa, Blau, Prout, & Latimer, 1977) and greater levels of within-session fear
activation are associated with poorer treatment outcomes (Meuret, Seidel, Rosenfield,
Hofmann, & Rosenfield, 1982, in press), practices should be designed to induce
manageable levels of fear so that patients’ underlying fear structures can be activated
and new learning can occur (Foa & McNally, 1996). Furthermore, although it
is typically recommended that patients continue their specified exposure practices
until the situation produces only mild to moderate fear, Meuret et al. (in press)
found that greater within- and between-session fear reduction was not related to
treatment outcome. Thus, future research is required to determine the extent to
which a patient’s fear needs to decrease before increasing the intensity of his or her
practice.
Role of Safety Behaviors

Safety behaviors include any overt or covert behaviors used to prevent a feared outcome
from occurring. Examples include subtle avoidance strategies (e.g., distraction or
thought suppression), overt actions (e.g., escape or complete avoidance), reliance
on safety objects (e.g., carrying medication or only entering a feared situation while
accompanied), or the overuse of alcohol or drugs to manage anxiety (Wells et al.,
1995). Safety behaviors may be best viewed as existing on a continuum; even adaptive
coping with anxiety includes cognitive and behavioral strategies aimed at managing
arousal, and it is only when such strategies are intended to prevent or minimize a feared
catastrophe that they may interfere with the potential to disconfirm maladaptive beliefs
(Thwaites & Freeston, 2005). Safety behaviors have been documented across several
psychological disorders, including anxiety disorders (e.g., Kim, 2005; Salkovskis,
Clark, Hackmann, Wells, & Gelder, 1999), sleep disorders (e.g., Hood, Carney,
& Harris, 2011), depression (e.g., Moulds, Kandris, Williams, & Lang, 2008), and
psychosis (e.g., Freeman et al., 2007).
Although safety behaviors help to alleviate an individual’s anxiety in the short term,
many researchers believe that these behaviors undermine the effectiveness of exposure
practices and thus maintain fear in the long term. Moreover, these behaviors may
also prevent individuals from fully engaging in their exposure practice, and ultimately
interfere with the acquisition of corrective information in the exposure environment.

For example, a patient with social anxiety disorder who fears attending a party because
of the possibility of being negatively evaluated or judged for sweating might wear
black clothing to a party to hide sweating. Although wearing black will likely reduce
anxiety at the party, it may also maintain the belief that sweating in front of others is
threatening because it prevents learning about what might happen if people were to
notice the sweating.
Given that the use of safety behaviors has been proposed as a maintaining fac-
tor for several psychological disorders, and the elimination of safety behaviors has
been found to improve treatment outcome (e.g., Morgan & Raffle, 1999; Wells
et al., 1995), the traditional recommendation has been to encourage patients to
drop their use of their safety behaviors during exposure therapy so that they can
encode and integrate new corrective information. However, recent studies of the
effect of safety behaviors have yielded mixed results. In a study of in vivo expo-
sure for snake fear, Milosevic and Radomsky (2008) found that participants who
were permitted to use safety behaviors (i.e., wearing protective gear) approached
closer to the snake at pretest than those who were not permitted to use safety
behaviors. Both groups showed significant and equivalent improvement following
the exposure session. Similar results were found by Hood, Antony, Koerner, and
Monson (2010) in a study of exposure for spider phobia. In this study, participants
who were encouraged to use idiographic safety behaviors (chosen from a list of
cognitive and behavioral possibilities) during exposure approached a tarantula at a
quicker rate than those who did not. Both groups showed comparable fear reduction
following exposure and were similarly able to approach the spider, though these
improvements tended to be more stable in individuals who refrained from using
safety behaviors. Taken together, these results suggest that safety behaviors may help
individuals approach feared stimuli more quickly without interfering with anxiety
reduction.
These results also support the notion that flexibility about safety behaviors in
clinical practice is warranted, and that judicious use of safety behaviors, particularly
at the beginning of treatment, may actually facilitate exposure and make treatment
more palatable to patients (Rachman, Radomsky, & Shafran, 2008). Accordingly,
research has found that the judicious use of safety behaviors does not diminish the
efficacy of exposure therapy (e.g., Deacon, Sy, Lickel, & Nelson, 2010), suggesting
that patients may be encouraged to drop their safety behaviors in a gradual way
(i.e., safety behavior use could be incorporated into one’s hierarchy, such that early
exposures permit the use of safety behaviors, and later exposures do not include such
behaviors).
Importantly, it has been noted that the effect of safety behaviors may vary with
the type of anxiety being treated. For instance, the majority of studies showing
beneficial effects of safety behavior have looked at specific phobia. In contrast,
there is little research regarding the effect of safety behaviors in disorders such
as PTSD or generalized anxiety disorder, for example. Furthermore, few studies
have employed meaningful follow-up assessments to investigate the long-term effects
of safety behavior use, and more research is needed in this area (Helbig-Lang &
Petermann, 2010).
Use of Medication During Exposure Therapy

There has been debate over whether use of medication during exposure therapy
facilitates or interferes with extinction learning. Literature reviews across psycho-
logical disorders indicate that there is no clear evidence that combination therapy
produces better long-term outcomes than exposure therapy alone (Foa, Franklin, &
Moser, 2002; Otto, Smits, & Reese, 2005). However, it is important to recognize
that many patients entering exposure treatments may already be receiving ongoing
pharmacotherapy (e.g., an antidepressant for anxiety, or benzodiazepines for relief
of anxiety symptoms during planned or naturalistic exposure to feared stimuli),
effectively resulting in combination treatment.
Barlow et al. (2000) investigated the separate and combined effects of imipramine
(a tricyclic antidepressant) and CBT (including interoceptive exposure) in a large-scale
study of panic disorder treatment. The addition of imipramine improved short-term
outcomes, but these gains were not maintained. In fact, at 1-year follow-up, patients
who had received combination therapy had higher relapse rates than did those who
received CBT alone or CBT plus placebo. This finding suggests that CBT confers
a more durable effect on outcome than imipramine in panic disorder, and that
medication may interfere with the long-term benefits of CBT for panic disorder.
However, because exposure was part of a comprehensive CBT package that included
other strategies, it is impossible from this study to make any conclusions about the
effects of medication on exposure in particular.
Marks et al. (1993) tested the effects of benzodiazepines on exposure for panic
disorder with agoraphobia in a study in which patients were randomly assigned to
receive alprazolam and exposure, alprazolam and relaxation (a psychological placebo),
placebo and exposure, or placebo and relaxation. The authors found that exposure
led to greater gains than did alprazolam. Adding alprazolam to exposure treatment
yielded little benefit during treatment and was associated with reduced gains at
follow-up (i.e., after treatment was withdrawn) than exposure alone. This finding
suggests that adding a benzodiazepine interferes with the effect of exposure. Westra,
Stewart, and Conrad (2002) found that this interference is true particularly when
benzodiazepines are taken on an as-needed (PRN) basis. In this study, patients
who took benzodiazepines PRN had worse outcomes after CBT for panic disorder
with agoraphobia, whereas those individuals who took benzodiazepines regularly had
outcomes equivalent to unmedicated patients. Lastly, the effect of benzodiazepines
on exposure may vary depending on timing of drug administration. For instance,
Marks, Viswanathan, Lipsedge, and Gardner (1972) found that conducting exposure
sessions when the effect of diazepam was waning resulted in greater improvement
of phobias than exposure sessions conducted when the effect of diazepam was at its
peak, or when placebo was administered.
Medications may interfere with exposure by blocking the activation of fear structures
that is presumed necessary for cognitive change in exposure treatments (Foa & Kozak,
1986). In addition, the use of medication during exposure may create context-specific
extinction that may not generalize when medication is withdrawn (e.g., Bouton,
2002). Although exposure therapy and medication appear to work via different and
not necessarily compatible pathways, the ways in which medications and exposure
therapy interact remain poorly understood.
Cognitive Enhancers
A substantial body of evidence supports the involvement of the amygdala in fear-
based learning (LaBar, Gatenby, Gore, LeDoux, & Phelps, 1998; Phillips & LeDoux,
1992). In particular, both fear learning and extinction learning are dependent on the
N-methyl-D-aspartate (NMDA) glutamatergic receptor in the amygdala. Interfering
with the activity of the NMDA receptor has been shown to block extinction learning
(Falls, Miserendino, & Davis, 1992), whereas enhancing the activity of the NMDA
receptor with d-cycloserine (DCS; a partial agonist of the NMDA receptor) has been
shown to facilitate fear extinction in rats (Ledgerwood, Richardson, & Cranney,
2003; Walker, Ressler, Lu, & Davis, 2002). These findings have stimulated a line
of research investigating the effects of DCS on extinction learning during exposure
therapy for individuals with anxiety disorders.
Ressler et al. (2004) found that administering DCS 2 to 4 hours prior to two sessions
of VR exposure therapy for individuals with acrophobia resulted in significantly larger
reductions in symptoms than exposure therapy plus placebo. These results were
maintained at 1-week and 3-month follow-up. DCS has also been shown to improve
outcomes relative to placebo when combined with exposure therapy in two separate
investigations involving individuals with social anxiety disorder (Guastella et al., 2008;
Hofmann et al., 2006). Both of these studies used 50 mg of DCS administered 1 hour
prior to therapy sessions, with four exposure sessions in total, and in the Hofmann
et al. (2006) study, gains were maintained at 1-month follow-up.
Investigations of augmentation of exposure with DCS for OCD have yielded
mixed results, and seem to vary depending on timing, dosage, and frequency of DCS
administration. Storch et al. (2007) augmented 12 ERP sessions with 250 mg DCS or
placebo administered 4 hours prior to weekly treatment sessions. These researchers did
not find any differences between groups on OCD symptoms at posttreatment or at 2-
month follow-up. In contrast, two studies found that augmentation with DCS during
ERP leads to quicker reductions in symptom severity during treatment, but these
gains do not exceed those of exposure alone at posttreatment or follow-up. Kushner
et al. (2007) administered 125 mg DCS 2 hours before 10 twice-weekly exposure
sessions and found differences at midtreatment on subjective units of discomfort and
anxiety, but no differences in OCD symptoms at posttreatment. Wilhelm et al. (2008)
administered 100 mg DCS 1 hour prior to 10 twice-weekly exposure therapy sessions
and found that augmentation with DCS was associated with reduced OCD severity
at midtreatment but not at posttreatment or at 1-month follow-up.
Thus, a key question with respect to results of DCS clinical studies is whether
DCS actually enhances extinction learning (as suggested by some animal studies;
e.g., Ledgerwood, Richardson, & Cranney, 2005) or merely speeds up the “normal”
response. Investigations of DCS augmentation of interoceptive exposure for panic
disorder support the latter notion. Otto et al. (2010) augmented interoceptive
exposure sessions for individuals with panic disorder (the last three sessions of a
five-session CBT protocol) with 50 mg DCS administered 1 hour prior to treatment
sessions. Augmentation with DCS was associated with improved outcomes that were
maintained at 1-month follow-up. However, there was also evidence that some
patients who had received placebo continued to make gains posttreatment, thereby
eliminating group differences with respect to the proportion of patients who met
criteria for clinically significant change at follow-up. Chasson et al. (2010) examined
the slopes of treatment response for ERP with and without DCS, using the results
of Kushner et al.’s (2007) study. Treatment response was achieved 2.3 times faster
when ERP was augmented with DCS, leading the authors to conclude that DCS
“jump-starts” the effects of ERP but may not be useful beyond a certain number
of sessions. However, it is possible that a “jump-start” could lead to a reduced
number of sessions, thereby reducing treatment cost and being more palatable to
patients.
Finally, methodological variance in DCS investigations has made it difficult to
carry out level comparisons across studies. A meta-analysis of studies examining DCS
augmentation of fear extinction or exposure therapy (Norberg, Krystal, & Tolin,
2008) concluded that DCS is most effective when administered a limited number
of times and when given immediately before or after extinction training or exposure
therapy. This timing is thought to be optimal in order to achieve peak plasma levels
at the time of memory consolidation (Grillon, 2009).
Conclusion
Exposure, the systematic and controlled confrontation of feared objects and situations,
has been found to be an efficacious treatment technique for fear reduction. Current
evidence suggests that fear reduction during exposure occurs because patients learn
new information that is incompatible with their expected fear outcome. Numerous
variables, including predictability and perceived control, frequency, duration, and
intensity of exposure practice, have been found to influence the process and outcome
of exposure therapy, which suggests that many factors need to be taken into account
when trying to optimize a patient’s exposure practice. Despite the well-established
efficacy of exposure-based therapies, a number of controversies remain. Specifically,
future studies are needed to elucidate the relationship between treatment out-
come and within-session fear reduction, the use of safety behaviors and medication
during exposure therapy, and the beneficial effect of cognitive enhancers such as
d-cycloserine.
References
Abramowitz, J. S. (1996). Variants of exposure and response prevention in the treatment of
obsessive compulsive disorder: A meta-analysis. Behavior Therapy, 27 , 583–600.
Abramowitz, J. S. (2006). Understanding and treating obsessive-compulsive disorder: A cognitive-
behavioral approach. Mahwah, NJ: Erlbaum.
Abramowitz, J. S., Deacon, B. J., & Whiteside, S. P. H. (2011). Exposure therapy for anxiety:
Principles and practice. New York, NY: Guilford Press.
Abramowitz, J. S., Foa, E. B., & Franklin, M. E. (2003). Exposure and ritual prevention for
obsessive-compulsive disorder: Effects of intensive versus twice-weekly sessions. Journal
American Psychological Association Presidential Task Force on Evidence-Based Practice.
(2006). Evidence-based practice in psychology. American Psychologist, 61, 271–285.
Antony, M. M., Ledley, D. R., Liss, A., & Swinson, R. P. (2006). Responses to symptom
induction exercises in panic disorder. Behaviour Research and Therapy, 44, 85–98.
Antony, M. M., & Rowa, K. (2008). Social anxiety disorder: Psychological approaches to assessment
and treatment. Göttingen, Germany: Hogrefe.
Antony, M. M., & Swinson, R. P. (2000). Phobic disorders and panic in adults: A guide to
assessment and treatment. Washington, DC: American Psychological Association.
Barlow, D. H., Craske, M. G., Cerny, J. A., & Klosko, J. S. (1989). Behavioral treatment of
panic disorder. Behavior Therapy, 20, 261–282.
Barlow, D. H., Gorman, J. M., Shear, M. K., & Woods, S. W. (2000). Cognitive-behavioral
therapy, imipramine, or their combination for panic disorder. Journal of the American
Medical Association, 283, 2529–2536.
Bohni, M. K., Spindler, H., Arendt, M., Hougaard, E., & Rosenberg, N. K. (2009). A
randomized study of massed three-week cognitive behavioural therapy schedule for panic
disorder. Acta Psychiatrica Scandinavica, 120, 187–195.
Bouton, M. E. (1988). Context and ambiguity in the extinction of emotional learning:
Implications for exposure therapy. Behaviour Research and Therapy, 26, 137–149.
Bouton, M. E. (2000). A learning theory perspective on lapse, relapse, and the maintenance of
behavior change. Health Psychology, 19, 57–63.
Bouton, M. E. (2002). Context, ambiguity, and unlearning: Sources of relapse after behavioral
extinction. Biological Psychiatry, 52, 976–986.
Bouton, M. E., Kenney, F. A., & Rosengard, C. (1990). State-dependent fear extinction with
two benzodiazepine tranquilizers. Behavioral Neuroscience, 104, 44–55.
Bryant, R. A., Moulds, M. L., Guthrie, R. M., Dang, S. T., Mastrodomenico, J., Nixon,
R. D. V., … Creamer, M. (2008). A randomized controlled trial of exposure therapy
and cognitive restructuring for posttraumatic stress disorder. Journal of Consulting and
Chambless, D. L. (1990). Spacing of exposure sessions in treatment of agoraphobia and simple
phobia. Behavior Therapy, 21, 217–229.
Chaplin, E. W., & Levine, B. A. (1981). The effects of total exposure duration and interrupted
versus continuous exposure in flooding therapy. Behavior Therapy, 12, 360–368.
Chasson, G. S., Buhlmann, U., Tolin, D. F., Rao, S. R., Reese, H. E., Rowley, T., … Wilhelm,
S. (2010). Need for speed: Evaluating slopes of OCD recovery in behavior therapy
enhanced with d-cycloserine. Behaviour Research and Therapy, 48, 675–679.
Craske, M. G., & Barlow, D. H. (2007). Mastery of your anxiety and panic: Therapist guide
(4th ed.). New York, NY: Oxford University Press.
Craske, M. G., Bunt, R., Rapee, R. M., & Barlow, D. H. (1991). Perceived control and
controllability during in vivo exposure: Spider phobics. Journal of Anxiety Disorders, 5,
285–292.
Craske, M. G., & Mystkowski, J. L. (2006). Exposure therapy and extinction: Clinical studies.
In M. G. Craske, D. Hermans, & D. Vansteenswegen (Eds.), Fear and learning: From basic
processes to clinical implications (pp. 217–233). Washington, DC: American Psychological
Association.
Craske, M. G., Rowe, M., Lewin, M., & Noriega-Dimitri, R. (1997). Interoceptive exposure
versus breathing retraining within cognitive-behavioural therapy for panic disorder with
agoraphobia. British Journal of Clinical Psychology, 36, 85–99.
Deacon, B. J., & Abramowitz, J. S. (2004). Cognitive and behavioral treatments for anxiety
disorders: A review of meta-analytic findings. Journal of Clinical Psychology, 60, 429–441.
Deacon, B. J., Sy, J. T., Lickel, J. J., & Nelson, E. A. (2010). Does the judicious use of safety
behaviors improve the efficacy and acceptability of exposure therapy for claustrophobic
fear? Journal of Behavior Therapy and Experimental Psychiatry, 41, 71–80.
De Moor, W. (1970). Systematic desensitization versus prolonged high intensity stimulation
(flooding). Journal of Behavior Therapy and Experimental Psychiatry, 1, 45–52.
Dua, P. S. (1972). Group desensitization of a phobia with three massing procedures. Journal
of Counseling Psychology, 19, 125–129.
Emmelkamp, P. M. G., & Wessels, H. (1975). Flooding in imagination vs flooding in vivo: A
comparison with agoraphobics. Behaviour Research and Therapy, 13, 7–15.
Epp, A. M., Dobson, K. S., & Cottraux, J. (2009). Efficacy, indications and applications of
individual cognitive-behavioral therapy for psychiatric patients. In G. O. Gabbard (Ed.),
Textbook of psychiatric treatments (pp. 239–262). Washington, DC: American Psychiatric
Publishing.
Falls, W., Miserendino, M., & Davis, M. (1992). Extinction of fear-potentiated startle: Blockade
by infusion of an NMDA antagonist into the amygdala. Journal of Neuroscience, 12,
854–863.
Foa, E. B., Blau, J. S., Prout, M., & Latimer, P. (1977). Is horror a necessary component of
flooding (implosion)? Behaviour Research and Therapy, 15, 397–402.
Foa, E. B., Franklin, M. E., & Moser, J. (2002). Context in the clinic: How well do cognitive-
behavioral therapies and medications work in combination? Biological Psychiatry, 52,
987–997.
Foa, E. B., Huppert, J. D., & Cahill, S. P. (2006). Emotional processing theory: An update. In
B. O. Rothbaum (Ed.), Pathological anxiety: Emotional processing in etiology and treatment
(pp. 3–24). New York, NY: Guilford Press.
Foa, E. B., Jameson, J. S., Turner, R. M., & Payne, L. L. (1980). Massed vs. spaced exposure
sessions in the treatment of agoraphobia. Behaviour Research and Therapy, 18, 333–338.
Foa, E. B., & Kozak, M. J. (1986). Emotional processing of fear: Exposure to corrective
information. Psychological Bulletin, 99, 20–35.
Foa, E. B., & McNally, R. J. (1996). Mechanisms of change in exposure therapy. In R.
Rapee (Ed.), Current controversies in the anxiety disorders (pp. 329–343). New York, NY:
Guilford Press.
Foa, E. B., Steketee, G., & Grayson, J. B. (1985). Imaginal and in vivo exposure: A comparison
with obsessive-compulsive checkers. Behavior Therapy, 16, 292–302.
Freeman, D., Garety, P. A., Kuipers, E., Fowler, D., Bebbington, P. E., & Dunn, G. (2007).
Acting on persecutory delusions: The importance of safety-seeking. Behaviour Research
and Therapy, 45, 89–99.
Freud, S. (1950). Turnings in the world of psychoanalytic therapy. In J. Strachey (Ed.),
Collected papers of Sigmund Freud (Vol. 2, pp. 399–400). London, England: Hogarth
and Institute of Psychoanalysis. (Original work published 1919)
Garcia-Palacios, A., Botella, C., Hoffman, H., & Fabregat, S. (2007). Comparing acceptance
and refusal rates of virtual reality exposure vs. in vivo exposure by patients with specific
phobias. Cyberpsychology and Behavior, 10, 722–724.
Gelder, M. G., Bancroft, J. J., Gath, D. H., Johnson, D. W., Mathew, A. M., & Shaw, P. M.
(1973). Specific and non-specific factors in behavior therapy. British Journal of Psychiatry,
123, 445–462.
Goldstein, A. J., & Chambless, D. L. (1978). A reanalysis of agoraphobia. Behavior Therapy,
9, 47–59.
Grey, S., Rachman, S., & Sartory, G. (1981). Return of fear: The role of inhibition. Behaviour
Grillon, C. (2009). D-cycloserine facilitation of fear extinction and exposure-based therapy
might rely on lower-level, automatic mechanisms. Biological Psychiatry, 66, 636–641.
Guastella, A. J., Richardson, R., Lovibond, P. F., Rapee, R. M., Gaston, J. E., Mitchell, P.,
& Dadds, M. R. (2008). A randomized controlled trial of d-cycloserine enhancement of
exposure therapy for social anxiety disorder. Biological Psychiatry, 63, 544–549.
Gunther, L. M., Denniston, J. C., & Miller, R. R. (1998). Conducting exposure treatment in
multiple contexts can prevent relapse. Behaviour Research and Therapy, 36, 75–91.
Helbig-Lang, S., & Petermann, F. (2010). Tolerate or eliminate? A systematic review on the
effects of safety behavior across anxiety disorders. Clinical Psychology: Science and Practice,
17 , 218–233.
Hofmann, S. G., Meuret, A. E., Smits, J. A. J., Simon, N. M., Pollack, M. H., Eisenmenger,
K., … Otto, M. W. (2006). Augmentation of exposure therapy with d-cycloserine for
social anxiety disorder. Archives of General Psychiatry, 63, 298–304.
Hood, H. K., Antony, M. M., Koerner, N., & Monson, C. M. (2010). Effects of safety behaviors
on fear reduction during exposure. Behaviour Research and Therapy, 48, 1161–1169.
Hood, H. K., Carney, C. E., & Harris, A. L. (2011). Rethinking safety behaviors in insomnia:
Examining the perceived utility of sleep-related safety behaviors. Behavior Therapy, 42,
644–654.
Hunt, M., Bylsma, L., Brock, J., Fenton, M., Goldberg, A., Miller, R., … Urgelles, J. (2006).
The role of imagery in the maintenance and treatment of snake fear. Journal of Behavior
Therapy and Experimental Psychiatry, 37 , 283–298.
Jacobson, E. (1938). Progressive relaxation. Chicago, IL: University of Chicago Press.
Janet, P. (1925). Psychological healing: A historical and clinical study. London, England: Allen
& Unwin.
Jones, M. C. (1924). A laboratory study of fear: The case of Peter. Journal of General Psychology,
31, 308–315.
Katerelos, M., Hawley, L. L., Antony, M. M., & McCabe, R. E. (2008). The exposure hierarchy
as a measure of progress and efficacy in the treatment of social anxiety disorder. Behavior
Modification, 32, 504–518.
Kazdin, A. E., & Wilson, G. T. (1978). Evaluation of behavior therapy: Issues, evidence, and
research strategies. Oxford, England: Ballinger.
Kim, E. J. (2005). The effect of the decreased safety behaviors on anxiety and negative thoughts
in social phobics. Journal of Anxiety Disorders, 19, 69–86.
Kushner, M. G., Kim, S. W., Donahue, C., Thuras, P., Adson, D., Kotlyar, M., … Foa, E.
B. (2007). D-cycloserine augmented exposure therapy for obsessive-compulsive disorder.
Biological Psychiatry, 62, 835–838.
LaBar, K. S., Gatenby, J. C., Gore, J. C., LeDoux, J. E., & Phelps, E. A. (1998). Human
amygdala activation during conditioned fear acquisition and extinction: A mixed-trial
fMRI study. Neuron, 20, 937–945.
Lang, P. J. (1977). Imagery in therapy: An information processing analysis of fear. Behavior
Therapy, 8, 862–886.
Lang, P. J. (1979). A bio-informational theory of emotional imagery. Psychophysiology, 16,
495–512.
Ledgerwood, L., Richardson, R., & Cranney, J. (2003). Effects of d-cycloserine on extinction
of conditioned freezing. Behavioral Neuroscience, 117 , 341–349.
Ledgerwood, L., Richardson, R., & Cranney, J. (2005). D-cycloserine facilitates extinction of
learned fear: Effects on reacquisition and generalized extinction. Biological Psychiatry, 57 ,
841–847.
Lopatka, C. L. (1989). The role of unexpected events in avoidance (Unpublished master’s thesis).
University of Albany, State University of New York.
Marks, I. M., Boulougouris, J., & Marset, P. (1971). Flooding versus desensitization in
the treatment of phobic patients: A crossover study. British Journal of Psychiatry, 119,
353–375.
Marks, I. M., Swinson, R. P., Basoglu, M., Kuch, K., Noshirvani, H., O’Sullivan, G., …
Sengun, S. (1993). Alprazolam and exposure alone and combined in panic disorder with
agoraphobia: A controlled study in London and Toronto. British Journal of Psychiatry,
162, 776–787.
Marks, I. M., Viswanathan, R., Lipsedge, M., & Gardner, R. (1972). Enhanced relief of phobias
by flooding during waning diazepam effect. British Journal of Psychiatry, 121, 493–505.
McGlynn, F. D., Rose, M. P., & Jacobson, N. (1995). Effects of control and of attentional
instructions on arousal and fear during exposure to phobia-cue stimuli. Journal of Anxiety
Disorders, 9, 451–461.
McGlynn, F. D., Rose, M. P., & Lazarte, A. (1994). Control and attention during exposure
influence arousal and fear among insect phobias. Behavior Modification, 18, 371–388.
Meuret, A. E., Seidel, A., Rosenfield, B., Hofmann, S. G., & Rosenfield, D. (in press). Does
fear reactivity during exposure predict panic symptom reduction? Journal of Consulting
and Clinical Psychology.
Meyer, V. (1966). Modification of expectations in cases with obsessional rituals. Behaviour
Milosevic, I., & Radomsky, A. S. (2008). Safety behaviour does not necessarily interfere with
exposure therapy. Behaviour Research and Therapy, 46, 1111–1118.
Morgan, H., & Raffle, C. (1999). Does reducing safety behaviors improve treatment response
in patients with social phobia? Australian and New Zealand Journal of Psychiatry, 33,
503–510.
Moscovitch, D. A., Antony, M. M., & Swinson, R. P. (2009). Exposure-based treatment
for anxiety disorders: Theory and process. In M. M. Antony & M. B. Stein (Eds.),
Oxford handbook of anxiety and related disorders (pp. 461–475). New York, NY: Oxford
University Press.
Moulds, M. L., Kandris, E., Williams, A. D., & Lang, T. J. (2008). The use of safety
behaviours to manage intrusive memories in depression. Behaviour Research and Therapy,
46, 573–580.
Mowrer, O. (1939). A stimulus–response analysis of anxiety and its role as a reinforcing agent.
Psychological Review, 46, 553–565.
Mowrer, O. (1960). Learning theory and behavior. New York, NY: John Wiley & Sons, Inc.
Mystkowski, J. L., Craske, M. G., Echiverri, A. M., & Labus, J. S. (2006). Mental reinstatement
of context and return of fear in spider-fearful participants. Behavior Therapy, 37 , 49–60.
Mystkowski, J. L., Mineka, S., Vernon, L. L., & Zinbarg, R. E. (2003). Changes in caffeine
states enhance return of fear in spider phobia. Journal of Consulting and Clinical
Norberg, M. M., Krystal, J. H., & Tolin, D. F. (2008). A meta-analysis of d-cycloserine and
the facilitation of fear extinction and exposure therapy. Biological Psychiatry, 63, 1118–
1126.
Öst, L.-G., Salkovskis, P. M., & Hellström, K. (1991). One-session therapist-directed exposure
vs. self-exposure in the treatment of spider phobia. Behavior Therapy, 22, 407–422.
Otto, M. W., Smits, J. A. J., & Reese, H. E. (2005). Combined psychotherapy and phar-
macotherapy for mood and anxiety disorders in adults: Review and analysis. Clinical
Psychology: Science and Practice, 12, 72–86.
Otto, M. W., Tolin, D. F., Simon, N. M., Pearlson, G. D., Basden, S., Meunier, S. A., …
Pollack, M. H. (2010). Efficacy of d-cycloserine for enhancing response to cognitive-
behavior therapy for panic disorder. Biological Psychiatry, 67 , 365–370.
Parsons, T. D., & Rizzo, A. A. (2008). Affective outcomes of virtual reality exposure therapy
for anxiety and specific phobias: A meta-analysis. Journal of Behavior Therapy and
Experimental Psychiatry, 39, 250–261.
Phillips, R., & LeDoux, J. (1992). Differential contribution of amygdala and hippocampus to
cued and contextual fear conditioning. Behavioral Neuroscience, 106, 274–285.
Powers, M. B., Smits, J. A. J., Leyro, T. M., & Otto, M. W. (2007). Translational research
perspectives on maximizing the effectiveness of exposure therapy. In D. C. S. Richard &
D. Lauterbach (Eds.), Handbook of exposure therapies (pp. 109–126). San Diego, CA:
Elsevier.
Rachman, S. (1976). The passing of the two-stage theory of fear and avoidance: Fresh
possibilities. Behaviour Research and Therapy, 14, 125–131.
Rachman, S. (1980). Emotional processing. Behaviour Research and Therapy, 14, 349–355.
Rachman, S., Radomsky, A. S., & Shafran, R. (2008). Safety behaviour: A reconsideration.
Behaviour Research and Therapy, 46, 163–173.
Ramsay, R. W., Barends, J., Breuker, J., & Kruseman, A. (1966). Massed versus spaced
desensitization of fear. Behaviour Research and Therapy, 4, 205–207.
Rescorla, R. A. (2001). Experimental extinction. In R. R. Mowrer & S. B. Klein (Eds.),
Handbook of contemporary learning theories (pp. 119–154). Mahwah, NJ: Erlbaum.
Ressler, K. J., Rothbaum, B. O., Tannenbaum, L., Anderson, P., Graap, K., Zimand, E., …
Davis, M. (2004). Cognitive enhancers as adjuncts to psychotherapy: Use of d-cycloserine
in phobic individuals to facilitate extinction of fear. Archives of General Psychiatry, 61,
1136–1144.
Rodriguez, B. I., Craske, M. G., Mineka, S., & Hladek, D. (1999). Context-specificity of
relapse: Effects of therapist and environmental context on return of fear. Behaviour
Research and Therapy, 37 , 845–862.
Rose, M. P., McGlynn, F. D., & Lazarte, A. (1995). Control and attention influence snake
phobics’ arousal and fear during laboratory confrontations with a caged snake. Journal of
Anxiety Disorders, 9, 293–302.
Salkovskis, P. M., Clark, D. M., Hackmann, A., Wells, A., & Gelder, M. G. (1999). An
experimental investigation of the role of safety-seeking behaviours in the maintenance of
panic disorder with agoraphobia. Behaviour Research and Therapy, 37 , 559–574.
Stampfl, T. G., & Levis, D. J. (1967). Essentials of implosive therapy: A learning-theory-based
psychodynamic behavioral therapy. Journal of Abnormal Psychology, 72, 496–503.
Stern, R. S., & Marks, I. M. (1973). Brief and prolonged exposure: A comparison in
agoraphobic patients. Archives of General Psychiatry, 28, 270–276.
Storch, E. A., Merlo, L. J., Bengtson, M., Murphy, T. K., Lewis, M. H., Yang, M. C., … Good-
man, W. K. (2007). D-cycloserine does not enhance exposure-response prevention therapy
in obsessive-compulsive disorder. International Journal of Clinical Psychopharmacology,
22, 230–237.
Thwaites, R., & Freeston, M. H. (2005). Safety-seeking behaviours: Fact or function? How
can we clinically differentiate between safety behaviours and adaptive coping strategies
across anxiety disorders? Behavioural and Cognitive Psychotherapy, 33, 177–188.
Tryon, W. W. (2005). Possible mechanisms for why desensitization and exposure therapy work.
van Minnen, A., & Foa, E. B. (2006). The effect of imaginal exposure length on outcome of
treatment for PTSD. Journal of Traumatic Stress, 19, 427–438.
Vogel, P. A., Stiles, T. C., & Götestam, K. G. (2004). Adding cognitive therapy elements to
exposure therapy for obsessive compulsive disorder: A controlled study. Behavioural and
Cognitive Psychotherapy, 32, 275–290.
Walker, D. L., Ressler, K. J., Lu, K. T., & Davis, M. (2002). Facilitation of conditioned
fear extinction by systemic administration or intra-amygdala infusions of d-cycloserine as
assessed with fear-potentiated startle in rats. Journal of Neuroscience, 22, 2343–2351.
Wells, A., Clark, D. M., Salkovskis, P., Ludgate, J., Hackmann, A., & Gelder, M. (1995).
Social phobia: The role of in-situation safety behaviors in maintaining anxiety and negative
beliefs. Behavior Therapy, 26, 153–161.
Westra, H. A., Stewart, S. H., & Conrad, B. E. (2002). Naturalistic manner of benzodiazepine
use and cognitive behavioral therapy outcome in panic disorder with agoraphobia. Journal
of Anxiety Disorders, 16, 233–246.
Wiederhold, B. K., Gevirtz, R. N., & Spira, J. L. (2001). Virtual reality exposure therapy
vs. imagery desensitization therapy in the treatment of flying phobia. In G. Riva & C.
Galimberti (Eds.), Towards cyberpsychology: Mind, cognition and society in the internet age
(pp. 253–272). Amsterdam, The Netherlands: IOS Press.
Wilhelm, S., Buhlmann, U., Tolin, D., Meunier, S., Pearlson, G., Reese, H., … Rauch, S. L.
(2008). Augmentation of behavior therapy with d-cycloserine for obsessive-compulsive
disorder. American Journal of Psychiatry, 165, 335–341.
Wolitzky-Taylor, K. B., Horowitz, J. D., Powers, M. B., & Telch, M. J. (2008). Psychological
approaches in the treatment of specific phobias: A meta-analysis. Clinical Psychology
Review, 28, 1021–1037.
Wolpe, J. (1958). Psychotherapy by reciprocal inhibition. Stanford, CA: Stanford University
Press.
4
Problem-Solving Strategies
Arthur M. Nezu and Christine Maguth Nezu
Drexel University, United States
Problem-solving therapy (PST) is a psychosocial intervention, generally considered to

be under a cognitive behavioral therapy umbrella, that is based on a biopsychosocial,
diathesis–stress model of psychopathology. PST involves training in a series of skills
geared to enhance one’s ability to cope effectively with a variety of life stressors
thought to engender negative health and mental health outcomes. Life stressors
include both major negative life events (e.g., death of a loved one, diagnosis and
treatment of a chronic illness, loss of a job, incarceration, combat) and chronic
daily problems (e.g., continuous tension with coworkers, reduced financial resources,
discrimination, marital difficulties). A basic tenet of PST is that much of what is
conceptualized as psychopathology and behavioral difficulties, including significant
emotional problems, is a function of ineffective coping with such stressors. As such,
teaching individuals to become better problem solvers as a means of coping with life
stress is hypothesized to eventuate in decreased extant physical and mental health
problems. As such, the overarching goal of PST is to foster the adoption and effective
implementation of adaptive problem-solving attitudes (i.e., optimism, enhanced self-
efficacy) and behaviors (i.e., adaptive emotional regulation, planful problem solving)
as a means of reducing distress and improving one’s overall well-being.
Historically, the genesis of PST from a cognitive behavioral perspective can be
traced to the seminal article by D’Zurilla and Goldfried (1971) who developed a
prescriptive model of training for individuals who present with significant deficits
in their ability to cope effectively with problems encountered in daily living. Since
that time, researchers and clinicians all over the world have applied variations of
this model to a wide variety of psychological and health problems and clinical
populations (see D’Zurilla & Nezu, 2007, and A. M. Nezu, D’Zurilla, Zwick, &
Nezu, 2004, for overviews of this literature base). Targeted problems and diagnoses
have included depression, depression comorbid with a variety of medical illnesses

DOI: 10.1002/9781118528563.wbcbt04
(e.g., cancer, Alzheimer’s disease, cardiovascular disease, heart failure, diabetes),

generalized anxiety disorder, posttraumatic stress disorder, hypertension, psychiatric
and behavioral problems of individuals with intellectual disabilities, obesity, personality
disorders, sexual offending behavior, back pain, behavioral functioning of adults with
schizophrenia, suicidal ideation and self-harm, and traumatic brain injury. An adapted
version of PST (problem-solving therapy for primary care patients; PST-PC) has been
extensively evaluated and found to be highly effective in treating depression among
primary care patients (e.g., Unützer et al., 2002). PST has also been demonstrated to
be an efficacious approach to help caregivers of a variety of medical patient populations
(e.g., individuals with stroke, traumatic brain injury, cancer, dementia) (see C. M.
Nezu, Palmatier, & Nezu, 2004, for a review of this literature). It has also been
applied as a means of enhancing one’s adherence to other psychosocial interventions
(A. M. Nezu, Nezu, & Perri, 2006).
In tandem with these research efforts, we have continuously revised and updated
the basic PST model to incorporate findings from the outcome literature, as well as
basic research from neuroscience, cognitive psychology, and clinical psychology. The
clinical guidelines described later in this chapter represent our most current thinking
and the most recently revised treatment protocol (A. M. Nezu, Nezu, & D’Zurilla,
2013). However, before we outline such treatment guidelines, we begin by addressing
the construct of social problem solving, the term used to describe the type of problem
solving that occurs in real-life settings, rather than problems of a more intellectual or
academic nature.
Social Problem Solving: A Definition
Social problem solving (SPS) is the process by which individuals attempt to identify,
discover, or create adaptive means of coping with a wide variety and range of
stressful problems, both acute and chronic, encountered during the course of living
(D’Zurilla & Nezu, 2007). More specifically, it reflects the process whereby people
direct their coping efforts at altering the problematic nature of a given situation,
their reactions to such problems, or both. Rather than representing a singular type
of coping behavior or activity, SPS represents the multidimensional meta-process of
ideographically identifying and selecting various coping responses to implement in
order adequately to match the unique features of a given stressful situation at a given
time (A. M. Nezu, 2004).
A Multidimensional Model of Social Problem Solving
According to contemporary SPS theory, problem-solving outcomes are largely deter-

mined by two general, but partially independent, dimensions: (a) problem orientation,
and (b) problem-solving style (D’Zurilla, Nezu, & Maydeu-Olivares, 2004). Problem
orientation (PO), previously referred to as “general orientation” (D’Zurilla & Nezu,
1982), represents the set of cognitive-affective schemas regarding individuals’ gener-
alized beliefs, attitudes, and emotional reactions concerning real-life problems, as well
Problem-Solving Strategies 69
as their ability to cope successfully with such difficulties. Originally thought of as being
two ends of the same continuum (e.g., D’Zurilla & Nezu, 1999), research during the
past several years has continued to characterize the two forms of problem orientation
as operating independent of each other (A. M. Nezu, 2004). These two orientation
components are positive problem orientation and negative problem orientation.
A positive problem orientation involves the tendency for individuals to (a) perceive
problems as challenges rather than major threats to one’s well-being, (b) be optimistic
in believing that problems are solvable, (c) have a strong sense of self-efficacy regarding
their ability to handle difficult problems, (d) believe that successful problem solving
usually involves time and effort, and (e) view negative emotions as important sources
of information necessary for effective problem solving.
A negative problem orientation refers to the tendency of individuals to (a) view
problems as major threats to one’s well-being, (b) generally perceive problems to be
unsolvable, (c) maintain doubts about their ability to cope with problems successfully,
and (d) become particularly frustrated and upset when faced with problems or when
they experience negative emotions.
Both orientations can have a strong impact on a person’s motivation and ability
actually to engage in focused attempts to solve problems. As such, the importance
of addressing the quality and valence of one’s dominant orientation is considered
a key component of the overall PST approach. We make this point in particular
to underscore the importance of including a specific and comprehensive focus on
orientation variables when conducting PST. There has been a tendency for some
researchers to equate PST with “rational or logical” problem-solving skills and either
to de-emphasize or actually to ignore problem orientation variables when conducting
this approach. Because PST involves helping people to cope effectively with real-life
stressful problems, which often engender strong emotional reactions, we firmly
believe that attention needs to be paid to such cognitive-affective variables. Moreover,
equating problem-solving skills with PST is similar to equating “cognitive restructur-
ing” with cognitive therapy. The first in both cases are specific techniques; the second,
systems of psychotherapy comprising multiple techniques and clinical strategies.
In support of the need to clarify this point, two recent meta-analytic reviews of
the extant literature of randomized controlled trials (RCTs) of PST, in addition to
an RCT that directly asked this question (A. M. Nezu & Perri, 1989), found that
the exclusion of a specific focus on problem orientation variables consistently led to
significantly less efficacious outcomes as compared to protocols that included such
training (Bell & D’Zurilla, 2009; Malouff, Thorsteinsson, & Schutte, 2007).
The second major dimension, problem-solving style (previously referred to as
“problem-solving proper,” e.g., A. M. Nezu & D’Zurilla, 1989), refers to the
core cognitive behavioral activities that people engage in when attempting to solve
stressful problems. Three differing styles have been identified (D’Zurilla, Nezu, &
Maydeu-Olivares, 2002; D’Zurilla et al., 2004)—rational problem solving (now
referred to as “planful problem solving”; A. M. Nezu et al., 2013), avoidant prob-
lem solving, and impulsive/careless problem solving. Planful problem solving is the
constructive approach that involves the systematic and planful application of the
following set of specific skills: (a) problem definition (i.e., clarifying the nature of
a problem, delineating a realistic set of problem-solving goals and objectives, and
identifying those obstacles that prevent one from reaching such goals), (b) generation
of alternatives (i.e., brainstorming a range of possible solution strategies geared to
overcome the identified obstacles), (c) decision making (i.e., predicting the likely
consequences of these various alternatives, conducting a cost–benefit analysis based
on these identified outcomes, and developing a solution plan that is geared to achieve
the problem-solving goal), and (d) solution implementation and verification (i.e.,
carrying out the solution plan, monitoring and evaluating the consequences of the
plan, and determining whether one’s problem-solving efforts have been successful or
need to continue).
In addition to planful problem solving, two social problem-solving styles have
been further identified, both of which, in contrast, are dysfunctional and maladaptive
in nature (D’Zurilla et al., 2002, 2004). An impulsive/careless style is the problem-
solving approach whereby an individual tends to engage in impulsive, hurried, and
careless attempts at problem resolution. Avoidant problem solving is the maladaptive
problem-solving style characterized by procrastination, passivity, and overdependence
on others to provide solutions. In general, both styles are associated with ineffective
or unsuccessful coping. Moreover, people who typically engage in these styles tend to
worsen existing problems and even create new ones.
It should be noted that we are not suggesting that individuals can be characterized
exclusively by either type of orientation or problem-solving style across all situations.
In other words, we are not suggesting that these are similar to “personality types.”
Rather, each represents a strong tendency either to view or to behave toward problems
from a particular perspective based on one’s learning experiences. For example, it is
possible (and common in our clinical experience) for individuals to be characterized
as having a positive orientation when dealing with problems related to achievement
goals, such as those involving work or career, while additionally having a negative
orientation when addressing affiliation themes, such as those involving romantic or
family relationships. The opposite can be true as well.
In addition, it should be noted that this five-component model of SPS (i.e.,
positive orientation, negative orientation, planful problem-solving style, avoidance
style, and impulsive/careless style) has been cross-validated numerous times across
various populations, ethnic minority cultures, and age groups (D’Zurilla & Nezu,
2007).
Social Problem Solving and Psychopathology
As noted previously, a major assumption underlying the relevance of PST as a

psychosocial intervention is the notion that SPS represents a set of strategies that
fosters effective coping with life stress. In support of this notion, research over the past
several decades has consistently identified a myriad of pathology-related differences
between individuals characterized as “effective” versus “ineffective” problem solvers
across differing age groups, populations, and cultures, and using differing measures
of SPS (see D’Zurilla & Nezu, 2007, and A. M. Nezu, Wilkins, & Nezu, 2004, for
overviews of this literature). In general, when compared to their effective counterparts,
ineffective problem solvers report a greater number of life problems, more health
and physical symptoms, more anxiety, more depression, and more psychological
maladjustment. Moreover, a negative problem orientation has been found to be
associated with negative moods under routine and stressful conditions in general, as
well as significantly related to pessimism, negative emotional experiences, and clinical
depression (A. M. Nezu, 2004). Persons with a negative orientation also tend to
worry and complain more about their health (Elliott, Grant, & Miller, 2004).
In addition, problem-solving deficits have been found to be significantly related
to poor self-esteem, hopelessness, suicidal risk, self-injury, anger proneness, increased
alcohol intake and substance risk taking, personality difficulties, criminal behavior,
alcoholism, secondary physical complications among persons with spinal cord injuries,
premenstrual and menstrual pain, physical health problems, diminished life satisfac-
tion, physical problems among adult cancer patients, and pain severity (D’Zurilla &
Nezu, 2007).
A Problem-Solving/Stress Model of Psychopathology
We have recently articulated a diathesis–stress model that delineates how SPS interacts
with various biological, psychological, and social variables to influence the likelihood
that a given individual will ultimately experience negative health and/or mental
health outcomes or adapt effectively in response to various life stressors (A. M. Nezu
et al., 2013). Essentially, as Figure 4.1 suggests, distal factors, in the form of genetic
propensities and early life stress, can produce certain biological (e.g., increased stress
sensitivity leading to lowered thresholds for triggering depressive reactions later in life;
Nugent, Tyrka, Carpenter, & Price, 2011) and psychosocial (e.g., lack of opportunity
to develop effective problem-solving skills due to stress-related overtaxed efforts to
cope; Wilhelm et al., 2007) vulnerabilities, making one more susceptible to negative
health outcomes later in life.
Focusing on more proximal variables, substantial research has documented the
causal role of stress (in the form of major negative life events and chronic daily
problems) in engendering initial onset, and/or exacerbating extant, psychopathol-
ogy (e.g., depression) and certain medical disorders (e.g., heart disease, diabetes;
Pandey, Quick, Rossi, Nelson, & Martin, 2011). Experiencing such stressors, in
the absence of effective coping, can lead to increased levels of stress and distress
Proximal factors
-Consequent biological
vulnerabilities (stress Health outcomes
Distal factors sensitivity) -Psychological/
-Genetic influences emotional disorders
-Life stressors: major life
-Early life stress events + chronic daily -Physical/health
problems (stress problems
generation)
-Problem-solving ability
Figure 4.1 Problem-solving/stress model of psychopathyology.

(termed “stress generation”). Individuals, as a function of early life stress and/or

a genetic vulnerability, in the face of this stress generation process, then, are espe-
cially vulnerable to negative health outcomes (e.g., Monroe et al., 2006), as seen in
Figure 4.1.
In this model, SPS is hypothesized to serve as an important moderator of the overall
stress–distress relationship. In other words, does the manner in which people cope
with stressful events, via effective SPS, affect the degree to which they will experience
both acute and/or long-term psychological distress? In general, studies directly asking
this question provide significant evidence that SPS is, in fact, a significant moderator
of the stress–distress relationship. For example, under similar levels of high stress,
individuals with ineffective or poor SPS have been found to experience significantly
higher levels of psychological distress, such as depression (e.g., Cheng, 2001; Frye &
Goodman, 2000; Miner & Dowd, 1996; A. M. Nezu, Nezu, Saraydarian, Kalmar,
& Ronan, 1986; A. M. Nezu & Ronan, 1988) and anxiety (e.g., Londahl, Tverskoy,
& D’Zurilla, 2005; Miner & Dowd, 1996; A. M. Nezu, 1986b), as compared to
individuals characterized by effective SPS. This conclusion is particularly important
given that this group of studies provides converging evidence for this hypothesis
across varying participant samples (e.g., college undergraduates, adolescent and child
populations, clinically depressed patients, adult cancer patients) and across differing
measures of SPS.
These studies therefore suggest that, as further noted in Figure 4.1, if a person’s
problem-solving ability is unable to cope adequately with life stress, not only is it
likely that he or she will experience negative health outcomes and psychological
distress, but such outcomes can also subsequently engender further life stress (i.e.,
continued chronic problems), as well as continuous assaults on his or her problem-
solving attempts. We suggest that this continuous reciprocal “downward spiral” of
stress–distress generation is responsible for engendering long-term clinical disorders.
In sum, the above research collectively supports the potential relevance of PST as
a psychosocial intervention that can enhance one’s ability to cope in order to reduce
extant pathology. We now turn to a brief overview of the research literature that
focuses on evaluating this hypothesis directly.
Efficacy of Problem-Solving Therapy
As noted in the introduction, PST has been applied, both as the sole intervention
strategy and as part of a larger treatment package, to a wide variety of patient
populations and problems. One approach to determining the overall efficacy of
PST is to focus on quantitative reviews of this literature. In the past several years,
three major meta-analyses of PST RCTs have been published and basically support
the overall efficacy of this approach across multiple populations and clinical prob-
lems. Specifically, Malouff et al. (2007) conducted a meta-analysis of 32 studies,
encompassing close to 3,000 participants, that evaluated the efficacy of PST across
a variety of mental and physical health problems. They found that PST was (a)
equally as effective as other psychosocial treatments, and (b) significantly more effec-
tive than both no treatment and attention placebo conditions. In addition, whether
the PST protocol included training in problem orientation and whether homework
was assigned were found to be significant moderators of treatment outcome (i.e.,
including training in problem orientation and assigning homework led to larger effect
sizes).
A second meta-analysis published in the same year was conducted by Cuijpers,
van Straten, and Warmerdam (2007). This analysis focused exclusively on trials of
PST for the treatment of depression. Specifically, they focused on 13 RCTs that
collectively included over 1,100 participants. Based on their results, Cuijpers et al.
concluded that, although additional research is needed due to an identified variability
in outcomes across studies, “there is no doubt that PST can be an effective treatment
for depression” (p. 9). Note that one possible explanation for such variability involves
the lack of a focus on problem orientation variables in some of the studies characterized
by lower effect sizes.
A subsequent meta-analysis that also focused exclusively on PST for depression
was conducted by Bell and D’Zurilla (2009), but included seven additional studies
beyond that encompassing the pool in the Cuijpers et al. meta-analysis. These
authors came to a similar conclusion about the efficacy of PST for depression when
looking at both posttreatment and follow-up results across the 20 investigations
(Bell & D’Zurilla, 2009). Specifically, PST was equally effective for the treatment
of depression compared to both alternative psychosocial therapies and psychiatric
medication, and more efficacious compared to supportive therapy and attention-
control conditions. In addition, Bell and D’Zurilla found that significant moderators
of treatment effectiveness included whether the PST program included problem-
orientation training and whether all four planful problem-solving skills were included
in the therapy protocol.
Flexibility of Problem-Solving Therapy: Examples of

Evidenced-Based Applications
Given that several meta-analytic reviews support PST as an evidenced-based treatment

approach, we now illustrate its flexible nature by describing examples of PST studies
that have been applied to differing populations, to differing clinical problems, and via
differing means of implementation. The following are a few such examples.
Group Problem-Solving Therapy

An example of PST applied in a group format is an RCT that evaluated the efficacy of
PST for adults diagnosed with unipolar depression (A. M. Nezu, 1986a). Individuals
seeking treatment for depression in an outpatient setting were randomly assigned to
one of three conditions: (a) PST, (b) problem-focused therapy (PFT), and (c) wait-list
control (WLC). Both treatment conditions were conducted in group settings over
eight weekly sessions. The PFT protocol involved therapeutic discussions of patients’
current life problems, but did not include systematic training in problem-solving
skills. Initial results indicated significant reductions in depression for the PST group
as compared to both the PFT and WLC conditions. Further analyses revealed that
PST participants improved significantly more than the other two groups in problem-
solving effectiveness and also improved significantly in locus-of-control orientation
(i.e., from external to internal). These overall results were found to be maintained at
a 6-month follow-up.
Problem-Solving Therapy for Individuals and Significant Others

PST has also been conducted on an individual basis. One example involved applying
PST as a means of improving the quality of life of cancer patients (A. M. Nezu,
Nezu, Felgoise, McClure, & Houts, 2003). In this study, adults diagnosed with a
variety of types of cancer, who also presented with clinically meaningful elevated
scores on measures of depression and psychological distress, were randomly assigned
to one of three conditions: (a) PST (10 individual sessions); (b) PST-plus (10
sessions of PST provided to both the patient and a patient-selected “significant
other”); and (c) WLC. The PST-plus condition was included in order to evaluate
the effects of including a caregiver as a “problem-solving coach.” Results of pre-post
analyses across multiple measures, that included self-reports, clinician evaluations,
and collateral ratings, provide strong evidence underscoring the efficacy of PST
for this population. Moreover, these results were maintained at 6-month and 1-
year follow-ups. Additional analyses indicated that including a significant other in
treatment served to enhance positive treatment effects beyond that attributable to
receiving PST by oneself. More specifically, at both follow-up assessment points,
cancer patients in the PST-plus condition were found to continue to experience
statistically and clinically significant improvement as compared to individuals in the
PST condition.
Problem-Solving Therapy as Part of a Larger Cognitive

Behavioral Treatment Package
PST has also been included as an important component of larger cognitive behavioral
treatment packages. For example, Garc ı́a-Vera, Labrador, and Sanz (1997) combined
PST with education and relaxation training for the treatment of essential hypertension.
Overall, compared to participants comprising a WLC, treated patients were found
at posttreatment to have significantly lowered blood pressure. These positive results
were maintained at a 4-month follow-up assessment. Whereas studies evaluating the
efficacy of a treatment package cannot provide direct evidence specific to any of
the included intervention components, a subsequent analysis of their outcome data
(Garc ı́a-Vera, Sanz, & Labrador, 1998) revealed that reductions in both systolic
and diastolic blood pressure were significantly correlated with improvements in
SPS. Moreover, SPS mediated the antihypertensive effects of their overall stress
management protocol, suggesting that PST was at the very least an important and
active treatment ingredient.
Another example involves a study conducted by van den Hout, Vlaeyen, Heuts,
Zijlema, and Wijen (2003), who evaluated whether PST provided a significant
supplemental value to a behavioral graded activity (GA) protocol in treating patients
with nonspecific lower back pain with regard to work-related disability. Their results
indicated that in the second half-year after the intervention, patients receiving both
GA and PST had significantly fewer days of sick leave than their counterparts who
received GA plus education. Further, work status was more favorable for the GA plus
PST participants in that more employees had a 100% return-to-work status and fewer
patients received disability pensions 1 year posttreatment.
Problem-Solving Therapy as a Means to Foster

Adherence and Compliance
Beyond applying PST as the major treatment modality to decrease psychological
distress and improve functioning, it has also been used as an adjunct to foster the
effectiveness of other behavioral intervention strategies (A. M. Nezu et al., 2006).
For example, Perri et al. (2001) hypothesized that PST would be an effective means
by which to foster improved adherence to a behavior therapy (BT) weight loss
intervention by helping participants to overcome various barriers to adherence, such
as scheduling difficulties, completing homework assignments, and the interference of
psychological distress. More specifically, after completing 20 weekly group sessions of
standard behavioral treatment for obesity, 80 women were randomly assigned to one
of three conditions: (a) no further contact (BT only), (b) relapse prevention training,
and (c) PST. At the end of 17 months, no differences in overall weight loss were
observed between relapse prevention and BT-only or between relapse prevention and
PST. However, PST participants had significantly greater long-term weight reductions
than BT-only participants, and a significantly larger percentage of PST participants
achieved clinically significant losses of 10% or more in body weight than did BT-only
participants (approximately 35% versus 6%).
Problem-Solving Therapy and Telephone Counseling

In order to improve access to treatment, researchers have attempted to provide
treatment over the telephone. With regard to PST, for example, Allen et al. (2002)
conducted a study where PST was delivered over the telephone as a means of
empowering women with breast carcinoma to cope with a range of difficulties when
diagnosed in midlife. Specifically, six PST sessions were provided to 87 women with
breast cancer—two were in person and the middle four were provided by a nurse
over the phone. Whereas PST was found generally to be an effective approach, results
were not as supportive of the efficacy of this method of providing PST across all
participants. More specifically, relative to the control group, patients receiving PST
who were characterized as “poor problem solvers” at baseline experienced no changes
in the number and severity of cancer-related difficulties. However, patients with
average or “good” problem-solving skills at baseline were found to have improved
mental health compared to controls as a function of the intervention. Collectively,
these results suggest that a more intensive form of this intervention (e.g., more
sessions, more face-to-face contact) may have been required for individuals with
particularly poor premorbid SPS ability.
Problem-Solving Therapy and the Internet

Another means to increase treatment access is via the Internet. Warmerdam, van
Straten, Twisk, Riper, and Cuijpers (2008), for example, adapted PST so that
it could be provided over the Internet to individuals living in the community
with elevated levels of depressive symptoms. The PST protocol was provided over
the course of five weeks and consisted of one lesson per week. The intervention
included information exercises, examples of individuals applying the principles of
PST, and a built-in feedback system. PST was compared to both an Internet-
based CBT program and a WLC. Both treatment groups received support from
master-level graduate psychology students directed at helping a participant use the
program, but not at developing a therapeutic relationship or providing individual
advice on how to cope with depression. Results indicated that both treatments
were equally effective in reducing depression and anxiety as compared to the
WLC; however, these effects appeared to be realized faster by PST than by
CBT.
Problem-Solving Therapy as Part of a Collaborative Care

Model of Health Care Delivery
PST has also been included as the form of psychotherapy that is an inherent part of a
collaborative care protocol combining antidepressant medication for the treatment of
depression in primary care patients. For example, Unützer et al. (2002), in focusing on
the elderly, developed a program entitled IMPACT, which had participants initially
meet with a depression clinical specialist. A stepped-care protocol was used and
initially entailed providing either pharmacotherapy or PST depending on a patient’s
choice. Treatments were switched (i.e., from medication to PST or vice versa) or
modified (e.g., change in antidepressant medication) if symptoms did not remit.
Although the RCT designed to evaluate the efficacy of IMPACT was not able to
assess the independent effects of PST, these researchers did find that overall, the
IMPACT protocol, as compared to usual care control patients, led to significant
reductions in baseline depressive symptoms, as well as less functional impairment and
more improved quality of life. Collaborative care models incorporating PST have also
been effectively applied to reduce depression among low-income, Hispanic adults
diagnosed with cancer (Ell et al., 2008) and for adults diagnosed with type 2 diabetes
(Katon et al., 2004).
Problem-Solving Therapy as a Prevention Strategy

More recently, we have been collaborating with the Department of Veterans Affairs
to develop a prevention program based on PST principles in order to help Veterans
who are experiencing challenges in adjusting from active duty to civilian life (Tenhula,
2010). The focus of this pilot program is on prevention and early intervention among
Veterans of the conflicts in Iraq and Afghanistan who may be experiencing distress.
The PST training has been designed to promote psychological resilience and prevent a
worsening of mental health. Evaluation of this program, entitled “Moving Forward,”
is underway at the time of writing. However, preliminary findings are very promising
(A. M. Nezu, Nezu, Tenhula, Karlin, & Beaudreau, 2012).
Problem-Solving Therapy: Overview of Clinical Guidelines
In the remaining section of this chapter, we provide a brief overview of the clinical
components of contemporary PST. Conceptually, we suggest that several major
obstacles can potentially exist for a given individual when attempting to successfully
resolve real-life stressful problems. These include:
1. the ubiquitous human presence of “cognitive overload,” especially under stressful

circumstances;
2. limited or deficient ability to engage in effective emotional regulation;
3. biased cognitive processing of various emotion-related information (e.g., negative
automatic thoughts, poor self-efficacy beliefs, difficulties in disengaging from
negative mood-congruent autobiographical memories);
4. poor motivation due to feelings of hopelessness; and
5. ineffective problem-solving strategies.
In order to achieve treatment goals and objectives, PST focuses on training

individuals in four major problem-solving “toolkits” that map on to the above
barriers. These toolkits include (a) problem-solving multitasking, (b) the “stop, slow
down, think, and act” (SSTA) method of approaching problems while under stress,
(c) healthy thinking and positive imagery, and (d) planful problem solving.
Note that whether all strategies in all toolkits are taught and emphasized is greatly
dependent on the assessment of a client’s problem-solving strengths and weaknesses,
as well as the therapist’s clinical judgment regarding the relevance and importance
of other related factors, such as the anticipated length of treatment, the severity of
negative symptoms, and the subsequent progress (or lack thereof ) being made by
the individual. In other words, it is not mandatory to engage in all training activities
across all four toolkits. Rather, the therapist should use assessment and outcome data
to inform various treatment decisions.
Problem-Solving Multitasking: Overcoming Cognitive Overload

This set of tools is geared to help an individual overcome the ubiquitous human
limitation when attempting to cope with stressful situations in real life—cognitive
overload (Rogers & Monsell, 1995). Due to basic human limitations in our ability
to manipulate large amounts of information in our working memory simultaneously
while attempting to solve complex problems or make effective decisions (what
Begley, 2011, recently referred to as “brain freeze”), especially when under stress,
individuals are taught to use three “multitasking enhancement” skills: externalization,
visualization, and simplification. These skills are considered foundational to effective
problem solving, and are similar to those skills that may be taught as basic to effective
aerobic exercise, such as stretching, breathing, and maintaining a healthy diet.
Externalization involves displaying information externally as often as possible.

More specifically, clients are taught to write ideas down, draw diagrams or charts to
determine relationships, draw maps, make lists, and audiotape ideas. In this manner,
one’s working memory is not overly taxed and this can allow one to concentrate more
on other activities, such as creatively thinking of various solutions. The visualization
tool is presented as using one’s “mind’s eye” or visual imagery to help clarify the
nature of a problem, practice carrying out a solution, and/or reduce high levels of
negative arousal (i.e., a form of guided imagery whereby one is directed imaginally
to go on a peaceful vacation). Simplification involves “breaking down” or simplifying
problems in order to make them more manageable. Clients are taught to break down
complex problems into more manageable smaller problems, and translate complex,
vague, and abstract concepts into more simple, specific, and concrete language.
“Stop, Slow Down, Think, and Act” (SSTA): Overcoming Emotional

Dysregulation and Maladaptive Problem Solving Under Stress
In situations where the primary goal of PST for a particular individual involves
the decrease of clinically significant emotional distress (e.g., depression, suicidal
ideation, generalized anxiety), emphasizing training in this toolkit to such clients
becomes especially important. It is also useful for training individuals as a means
of preventing extant emotional concerns from becoming particularly problematic.
In essence, clients are taught a series of steps to enhance their ability to modulate
(as opposed to “eradicate”) negative emotional arousal in order to more effectively
apply a systematic approach to solving problems (i.e., to be able to use the various
planful problem-solving skills optimally). It is also presented to individuals as the
overarching map to follow when attempting to cope with stressful problems that
engender strong emotional reactions and is included as the major treatment strategy
geared to foster adaptive emotional regulation skills. It is also included in PST as a
means of minimizing impulsive/careless attempts at problem solving.
According to the SSTA method, clients are first taught to become “emotionally
mindful” by being more aware of when and how they experience negative emotional
arousal. Specifically, they are taught to notice changes in physical (e.g., headache,
fatigue, pain), mood (e.g., sadness, anger, tension), cognitive (e.g., worry, thoughts
of negative outcomes), and/or behavioral (e.g., urge to run away, yelling, crying)
indicators. For certain individuals, additional training may be necessary to increase the
accuracy by which they attempt to identify and label emotional phenomena. Next,
they are taught to stop; that is, to engage in behaviors (e.g., shouting out loud,
raising one’s hands, holding up a stop sign) that help them to “put on the brakes”
in order to better modulate their emotional arousal (i.e., prevent the initial arousal
from evoking a more intense form of the emotion together with its “full blown”
concomitant negative thinking, state-dependent negative memories, negative affect,
and maladaptive behaviors).
Next, in order to meaningfully be able to stop, clients are further taught to slow
down; that is, to decrease the accelerated rate at which one’s negative emotionality
can occur. Various specific techniques are provided and practiced with clients in
order to offer them a choice among a pool of potentially effective “slowing down
tools.” These include counting down from 10 to 1, diaphragmatic breathing, guided

imagery or visualization, “fake smiling” (in keeping with the potential positive impact
related to the facial feedback hypothesis; Havas, Glenberg, Gutowski, Lucarelli, &
Davidson, 2010), “fake yawning” (in keeping with recent neuroscience research
demonstrating the efficacy of directed yawning as both a stress management strategy
and a means to enhance cognitive awareness; Newberg & Waldman, 2009; Walusinski,
2006), meditation, exercise, talking to others, and prayer (if relevant to a particular
individual). Individuals are also encouraged to use strategies that have been helpful
to them in the past.
The thinking and acting steps in SSTA refer to applying the four specific planful
problem-solving tasks (i.e., defining the problem and setting realistic goals, generating
alternative solutions, decision making, solution implementation and verification) after
one has “slowed down,” in attempting to resolve or cope with the stressful problem
situation that initially evoked the negative emotional stress reaction.
Healthy Thinking and Positive Imagery: Overcoming

Negative Thinking and Poor Motivation
This toolkit is included specifically to address additional problem orientation issues
if relevant to a particular individual, that is, negative thinking and feelings of hope-
lessness. Similar to cognitive restructuring strategies, clients are taught that “how
one thinks can affect how one feels.” In essence, this toolkit entails a variety of
cognitive change techniques geared to enhance optimism and enhanced self-efficacy.
For example, clients are taught to use the “ABC Model of Thinking” (where A is
the activating or triggering event, B is a given belief, attitude, or viewpoint, and
C is the emotional consequence that is based on that belief, as compared to “re-
ality”) in order to determine whether one needs to change such negative beliefs.
They are provided with a series of “healthy thinking” rules (e.g., “Nothing is
100% perfect”; “Problems are a normal part of life”; “Everyone makes mistakes”;
“Every minute I spend thinking negatively takes away from enjoying my life”),
as well as a list of “realistically optimistic self-statements” (e.g., “I can solve this
problem”; “I’m okay—feeling sad under these circumstances is normal”; “I can’t
direct the wind, but I can adjust the sails”; “Difficult and painful does not equal
hopeless!”), as more optimistic examples of ways to think in order to readjust their
orientation.
In addition, if a given individual has particular difficulty with changing his or her
negative thinking, we also advocate having the PST therapist conduct a “reverse
advocacy role play” exercise surrounding that individual’s unique negative thinking
patterns. In this exercise, a given maladaptive attitude is temporarily “adopted” by
the therapist using a role-play format. The individual, who now has to adopt the
role of “counselor,” has to provide reasons or arguments for why such an attitude
is incorrect, maladaptive, or dysfunctional. In this manner, the client is influenced
to begin verbalizing those aspects of a positive problem orientation. The process
of identifying a more appropriate set of beliefs toward problems and providing
justification for the validity of these attitudes helps the individual to begin personally
to adopt such an orientation.
The second tool in this toolkit focuses on using visualization to enhance motivation
and to decrease feelings of hopelessness. The use of visualization here, which is
different than that described within the multitasking toolkit, is to help the client to
experience sensorially what it “feels” like to solve a difficult problem successfully;
in other words, to “see the light at the end of the tunnel,” or “the ribbon across
the finishing line.” With this strategy, the therapist’s goal is to help patients create
the experience of the success in their mind’s eye, and vicariously experience the
potential reinforcement to be gained. Clients are specifically taught not to focus on
how the problem got solved, but rather to focus on the feelings associated with
having already solved it. The central goal of this strategy is to have individuals create
their own positive consequences (in the form of affect, thoughts, physical sensations,
and behavior) associated with solving a difficult problem as a major motivational step
toward overcoming low motivation and feelings of hopelessness, as well as minimizing
the tendency to engage in avoidant problem solving.
Planful Problem Solving: Fostering Effective Problem Solving

This last toolkit provides training in the four planful problem-solving tasks, the first
being problem definition. This activity involves having clients separate facts from
assumptions when describing a problem, delineate a realistic and attainable set of
problem-solving goals and objectives, and identify those obstacles that prevent one
from reaching such goals. Note that this model advocates delineating both problem-
focused goals, which include objectives that entail changing the nature of the situation
so that it no longer represents a problem, as well as emotion-focused goals, which
include those objectives that involve moderating one’s cognitive-emotional reactions
to those situations that cannot be changed. Strategies that might be effective in
reaching such emotion-focused goals might include stress management, forgiveness
of others, and acceptance that the situation cannot be changed.
The second task, generating alternatives, involves creatively brainstorming a range
of possible solution strategies geared to overcome the identified obstacles to their
goals using various brainstorming techniques. Decision making, the third planful
problem-solving task, involves predicting the likely consequences of the various
alternatives previously generated, conducting a cost–benefit analysis based on these
identified outcomes, and developing a solution plan geared to achieve the articulated
problem-solving goal. The last activity, solution implementation and verification,
entails having the person optimally carry out the solution plan, monitor and evaluate
the consequences of the plan, and determine whether his or her problem-solving
efforts have been successful or need to continue.
Guided Practice
A substantial majority of the overall PST intervention involves providing feedback
and additional training to individuals in the four toolkits as they continue to apply
the model to current problems they are experiencing. In addition, PST encourages
individuals to “forecast” future stressful situations, whether positive (e.g., getting a
promotion and moving to a new city) or negative (e.g., the break-up of a relationship)
in order to anticipate how such tools can be applied in the future in order to minimize
potential negative consequences.
Summary
This chapter focused on PST, a cognitive behavioral intervention that teaches indi-
viduals a series of adaptive problem-solving tasks geared to fostering their ability to
cope effectively with stressful life circumstances in order to reduce psychopathology
and negative physical symptoms. This approach is based on the notion that what is
often conceptualized as psychopathology and behavioral difficulties is a function of
ineffective coping with life stress. Research addressing differences between effective
and ineffective problem solving, the role of social problem solving as a modera-
tor of the stress–distress relationship, and the efficacy of PST interventions were
briefly presented in support of this tenet. In addition, examples were provided to
illustrate the flexibility of this approach with regard to applications with differing
clinical populations, problems, and methods of treatment implementation. Last,
a brief overview of the clinical components of contemporary PST was presented
that entailed four toolkits, each of which addressed a possible barrier to effective
problem solving under stress. These barriers included cognitive overload, emotional
dysregulation, negative thinking, poor motivation, and ineffective problem-solving
strategies.
References
Allen, S. M., Shah, A. C., Nezu, A. M., Nezu, C. M., Ciambrone, D., Hogan, J., & Mor,
V. (2002). A problem-solving approach to stress reduction among younger women with
breast carcinoma: A randomized controlled trial. Cancer, 94, 3089–3100.
Begley, S. (2011, March). I can’t think! Newsweek, 157 , 28–33.
Bell, A. C., & D’Zurilla, T. J. (2009). Problem-solving therapy for depression: A meta-analysis.
Cheng, S. K. (2001). Life stress, problem solving, perfectionism, and depressive symptoms in
Chinese. Cognitive Therapy and Research, 25, 303–310.
Cuijpers, P., van Straten, A., & Warmerdam, L. (2007). Problem solving therapies for
depression: A meta-analysis. European Psychiatry, 22, 9–15.
D’Zurilla, T. J., & Goldfried, M. R. (1971). Problem solving and behavior modification.
D’Zurilla, T. J., & Nezu, A. (1982). Social problem solving in adults. In P. C. Kendall (Ed.),
Advances in cognitive-behavioral research and therapy (Vol. 1, pp. 202–274). New York,
NY: Academic Press.
D’Zurilla, T. J., & Nezu, A. M. (1999). Problem-solving therapy: A social competence approach
to clinical intervention (2nd ed.). New York, NY: Springer.
D’Zurilla, T. J., & Nezu, A. M. (2007). Problem-solving therapy: A positive approach to clinical
intervention (3rd ed.). New York, NY: Springer.
D’Zurilla, T. J., Nezu, A. M., & Maydeu-Olivares, A. (2002). Manual for the Social Problem-
Solving Inventory—Revised. North Tonawanda, NY: Multi-Health Systems.
D’Zurilla, T. J., Nezu, A. M., & Maydeu-Olivares, A. (2004). Social problem solving:
Theory and assessment. In E. C. Chang, T. J. D’Zurilla, & L. J. Sanna (Eds.), Social
problem solving: Theory, research, and training (pp. 11–27). Washington, DC: American
Psychological Association.
Ell, K., Xie, B., Quon, B., Quinn, D. I., Dwight-Johnson, M., & Lee, P. (2008). Randomized
controlled trial of collaborative care management of depression among low-income
patients with cancer. Journal of Clinical Oncology, 26, 4488–4496.
Elliott, T. R., Grant, J. S., & Miller, D. M. (2004). Social problem-solving abilities and
behavioral health. In E. C. Chang, T. J. D’Zurilla, & L. J. Sanna (Eds.), Social problem
solving: Theory, research, and training (pp. 117–134). Washington, DC: American
Frye, A. A., & Goodman, S. H. (2000). Which social problem-solving components buffer
depression in adolescent girls? Cognitive Therapy and Research, 24, 637–650.
Garc ı́a-Vera, M. P., Labrador, F. J., & Sanz, J. (1997). Stress-management training for essential
hypertension: A controlled study. Applied Psychophysiology and Biofeedback, 22, 261–283.
Garc ı́a-Vera, M. P., Sanz, J., & Labrador, F. J. (1998). Psychological changes accompa-
nying and mediating stress-management training for essential hypertension. Applied
Psychophysiology and Biofeedback, 23, 159–178.
Havas, D. A., Glenberg, A. M., Gutowski, K. A., Lucarelli, M. J., & Davidson, R. J. (2010).
Cosmetic use of botulinum toxin-A affects processing of emotional language. Psychological
Science, 21, 895–900.
Katon, W. J., Von Korff, M., Lin, E. H. B., Simon, G., Ludman, E., Russo, J., … Bush, T.
(2004). The Pathways Study: A randomized trial of collaborative care in patients with
diabetes and depression. Archives of General Psychiatry, 61, 1042–1049.
Londahl, E. A., Tverskoy, A., & D’Zurilla, T. J. (2005). The relations of internalizing symptoms
to conflict and interpersonal problem solving in close relationships. Cognitive Therapy and
Research, 29, 445–462.
Malouff, J. M., Thorsteinsson, E. B., & Schutte, N. S. (2007). The efficacy of problem solving
therapy in reducing mental and physical health problems: A meta-analysis. Clinical
Psychology Review, 27 , 46–57.
Miner, R. C., & Dowd, E. T. (1996). An empirical test of the problem solving model
of depression and its application to the prediction of anxiety and anger. Counseling
Psychology Quarterly, 9, 163–176.
Monroe, S. M., Torres, L. D., Guillaumont, J., Harkness, K. L., Roberts, J. E., Frank,
E., & Kupfer, D. (2006). Life stress and the long-term treatment course of recurrent
depression: III. Nonsevere life events predict recurrence for medicated patients over three
years. Journal of Consulting and Clinical Psychology, 74, 112–120.
Newberg, A., & Waldman, M. R. (2009). How God changes your brain. New York, NY:
Ballantine Books.
Nezu, A. M. (1986a). Efficacy of a social problem-solving therapy approach for unipolar
Nezu, A. M. (1986b). Negative life stress and anxiety: Problem solving as a moderator variable.
Psychological Reports, 58, 279–283.
Nezu, A. M. (2004). Problem solving and behavior therapy revisited. Behavior Therapy, 35,
1–33.
Nezu, A. M., & D’Zurilla, T. J. (1989). Social problem solving and negative affective states.
In P. C. Kendall & D. Watson (Eds.), Anxiety and depression: Distinctive and overlapping
features (pp. 285–315). New York, NY: Academic Press.
Nezu, A. M., D’Zurilla, T. J., Zwick, M. L. & Nezu, C. M. (2004). Problem-solving therapy
for adults. In E. C. Chang, T. J. D’Zurilla, & L. J. Sanna (Eds.), Social problem solving:
Theory, research, and training (pp. 171–191). Washington, DC: American Psychological
Association.
Nezu, A. M., Nezu, C. M., & D’Zurilla, T. J. (2013). Problem-solving therapy: A treatment
manual. New York, NY: Springer.
Nezu, A. M., Nezu, C. M., Felgoise, S. H., McClure, K. S., & Houts, P. S. (2003). Project
Genesis: Assessing the efficacy of problem-solving therapy for distressed adult cancer
patients. Journal of Consulting and Clinical Psychology, 71, 1036–1048.
Nezu, A. M., Nezu, C. M., & Perri, M. G. (2006). Problem solving to promote treatment
adherence. In W. T. O’Donohue & E. R. Levensky (Eds.), Promoting treatment adherence:
A practical handbook for health care providers (pp. 135–148). New York, NY: Sage.
Nezu, A. M., Nezu, C. M., Saraydarian, L., Kalmar, K., & Ronan, G. F. (1986). Social
problem solving as a moderator variable between negative life stress and depressive
symptoms. Cognitive Therapy and Research, 10, 489–498.
Nezu, A. M., Nezu, C. M., Tenhula, W., Karlin, B., & Beaudreau, S. (2012). Problem-solving
training to enhance readjustment among returning veterans: Initial evaluation results.
Paper presented at the Annual Convention of the Association of Behavioral and Cognitive
Therapies, National Harbor, MD.
Nezu, A. M., & Perri, M. G. (1989). Social problem solving therapy for unipolar depression:
An initial dismantling investigation. Journal of Consulting and Clinical Psychology, 57 ,
408–413.
Nezu, A. M., & Ronan, G. F. (1988). Stressful life events, problem solving, and depressive
symptoms among university students: A prospective analysis. Journal of Counseling
Nezu, A. M., Wilkins, V. M., & Nezu, C. M. (2004b). Social problem solving, stress, and
negative affective conditions. In E. C. Chang, T. J. D’Zurilla, & L. J. Sanna (Eds.), Social
problem solving: Theory, research, and training (pp. 49–65). Washington, DC: American
Nezu, C. M., Palmatier, A., & Nezu, A. M. (2004). Social problem-solving training for
caregivers. In E. C. Chang, T. J. D’Zurilla, & L. J. Sanna (Eds.), Social problem solving:
Theory, research, and training (pp. 223–238). Washington, DC: American Psychological
Association.
Nugent, N. R., Tyrka, A. R., Carpenter, L. L., & Price, L. N. (2011). Gene-environment inter-
actions: Early life stress and risk for depressive and anxiety disorders. Psychopharmacology,
214, 175–196.
Pandey, A., Quick, J. C., Rossi, A. M., Nelson, D. L., & Martin, W. (2011). Stress and the
workplace: 10 years of science, 1997–2007. In R. J. Contrada & A. Baum (Eds.), The
handbook of stress science: Biology, psychology, and health (pp. 137–149). New York, NY:
Springer.
Perri, M. G., Nezu, A. M., McKelvey, W. F., Schein, R. L., Renjilian, D. A., & Viegener,
B. J. (2001). Relapse prevention training and problem-solving therapy in the long-term
management of obesity. Journal of Consulting and Clinical Psychology, 69, 722–726.
Rogers, R. D., & Monsell, S. (1995). The cost of predictable switch between simple cognitive
tasks. Journal of Experimental Psychology: General, 124, 207–231.
Tenhula, W. N. (2010, Fall issue). Problem-solving training. Health Power Prevention News,
3–4.
Unützer, J., Katon, W., Callahan, C., Williams, J. W., Hunkeler, E. M., Harpole, L., …
Langston, C. A. (2002). Collaborative care management of late-life depression in the
primary care setting: A randomized controlled trial. Journal of the American Medical
Association, 288, 2836–2845.
van den Hout, J. H. C., Vlaeyen, J. W. S., Heuts, P. H. T., Zijlema, J. H. L., & Wijen, J. A.
G. (2003). Secondary prevention of work-related disability in nonspecific low back pain:
Does problem-solving therapy help? A randomized clinical trial. Clinical Journal of Pain,
19, 87–96.
Walusinski, O. (2006). Yawning: An unsuspected avenue for a better understanding of arousal
and interoception. Medical Hypotheses, 67 , 6–14.
Warmerdam, L., van Straten, A., Twisk, J., Riper, H., & Cuijpers, P. (2008). Internet-based
treatment for adults with depressive symptoms: Randomized controlled trial. Journal of
Medical Internet Research, 10, e44.
Wilhelm, K., Siegel, J. E., Finch, A. W., Hadzi-Pavlovic, D., Mitchell, P. B., Parker, G., &
Schofield, P. R. (2007). The long and the short of it: Associations between 5-HTT
genotypes and coping with stress. Psychosomatic Medicine, 69, 614–620.
5
Emotion Regulation Strategies
Shauna L. Clen
Kent State University, United States
Douglas S. Mennin
Hunter College, City University of New York, United States
David M. Fresco
Kent State University, United States
Introduction
Whether it is the sense of dread as one’s heart beats furiously and unexpectedly, the
vivid memory of a horrific event, or the sharp craving for a substance to help take
away despair, emotions prominently color the experiences of individuals suffering with
psychopathology. Despite this centrality, cognitive behavioral approaches traditionally
downplayed the importance of emotional factors and implied that difficult emotions
were indicative of dysfunction and necessitated diminishment (Greenberg & Safran,
1987; Samoilov & Goldfried, 2000). It is not surprising, then, that traditional
cognitive behavioral therapy has been characterized by less activation of emotions
within session as compared to other forms of therapy (Goldfried, Castonguay, Hayes,
Drozd, & Shapiro, 1997).
This historical neglect of emotional factors in cognitive behavioral approaches has
been influenced by a lack of conceptual clarity regarding emotions and confusion
regarding how to address emotional processes effectively in treatment (Samoilov &
Goldfried, 2000). More recently, affect science has become a flourishing area of
research that offers novel perspectives on emotional functioning that have impor-
tant implications for the treatment of psychopathology (e.g., Davidson, Pizzagalli,
Nitschke, & Putnam, 2002; Rottenberg, Gross, & Gotlib, 2005). Recently, inno-
vative cognitive behavioral treatments have emerged that offer a more functional
approach to difficult emotions. Cognitive behavioral treatments such as dialectical
behavioral therapy (DBT; Linehan, 1993a), acceptance and commitment therapy
(ACT; S. C. Hayes, Strosahl, & Wilson, 1999), mindfulness-based cognitive therapy

DOI: 10.1002/9781118528563.wbcbt05
(MBCT; Segal, Williams, & Teasdale, 2002), the unified protocol for transdiagnostic
treatment of emotional disorders (UP; Barlow et al., 2011), acceptance-based behav-
ioral therapy (ABBT; Roemer & Orsillo, 2005), compassion-focused therapy (CFT;
Gilbert, 2009), and emotion regulation therapy (ERT; Mennin & Fresco, 2009)
conceptualize painful emotions as natural responses to life’s challenges and provide
validation regarding difficult emotional experiences. These treatments do not view dif-
ficult emotions as inherently problematic but instead focus on the functional qualities
of emotions and how individuals understand and respond to their emotional experi-
ences. As such, these treatments provide novel perspectives that advance functional
approaches to emotions within cognitive behavioral therapy.
In this chapter, we (a) briefly review an affect science approach to emotional
functioning, (b) present an argument for utilizing an emotion regulation framework
to improve upon traditional cognitive behavioral therapy, (c) provide a rationale for
targeting four specific emotion regulatory mechanisms in treatment, and (d) outline
and briefly review relevant research and interventions regarding four important
emotion regulatory mechanisms.
An Affect Science Approach
Theories underlying affect science propose that emotions actively shape and influence
human experience. Consequently, emotions are viewed as highly adaptive, informative,
and integral to human functioning (Frijda, 1986). Although definitions of emotions
vary, emotions are generally seen as short-lived states that reflect the activation of
approach and avoidance motivational systems (Gray & McNaughton, 2000; Higgins,
1997) and are triggered when attention is allocated to real or imagined events that are
relevant to one’s goals or values (Lang, 1978). For instance, sadness can be triggered
by the loss of something cherished or desired, such as the expectation of a certain
outcome (Barr-Zisowitz, 2000). Emotions usually involve a loosely coordinated
pattern of experiential, physiological, and behavioral responses (Mauss, Levenson,
McCarter, Wilhelm, & Gross, 2005).
Functionally, emotions can provide intrapersonal information reflective of one’s
motivations, goals, or values in a given situation (Lang, 1978), which can range
from long-lasting, conscious, and complex values that are integral to one’s sense
of self, such as maintaining a supportive romantic relationship, to motivations that
are momentary, unconscious, and simple, such as protecting oneself from immediate
bodily harm (Gross & Thompson, 2007). Emotions also contribute to decision
making and planning. For instance, positive emotions such as joy can widen one’s
array of cognitions and actions and encourage new approach behaviors (Fredrickson,
2001). Negative emotions such as anxiety can focus one’s attention toward a specific
problem area (e.g., being unprepared for an upcoming exam) so that goals can be
clarified and solutions to a given issue generated (Parrott, 2001).
Emotions are also integral components of interpersonal interactions and relation-
ships (Tooby & Cosmides, 1990). For instance, emotional expressions such as smiling
can initiate and maintain social interactions (Ekman, 1993). Emotional expressions
can also communicate how a person is reacting to the environment and can help other
Emotion Regulation Strategies 87
individuals predict how the person is likely to behave (Izard, 1991). Emotions also
serve a central role in shaping the nature of romantic (Levenson & Gottman, 1983)
and familial relationships (Bowlby, 1969).
Although emotions serve important functions, emotional responses are not always
effective, adaptive, or conducive to mental health. The processes by which individuals
influence the provocation, experience, and expression of their emotions is commonly
referred to as emotion regulation (Gross, 1998b). The ability to regulate one’s
emotions in a manner that allows for flexible adjustment to environmental demands
is important to well-being and mental health. Individuals with psychopathology
often exhibit emotional responses that reflect contextually invariant excesses, deficits,
or lability as well as regulatory efforts that are deficient, excessively employed, or
enacted in rigid and inflexible ways (Kring & Werner, 2004). Numerous emotion
regulation strategies have been studied in relation to psychopathology. In general,
emotion regulation strategies that involve actively addressing triggering situations
(e.g., cognitive reappraisal, defined as employing a different cognitive vantage point
regarding an emotionally provocative event; see Gross, 2001) or actively approaching
painful emotions (e.g., emotional acceptance, defined as openly turning toward,
allowing, and remaining in personal contact with an emotional experience; see S.
C. Hayes et al., 1999) tend to be associated with adaptive outcomes (e.g., Aldao,
Nolen-Hoeksema, & Schweizer, 2010; Campbell-Sills, Barlow, Brown, & Hofmann,
2006; Ray, Wilhelm, & Gross, 2008). However, emotion regulation strategies that
involve passive, repetitive responses (e.g., rumination, worry) or attempts to eliminate
or avoid awareness of painful emotions (e.g., experiential suppression, emotional
avoidance) tend to be associated with maladaptive outcomes (e.g., Aldao et al., 2010;
Campbell-Sills et al., 2006; Eifert & Heffner, 2003; Hofmann et al., 2005).
Target Regulatory Mechanisms of Skills-Based Treatment
Although cognitive behavioral treatments demonstrate considerable efficacy, some

conditions remain characterized by relapse (e.g., major depressive disorder; Segal et al.,
2002), poor ability to function adaptively (e.g., chronic posttraumatic stress disorder;
Cloitre, Koenen, Cohen, & Han, 2002), or persistent symptomatic recurrence (e.g.,
generalized anxiety disorder; Borkovec & Ruscio, 2001). These conditions suggest the
need for further advances in our conceptualizations and approaches to intervention to
instill a consistent level of symptom amelioration, functionality, and life satisfaction.
In hopes of improving treatment efficacy, the National Institute of Mental Health
has promoted two initiatives with the goal of accelerating the payoff from basic
and translational research into treatment application. First, the Research Domain
Criteria (Sanislow et al., 2010) aim to understand what is expected in normative
functioning in various biopsychosocial domains so that these normative findings can be
contrasted with disordered subgroups to identify mechanistic regions of interest that
may become targets of treatment development. Second, “treatment personalization”
aims to identify factors that predict who will benefit from a given treatment in
order to systematically determine ways of optimizing care. Taken together, these
initiatives highlight the need to specify transdiagnostic dysfunctional mechanisms
within individuals and to further the development of treatment intervention processes

to specifically target these mechanisms.
A common principle of many cognitive behavioral treatments is teaching clients skills
that improve various capacities to promote adaptive, flexible engagement with their
environment. Emotion regulation may provide an important framework for capacity
development through the training of skills that specifically seek to improve various
emotion regulation abilities. Specific target regulatory mechanisms may include
directed attention, emotional acceptance, cognitive distancing, and cognitive change.
Enhancing directed attention (i.e., the ability to focus, sustain, and flexibly move
attention) may help clients become more aware of their external environment and
their internal feelings and sensory experiences. Increasing emotional acceptance
(i.e., the ability to turn openly toward, allow, and remain in personal contact with
an emotional experience) may help clients become more comfortable with their
own emotions and less wary of encountering emotionally provocative situations.
Improving cognitive distancing from emotional states (i.e., the ability to identify,
observe, and generate psychological perspective from inner experiences) may help
clients to disengage from psychological immersion in strong emotions and identify
difficult inner experiences without getting overwhelmed. Facilitating cognitive change
(i.e., the ability to change one’s evaluation of an event such that the event is altered
in its emotional significance) may help clients develop new understanding regarding
the manner in which they interpret certain events and may promote new insights
and flexibility in thinking. Gross (2001) has stressed that regulatory efforts can be
enacted across a temporal continuum from early attentional processes to later, more
elaborative, cognitive processes. Thus, these strategies can be viewed as differing entry
points to affecting an emotional cascade and can also be considered sequentially from
least (i.e., directed attention) to most (i.e., cognitive change) cognitively elaborative
and resource-depleting (Muraven & Baumeister, 2000).
Developing abilities in any and all of these capacities may promote greater flexi-
bility in clients’ responses to their environment, their emotions, and their pursuit of
meaningful endeavors. These four regulatory mechanisms and examples of associated
therapeutic processes that target these mechanisms are reviewed herein. Of course,
most therapeutic processes are blunt instruments that change a myriad of mechanisms
(e.g., behavioral activation might increase attentional abilities in addition to strength-
ening reward learning). Thus, the therapeutic processes that will be discussed are
specific interventions that are purposefully employed to target a given mechanism.
Directed Attention
Directed attention represents the ability voluntarily to focus attention toward target
stimuli, sustain attention on the chosen stimuli, and flexibly move attention to
different stimuli. This mechanism entails the ability to attend to stimuli without being
dissuaded by elaborative thought processes (e.g., judgments about an experience).
Focusing attention involves actively choosing the stimuli to which one will attend
(Kabat-Zinn, 2005). Sustaining attention involves maintaining one’s attention on
target stimuli (Parasuraman, 1998) and actively redirecting attention back to the
target stimuli when one notices that attention has wandered to automatic, habitual
thought processes (Hasenkamp, Wilson-Mendenhall, Duncan, & Barsalou, 2012;

Kabat-Zinn, 2005). Flexibly moving attention entails deliberately shifting the focus of
one’s attention to various aspects of an experience (Kabat-Zinn, 2005).
An important aspect of directed attention is attending to external stimuli such as
objects in the visual field or sounds. When it is advantageous to do so, individuals
with highly developed capacities to direct their attention can disengage attention
from internal, elaborative processes (e.g., habitual, passive thoughts) and extend
their attention outward, which encourages awareness of and engagement with their
environment. Increased environmental awareness and engagement may facilitate the
selection of action that is flexible and adaptive for current circumstances (Langer &
Moldoveanu, 2000). Directed attention also involves the ability to attend to internal,
nonverbal stimuli, or stimuli that can be felt in the body. Individuals with highly
developed capacities to direct their attention to internal, nonverbal stimuli are more
aware of and engaged with their internal feelings and sensations and are able to
disengage from elaborative processes about their sensory experiences. The ability
to direct attention to internal states is closely related to emotional functioning, as
conscious awareness of emotions may involve sensing the visceral condition of the
body during emotional experiences (Damasio, 1999; Paulus & Stein, 2006) and
utilizing this information in the awareness of subjective emotional feelings (Craig,
2009). Finally, directed attention entails the capacity to flexibly move one’s attention
or shift the focus of attention in response to environmental demands. This ability
also includes being able to disengage from elaborative processes that would detract
attention away from the current task. Individuals with highly developed capacities to
flexibly move their attention are more able to adjust to the flux of a given situation.
At the neural level, directing attention to external stimuli involves the amygdala,
which plays a key role in reflexive attending to stimuli that is motivationally salient
(Zald, 2003). Further, directing attention to internal, nonverbal stimuli involves the
insula, which is central to the awareness of internal bodily states, including awareness
of sympathetic and parasympathetic changes, bodily movements, and cross-modal
sensory information (Craig, 2009). Both the insula and the amygdala share reciprocal
connections with prefrontal areas such as the medial prefrontal cortex (mPFC). These
areas are integral for flexibly directing attention, including focusing, concentrating
(i.e., inhibiting an attentional shift), or effectively shifting the focus of attention in
response to contextual demands (Phillips, Drevets, Rauch, & Lane, 2003).
Individuals with psychopathology often have difficulties directing their attention,
including having their attention habitually “captured” by personally significant stimuli
(e.g., stimuli related to threat, abandonment, mistreatment, rejection, failure), having
difficulties disengaging attention from unhelpful, elaborative processes (e.g., worrying,
brooding), experiencing difficulties attending to the objective qualities of their external
environment, and having difficulties attending to feelings and sensations without
being dissuaded by unhelpful elaborative processes. Indeed, difficulties related to
attentional processes have been implicated in various forms of psychopathology
including mood disorders (Joormann & Gotlib, 2007), anxiety disorders (Mogg,
Philippot, & Bradley, 2004), and personality disorders (Seres, Unoka, Bódi, Aspán,
& Kéri, 2009). For example, allocating disproportionate attention to threatening
stimuli may play a role in the onset and maintenance of anxiety disorders (Cisler &
Koster, 2010). Researchers have also begun to study the individual’s role in voluntarily
directing his or her attention. For instance, the extent to which individuals are able
to exercise “attentional control” is related to the extent of difficulty in disengaging
attention from threatening stimuli (Peers & Lawrence, 2009). On a neural level,
studies have consistently found increased amygdala activation during attentional tasks
across mood and anxiety disorders (Etkin & Wager, 2007). Also, several studies have
demonstrated heightened interoceptive sensitivity via increased insula activity across
anxiety and mood disorders (Etkin & Wager, 2007; Paulus & Stein, 2006).
Associated therapeutic processes. The client’s ability to direct his or her attention plays
an integral role in therapeutic interventions. For instance, if a cognitive behavioral
therapist is implementing behavioral activation for a client with major depressive
disorder, the impact of the ostensibly positive activity on the client’s emotional state
will be affected by the extent to which the client is able to disengage attention
away from maladaptive, elaborative processes (e.g., brooding) and direct his or her
attention externally toward the activity. Similarly, if a cognitive behavioral therapist
would like a client to monitor and record his or her emotions in a given situation, the
accuracy of this exercise will be affected by the extent to which the client is able to
direct attention toward his or her internal, feeling states.
In an effort to promote directed attention capacities, many recent cognitive
behavioral therapies incorporate mindfulness training into treatment (i.e., cultivat-
ing nonjudgmental, present-moment awareness through guided exercises involving
directing one’s attention to various internal and external stimuli; see Kabat-Zinn,
1982). Mindfulness training is associated with an array of positive outcomes related to
well-being and mental health (Baer, 2003; Hofmann, Sawyer, Witt, & Oh, 2010) as
well as improvements in working memory and ability to sustain attention (Chambers,
Lo, & Allen, 2008). Targeting directed attention to external stimuli can be seen in
exercises such as mindfulness of sounds, in which the client attends to sounds that
arise in the current environment (Segal et al., 2002), mindful walking, in which the
client attends to the surrounding environment while walking (Kabat-Zinn, 2005), and
informal/everyday mindfulness (i.e., anchoring in the present), in which the client
directs attention externally to what he or she sees, hears, and feels during various
activities throughout the day (Barlow et al., 2011; Linehan, 1993b). Similarly, Wells
(2008) encourages the development of directed external attention by having the client
close his or her eyes and focus attention on therapist-produced sounds in session (e.g.,
tapping on the wall, the sound of the therapist’s voice).
Other mindfulness exercises target the client’s ability to direct attention to internal,
nonverbal stimuli, including mindful breathing, in which the client focuses on bodily
sensations that accompany breathing (e.g., air passing by the nostrils), and the body
scan, in which the client directs attention to sensations in different parts of his or her
body (Kabat-Zinn, 2005). In addition, exercises traditionally employed for calming
the body such as diaphragmatic breathing, in which the client takes deep breaths
from the abdomen, and progressive muscle relaxation, in which the client tenses and
relaxes various muscle groups in the body (Bernstein, Borkovec, & Hazlett-Stevens,
2000), have been recently adapted to have greater emphasis on awareness of bodily
sensations, rather than on reducing distress (Hayes-Skelton, Usmani, Lee, Roemer,

& Orsillo, 2012; Roemer & Orsillo, 2005).
Although mindfulness training explicitly targets the mechanism of directed atten-
tion, many cognitive behavioral processes likely impact the client’s ability to attend
to external stimuli and internal, nonverbal stimuli. In support of this hypothesis,
many cognitive behavioral therapies have been shown to reduce attentional bias
toward threatening stimuli in individuals with social anxiety disorder (Pishyar, Har-
ris, & Menzies, 2008) and generalized anxiety disorder (Mathews, Mogg, Kentish,
& Eysenck, 1995). Finally, there has been an increasing interest in computer-based
training that focally targets the reversal of negative attentional biases through less ver-
bally elaborate attention tasks, which are administered in laboratory and ambulatory
contexts (Beard, 2011).
Emotional Acceptance
The pursuit of meaningful endeavors will inevitably engender difficult emotions as
one encounters setbacks, challenges, complex situations, and disappointing outcomes.
The ability to turn openly toward an emotional experience, allow the experience, and
remain in personal contact with the experience reflects emotional acceptance (S.
C. Hayes et al., 1999). Emotional acceptance involves psychologically embracing
emotional feelings and engaging experientially with these feelings (e.g., sensing
emotional feelings flowing through the body) without being dissuaded by elaborative
thought processes (e.g., judgments about the experience).
Individuals with highly developed capacities to accept their emotions are able to
notice and allow emotions that are elicited throughout their daily life, which facilitates
the understanding of their own emotional processes as they relate to environmental
events. In addition, given the open, allowing, and engaging nature of this mechanism,
individuals with highly developed capacities to accept their emotions are less likely to
avoid certain activities or situations solely due to the possibility that difficult emotions
could arise. Indeed, emotional acceptance is often presented as necessary to valued
living (S. C. Hayes et al., 1999).
Conversely, individuals with psychopathology often have difficulties accepting
their emotional experiences, including being dissuaded by negative beliefs regard-
ing difficult emotions, aversion toward difficult emotional experiences, engaging
in maladaptive elaborative responses when difficult emotions arise (e.g., worrying,
brooding, self-criticizing), attempting to reduce awareness of difficult emotions,
attempting to limit the experience of difficult emotions, and avoiding situations
and activities that could provoke difficult emotions, even when such activities
are important to them (e.g., Barlow et al., 2011; Eifert & Forsyth, 2005; S. C.
Hayes et al., 1999; Linehan, 1993a; Roemer & Orsillo, 2005; Segal et al., 2002).
Experimental studies on individuals with psychopathology reveal psychological ben-
efits from promoting experiential engagement and gentle allowance of difficult
emotions. Inducing emotional acceptance in individuals with clinical or analogue
psychopathology has been associated with better affective recovery from emotional
provocation (Campbell-Sills et al., 2006), less distress in response to emotional
provocation, reductions in negative beliefs regarding emotions (Singer & Dobson,
2007), less distress in response to carbon dioxide challenges (Eifert & Heffner,
2003; Feldner, Zvolensky, Eifert, & Spira, 2003; Levitt, Brown, Orsillo, & Bar-
low, 2004), and more willingness to undergo additional carbon dioxide challenges
(Eifert & Heffner, 2003; Levitt et al., 2004). Conversely, inducing experiential sup-
pression (i.e., attempting to minimize and limit emotional experiences) in individuals
with clinical or analogue psychopathology is associated with prolonged psycho-
logical distress (Campbell-Sills et al., 2006; Feldner et al., 2003; Levitt et al.,
2004).
To date, there is a paucity of research examining the neurobiology of accep-
tance strategies or interventions, as well as very limited physiological findings. In
relation to physiology, Hofmann, Heering, Sawyer, and Asnaani (2009) found that
instructing individuals to accept their emotions (or to reappraise an aversive task)
was associated with decreased heart rate (i.e., decreased physiological arousal) in
response to an emotion provocation in nonclinical individuals, as compared to
expressive suppression instructions. Reappraisal instructions were associated with the
lowest amount of self-reported anxiety. However, Aldao and Mennin (2012) demon-
strated that unlike healthy individuals, individuals with generalized anxiety disorder
experienced decreased heart rate variability when instructed to accept (or reap-
praise) experimentally-induced emotional responses, as compared to no instructions,
suggesting a failure of efficiency of these strategies for these individuals.
Associated therapeutic processes. The client’s ability to accept emotional experiences

plays an integral role in therapeutic interventions. For example, if a cognitive behavioral
therapist is encouraging in vivo exposure or undertaking a challenging values-based
action, compliance is likely to be affected by the client’s ability to observe and
gently allow the difficult emotions that these activities will provoke. In an effort to
promote emotional acceptance capacities, many recent forms of cognitive behavioral
therapy present a conceptualization of difficult emotions as natural responses to
life’s challenges, provide validation regarding difficult emotional experiences, and
encourage monitoring and recording of emotional experiences, activating situations,
and accompanying responses (e.g., UP; Barlow et al., 2011; CFT; Gilbert, 2009;
ACT; S. C. Hayes et al., 1999; DBT; Linehan, 1993a; ERT; Mennin & Fresco,
2009; ABBT; Roemer & Orsillo, 2005; MBCT; Segal et al., 2002).
Many recent forms of cognitive behavioral therapy also facilitate emotional accep-
tance by incorporating mindfulness exercises into treatment (e.g., exercises designed
to increase present-moment, nonjudgmental awareness; see Kabat-Zinn, 2005). Pro-
moting emotional acceptance is central to exercises such as mindfulness of emotions,
in which the client brings to mind an emotionally provocative situation and observes,
allows, and psychologically turns toward his or her internal, emotional experience
(Mennin & Fresco, 2009; Orsillo & Roemer, 2011), exercises involving visualizing
the emotion in the body by means of descriptive imagery (e.g., the client visualizes
what the emotion would look like and feel like if it could be tangibly encoun-
tered through the senses; see S. C. Hayes & Smith, 2005), and exercises that
promote present-moment awareness of many aspects of internal experience, including
emotional feelings (Segal et al., 2002).
In ACT, a common technique used to target emotional acceptance involves the use
of descriptive metaphors or analogies to encourage being gentle and open to difficult
emotional experiences (e.g., describing internally responding to emotional pain as akin
to how you would embrace a crying child; see S. C. Hayes & Smith, 2005). Clients
can also validate their own emotional experiences by imagining they are describing
their feelings to a caring friend who is interested and nonjudgmental (Gilbert,
2009). Additionally, clients have successfully approached their difficult emotions
by listening to personally emotionally-provocative songs and then recording their
feelings, thoughts, and behavioral responses (Barlow et al., 2011). Finally, traditional
cognitive behavioral techniques, such as providing psychoeducation regarding the
functional and biological nature of emotions (e.g., UP; Barlow et al., 2011; CFT;
Gilbert, 2009; DBT; Linehan, 1993b; ERT; Mennin & Fresco, 2009; ABBT; Roemer
& Orsillo, 2005), can reduce aversion to difficult emotions. Similarly, behavioral
experiments can illustrate how emotions change and are temporary (e.g., Beck, Rush,
Shaw, & Emery, 1979).
Although treatment mechanism research examining emotional acceptance is lim-
ited, increases in self-reported acceptance of difficult inner experiences (including
emotional experiences) are associated with positive treatment outcomes (e.g., For-
man, Herbert, Moitra, Yeomans, & Geller, 2007; S. A. Hayes, Orsillo, & Roemer,
2010; Lappalainen et al., 2007; McCracken, Vowles, & Eccleston, 2005). From a
neurological perspective, a recent investigation in chronic pain patients found that
ACT led to increased activations in the ventrolateral prefrontal cortex (VLPFC;
an area associated with symbolic processing of emotional information), lateral
orbitofrontal cortex (LOFC; involved in processing reward value of reinforcers),
and regions associated with executive cognitive control (Jensen et al., 2012). How-
ever, mechanisms of acceptance were not isolated from other components of the
intervention.
Cognitive Distancing
Distancing from emotional states (also referred to as “decentering”; Segal et al.,
2002), refers to the ability cognitively to “step back” when one is experiencing
intense emotions and a corresponding motivational impetus. This ability involves
observing and identifying inner experiences during strong emotional states and
creating separation from these experiences. Distancing involves recognizing that
one’s thoughts, feelings, and urges are subjective, transient internal events rather
than inherent, permanent aspects of the self or accurate representations of reality
(Fresco, Moore, et al., 2007; Fresco, Segal, Buis, & Kennedy, 2007; Segal et al.,
2002).
Individuals with highly developed capacities to distance from emotional states are
able to observe, separate from, and gain perspective on their inner experiences, and
thus are less likely to become immersed in an emotional state and have their actions
solely driven by an emotional impulse. Studies utilizing experimental methodologies
have found psychological benefits, including reduced distress (Ayduk & Kross, 2008;
Healy et al., 2008; Kalisch et al., 2005) and reduced blood pressure reactivity (Ayduk
& Kross, 2008), from instructing nonclinical individuals to observe and distance from
difficult inner experiences. In the laboratory, researchers have examined the effects of
cognitive distancing from inner experiencing by implementing techniques designed
to promote distance from the self in space (e.g., viewing inner experiences as physical
objects that are separate from oneself; Kalisch et al., 2005) and distance from the self in
personal perspective (e.g., processing inner experiences from an observational stance;
Ayduk & Kross, 2008; Healy et al., 2008). Additionally, the effects of distancing have
been examined in relation to aversive stimuli, with greater imagined spatial distance
between the stimuli and oneself being associated with reduced distress in nonclinical
participants (Davis, Gross, & Ochsner, 2011).
In neuroimaging investigations, experimental manipulations that increase cogni-
tive distance from affective stimuli or the processing of intrapersonal stimuli (e.g.,
autobiographical recall) have produced increased activation in prefrontal areas such as
the dorsolateral prefrontal cortex (DLPFC; an area implicated in top-down, effortful
cognitive control), the mPFC (an area implicated in attention to emotional states),
and the dorsal area of the anterior cingulate (dACC; an area involved in monitor-
ing conflict), while decreasing activity in the amygdala (Koenigsberg et al., 2009,
2010). Further, the ability to label affect from this distanced perspective has also
been shown to activate the VLPFC while deactivating the amygdala, a relation-
ship mediated by the mPFC (Cunningham, Johnson, Gatenby, Gore, & Banaji,
2003).
Individuals with psychopathology often experience difficulties distancing from
their emotional states, including becoming psychologically immersed in difficult
thoughts or feelings, becoming consumed with a single perspective in response
to complex events, mindlessly acting on emotional impulses or urges, engaging in
repetitive, maladaptive elaborative responses during difficult emotional states (e.g.,
worrying, brooding), and having problems undertaking meaningful, goal-directed
actions during difficult emotional states. Indeed, deficits in cognitive distancing from
emotional states may play a central role in psychopathology (e.g., Bateman & Fonagy,
2004; Beck et al., 1979; S. C. Hayes et al., 1999; Teasdale et al., 2002; Wells, 2008).
Likewise, several constructs conceptually related to distancing from emotional states
have been proposed as having an ameliorating effect on psychopathological processes
and symptoms, including metacognitive awareness (Teasdale et al., 2002), distancing
(Beck et al., 1979), cognitive defusion (S. C. Hayes et al., 1999), self-distancing
(Kross & Ayduk, 2009), detached mindfulness (Wells, 2008), and mentalization
(Bateman & Fonagy, 2004).
Research on cognitive distancing as it relates to psychopathology has begun to
grow. Fresco, Moore, and colleagues (2007) found that self-reported decenter-
ing (i.e., distancing) was negatively related to self-report measures of depressive
symptoms, anxiety symptoms, depressive rumination, experiential avoidance, and
expressive suppression. In the laboratory, individuals with psychopathology experience
distress-reducing benefits from experimental techniques designed to promote an
observational distance from difficult inner experiences (Kross & Ayduk, 2009;
Wisco & Nolen-Hoeksema, 2011). Furthermore, distancing manipulations reduce
depressotypic thought accessibility, diminish emotional recounting, and increase
accuracy of reconstruals of past events in depressed individuals (Kross, Gard, Deldin,
Clifton, & Ayduk, 2012).
Associated therapeutic processes. The client’s ability to distance from emotional states
plays an essential role in therapeutic interventions. For example, when encouraging
the client to undertake a behavioral change in a problematic area, the client’s
ability to enact a different behavior will likely be impacted by his or her ability to
identify, observe, and cognitively separate from the emotional state that the situation
has repeatedly provoked. To promote distancing capacities, many recent cognitive
behavioral therapies employ mindfulness techniques to facilitate the identification of
inner experiences while maintaining an observational perspective.
The targeting of distancing from emotional states can be seen in mindfulness and
acceptance-based exercises that promote distance from the self in personal perspective
by having the client observe his or her inner experience, including difficult thoughts,
emotions, and urges (Segal et al., 2002). Many mindfulness exercises also target
distancing from emotional states by promoting distance from the self in space
(i.e., the client imagines assigning a physical form to difficult inner experiences).
Common acceptance-based exercises that promote distance in personal perspective
and distance in space include “leaves on a stream,” in which the client imagines
placing difficult thoughts on leaves floating down a moving stream; “watching the
mind train,” in which the client imagines placing difficult feelings, thoughts, and
urges in specific train cars that are moving down railroad tracks (S. C. Hayes &
Smith, 2005); “mindfulness of clouds and sky,” in which the client imagines placing
difficult thoughts and feelings on clouds, while viewing his or her mind as the sky
(Orsillo & Roemer, 2011); and the observer exercise, in which the client creates
mental separation from aspects of his or her inner experience and imagines placing
thoughts, feelings, and physical sensations in physical space (S. C. Hayes et al.,
1999; Mennin & Fresco, 2009). The “mountain meditation” (Kabat-Zinn, 2005)
is also used to promote distance from the self in time, as the client visualizes
him- or herself as a stable, permanent mountain that is experiencing emotional
“weather.”
Analogies and metaphors also promote distance from the self in personal perspective,
such as the recalcitrant child analogy, which equates observing difficult thoughts
and emotions as akin to looking after, but not engaging with, a child who is
distressed and throwing a tantrum (Wells, 2008). In addition, acceptance-based and
cognitive behavioral techniques that involve the identification and recognition of
difficult thoughts and feelings also promote distancing (i.e., observation and partial
separation), such as labeling private experiences with a descriptive prefix (e.g., “I am
having the thought that …,” “I am having the emotion of …”; see S. C. Hayes &
Smith, 2005), or recording difficult thoughts on a whiteboard and stepping back and
looking at the thoughts in a written form (Beck, Emery, & Greenberg, 1985).
Although treatment research examining distancing is limited, meaningful clin-
ical change is associated with gains in self-reported decentering (Bieling et al.,
2012; Fresco, Segal, et al., 2007; Mennin & Fresco, 2011) and interview-coded
metacognitive awareness (e.g., viewing difficult inner experiences as temporary men-
tal events that are not synonymous with the self; Teasdale et al., 2002). ACT research
also supports a reduction in the believability of unhelpful internal experiences (e.g.,
depressotypic thoughts, delusional thoughts) as being positively related to treatment
outcome (Gaudiano, Herbert, & Hayes, 2010; Zettle, Rains, & Hayes, 2011).
Cognitive Change
When an event is encountered, individuals often automatically interpret the event,
thereby influencing the nature and intensity of the emotional response (Scherer,
Schorr, & Johnstone, 2001). Cognitive change refers to the ability to change the
evaluation of an event, or one’s ability to cope with the event, such that the event is
altered in its emotional significance (Gross & Thompson, 2007). Cognitive change
involves viewing an intrapersonal, interpersonal, or environmental event from a
different perspective than one’s initial interpretation. Thus, cognitive change entails
flexibility, rather than rigidity, in one’s thinking.
The manner in which individuals interpret difficult events may have important
implications for well-being. Individuals with highly developed capacities to change
cognitive appraisals are able to relinquish their original, automatic interpretation
of an event, thus freeing themselves from getting “stuck” on a single unhelpful or
unrealistic interpretation. Considering alternative appraisals and perspectives regarding
an emotionally provocative event may undermine passive, repetitive, elaborative
processes (e.g., rumination), which can maintain difficult emotional states (Ray et al.,
2008).
Reappraisal is one way an individual can consider a different perspective regarding
an emotionally provocative event. Reappraisal is the active process of adopting a
cognitive vantage point that is different than the manner in which one initially
evaluated an event (Gross, 2001). Three of the most common reappraisal techniques
include realistic reappraisal, positive reappraisal, and self-compassionate reappraisal.
Realistic reappraisal refers to reevaluating an event in a manner that is more accurate,
objective, factual, and sensitive to contextual factors than the original appraisal (e.g.,
Ray et al., 2008). Positive reappraisal refers to reevaluating an event in a manner
that orients toward possible desired, rewarding, or beneficial aspects of the event or
consequences of the event that may have been overlooked in the original appraisal
(e.g., Ray et al., 2008). Self-compassionate reappraisal refers to reevaluating an event
in a manner that appreciates that one is in emotional pain, validates the pain, desires to
alleviate the pain, and identifies the pain as a natural aspect of the human experience
(see Gilbert, 2009).
Self-reported tendency to engage in reappraisal is positively associated with interper-
sonal functioning (Gross & John, 2003) and is negatively associated with depressive
and anxiety symptoms (Aldao et al., 2010). Researchers have also manipulated cog-
nitive appraisal in the laboratory and have found distress-reducing benefits from
preemptively instructing nonclinical participants to appraise aversive stimuli (Gross,
1998a) or aversive tasks (Hofmann et al., 2009) in a manner designed to promote
personal detachment or objectivity before the individuals encounter the stimuli or task.
In addition to influencing initial appraisals, studies on nonclinical individuals have also
found distress-reducing benefits from inducing realistic/objective reappraisal, posi-
tive reappraisal (Ray et al., 2008), other-focused compassionate reappraisal (Witvliet,
DeYoung, Hofelich, & DeYoung, 2011), and self-compassionate reappraisal (Leary,
Tate, Adams, Batts, & Hancock, 2007) of personally emotionally-provocative events
that have already occurred. Beginning with a seminal study by Ochsner, Bunge,
Gross, and Gabrieli (2002), several investigations of the neural correlates of cognitive
reappraisal have emerged over the last decade (Berkman & Lieberman, 2009). These
studies involve instructing participants to appraise emotional stimuli in a manner that
will influence extent of emotional experience. Reappraisal instructions are associated
with increased activation in the VLPFC, DLPFC, dorsal region of the mPFC, and
dACC, as well as decreased activity in the amygdala and orbitofrontal cortex.
Individuals with psychopathology often exhibit habitual, rigid, unrealistic, or
unhelpful appraisals (e.g., pessimistic, hopeless, self-critical, or low mastery appraisals),
engage in maladaptive, repetitive, elaborative responses based upon these unrealistic
or unhelpful appraisals, and are uncomfortable considering alternative ways of viewing
events (e.g., Alloy, Kelly, Mineka, & Clements, 1990; Barlow, Allen, & Choate, 2004;
Beck et al., 1979; Resick & Schnicke, 1993). Experimental studies reveal distress-
reducing benefits from instructing individuals with psychopathology to appraise
threatening stimuli (Goldin, Manber, Hakimi, Canli, & Gross, 2009) and reap-
praise personally emotionally-provocative events and associated negative, self-referent
thoughts (Goldin, Manber-Ball, Werner, Heimberg, & Gross, 2009) in a manner
designed to promote personal detachment or objectivity.
Increasingly, studies are examining neural activity in response to experimentally
induced cognitive changes in individuals with psychopathology. Individuals with
psychopathology demonstrate paradoxical patterns of activation as compared to
healthy individuals in response to reappraisal manipulations (e.g., Aldao & Mennin,
2012; Goldin, Manber-Ball, et al., 2009; Johnstone, van Reekum, Urry, Kalin, &
Davidson, 2007). For instance, whereas control participants demonstrate a negative
relationship between activation in the VLPFC and the amygdala that is mediated by
the ventromedial prefrontal cortex (VMPFC), participants with depression show a
positive association between activation in the VMPFC and the amygdala and do not
exhibit VLPFC activation (Johnstone et al., 2007). Also, Goldin, Manber-Ball, et al.
(2009) found a temporal lag in DLPFC activation following activation of the mPFC
and amygdala in response to self-relevant statements in social anxiety disorder patients
as compared to controls. These findings suggest that whereas utilizing cognitive
control strategies such as reappraisal to modulate limbic responses is possible in
clinical populations, these individuals must first overcome an initial increased aversive
response, and subsequently cognitive change is accomplished with much greater effort
than in healthy individuals.
Associated therapeutic processes. The client’s ability to change cognitive appraisals is

often a central target of cognitive behavioral interventions. In an effort to promote
cognitive change capacities, many cognitive behavioral therapists encourage clients
to record emotionally provocative events and their interpretation of these events.
If the interpretation is found to be unrealistic or unhelpful, therapists help clients
to challenge the ascribed meaning through logical questioning and identification
of cognitive “distortions” (i.e., interpretations that are not based on logic), and
encourage the client to generate new possible meanings that are more rational and
realistic (Beck et al., 1979; Resick & Schnicke, 1993). Cognitive behavioral therapists
also use behavioral experiments to demonstrate to clients that certain unhelpful or
unrealistic meanings that have been ascribed to events are not in line with what
objectively occurs (Beck et al., 1979). Cognitive change is also targeted through
psychoeducation regarding the benefits of being flexible in one’s appraisals of

emotionally provocative events, monitoring and recording one’s automatic appraisals
of emotionally provocative events, identifying “thinking traps” in appraisals, and
generating alternative, more flexible appraisals (Barlow et al., 2011). Another
common technique that facilitates cognitive change is encouraging clients to make
decisions from a “wise mind” perspective, which is a state of intuitive knowing,
understanding, and truth that integrates people’s capacity for reasoning and logic
with their strong emotional responses and desires (Linehan, 1993b).
Cognitive behavioral therapists also target cognitive change by enhancing clients’
abilities to employ self-compassionate reappraisal. Self-compassionate techniques
include having clients imagine telling a very caring and interested individual about
their difficult thoughts and feelings, asking themselves factual questions about the real-
ity of their situation in a caring and understanding manner, reminding themselves of
their strengths and coping abilities, empathically reflecting on the perspective of other
individuals in the situation, and offering soothing and helpful alternative thoughts
while talking to themselves in the mirror (Gilbert, 2009). Cognitive behavioral ther-
apists have also encouraged self-compassion through loving-kindness meditation, in
which clients imagine extending kindness to loved ones, to themselves, to neutral
people, to individuals who have caused them harm, and to all living beings (Carson
et al., 2005). Another relevant exercise involves having clients observe self-critical
thoughts and generate statements of self-validation and self-compassion (Mennin &
Fresco, 2009; Orsillo & Roemer, 2011; Segal et al., 2002).
Although treatment research examining cognitive change is limited, there is some
support linking self-reported tendency to engage in reappraisal (Bryant, Moulds, &
Guthrie, 2001) and self-reported capability of employing reappraisal (Goldin et al.,
2012) with positive clinical change. Goldin and colleagues (2012) found that increases
in cognitive reappraisal self-efficacy mediated the effect of cognitive behavioral therapy
on treatment outcome. In a recent meta-analysis, Smits, Julian, Rosenfield, and Powers
(2012) examined 25 studies that examined the relationship between threat reappraisal
and symptom change in cognitive behavioral treatment of anxiety disorders. These
researchers found that although a slight majority of these studies had established
statistical mediation, only a few studies established that threat reappraisal preceded
anxiety reduction and even fewer studies demonstrated specificity in this effect.
Conclusions
As life is full of disappointing outcomes and unforeseen challenges, emotion regula-

tion abilities are essential to valued living. Targeting regulatory mechanisms through
skills-based cognitive behavioral interventions may help alleviate suffering and pro-
mote adaptive, flexible engagement with one’s environment among individuals with
psychopathology. Employing techniques designed to enhance clients’ capacities for
directed attention may help clients become more aware of their external environment
and their internal feelings and sensory experiences. Utilizing exercises designed to
encourage clients’ capacities for emotional acceptance may help clients become more
comfortable with their own emotions and less wary in encountering emotionally
provocative situations. Using strategies designed to facilitate clients’ capacities to

cognitively distance from emotional states may help clients to disengage from psycho-
logical immersion in strong emotions and identify difficult inner experiences without
getting overwhelmed. Targeting clients’ capacities to employ cognitive change may
help clients develop new understanding regarding the manner in which they interpret
certain events and may promote new insights and flexibility in thinking. Developing
abilities in any and all of these capacities may promote greater flexibility in clients’
responses to their environment, their emotions, and their pursuit of meaningful
endeavors.
Affect science and emotion regulation are relative newcomers to the fields of psy-
chopathology and treatment research. As such, research regarding specific regulatory
mechanisms is very limited at this time. Additional experimental research is needed to
further delineate and examine specific regulatory mechanisms. Further research in the
context of cognitive behavioral interventions is also needed to elucidate the poten-
tial causal mediating role of regulatory mechanisms in relation to clinical outcome.
Despite these challenges, emotion regulation may provide an important framework
for delineating particular intrapersonal mechanisms of capacity development such as
directed attention, emotional acceptance, cognitive distancing, and cognitive change.
Further, with increased precision in research regarding regulatory mechanisms, cog-
nitive behavioral skills training can be honed to influence these areas more effectively,
thereby clarifying essential pathways for successful intervention as well as providing
direction for improving treatment for refractory conditions.
References
Aldao, A., & Mennin, D. S. (2012). Paradoxical physiological effects of implementing adaptive
emotion regulation strategies in generalized anxiety disorder. Behaviour Research and
Therapy, 50, 122–130.
Aldao, A., Nolen-Hoeksema, S., & Schweizer, S. (2010). Emotion-regulation strategies across
psychopathology: A meta-analytic review. Clinical Psychology Review, 30, 217–237.
Alloy, L. B., Kelly, K., Mineka, S., & Clements, C. (1990). Comorbidity of anxiety and
depressive disorders: A helplessness-hopelessness perspective. In J. D. Maser & C. R.
Cloninger (Eds.), Comorbidity of mood and anxiety disorders (pp. 499–543). Washington,
DC: American Psychiatric Press.
Ayduk, Ö., & Kross, E. (2008). Enhancing the pace of recovery: Self-distanced analysis of
negative experiences reduces blood pressure reactivity. Psychological Science, 19, 229–231.
Baer, R. A. (2003). Mindfulness training as clinical intervention: A conceptual and empirical
review. Clinical Psychology: Science and Practice, 10, 125–143.
Barlow, D. H., Allen, L. B., & Choate, M. L. (2004). Toward a unified treatment for emotional
disorders. Behavior Therapy, 35, 205–230.
Barlow, D. H., Farchione, T. J., Fairholme, C. P., Ellard, K. K., Boisseau, C. L., Allen, L. B., &
Ehrenreich-May, J. (2011). The unified protocol for transdiagnostic treatment of emotional
disorders: Client workbook. New York, NY: Oxford University Press.
Barr-Zisowitz, C. (2000). “Sadness”—Is there such a thing? In M. Lewis & J. M. Haviland-
Jones (Eds.), Handbook of emotions (2nd ed., pp. 607–622). New York, NY: Guilford
Press.
Bateman A., & Fonagy, P. (2004) Psychotherapy for borderline personality disorder: A
mentalization-based treatment. Oxford, England: Oxford University Press.
Beard, C. (2011). Cognitive bias modification for anxiety: Current evidence and future
directions. Expert Review of Neurotherapeutics, 11, 299–311.
Beck, A. T., Emery, G., & Greenberg, R. L. (1985). Anxiety disorders and phobias: A cognitive
perspective. New York, NY: Basic Books.
Berkman, E. T., & Lieberman, M. D. (2009). Using neuroscience to broaden emotion reg-
ulation: Theoretical and methodological considerations. Social and Personality Psychology
Compass, 3, 475–493.
Bernstein, D. A., Borkovec, T. D., & Hazlett-Stevens, H. (2000). New directions in progressive
relaxation training: A guidebook for helping professionals. Westport, CT: Praeger.
Bieling, P. J., Hawley, L. L., Bloch, R. T., Corcoran, K. M., Levitan, R. D., Young, L. T., …
Segal, Z. V. (2012). Treatment-specific changes in decentering following mindfulness-
based cognitive therapy versus antidepressant medication or placebo for prevention of
depressive relapse. Journal of Consulting and Clinical Psychology, 80, 365–372.
Borkovec, T. D., & Ruscio, A. M. (2001). Psychotherapy for generalized anxiety disorder.
Journal of Clinical Psychiatry, 62, 37–42.
Bowlby, J. (1969). Attachment. New York, NY: Basic Books.
Bryant, R. A., Moulds, M., & Guthrie, R. M. (2001). Cognitive strategies and the resolution
of acute stress disorder. Journal of Traumatic Stress, 14, 213–219.
Campbell-Sills, L., Barlow, D. H., Brown, T. A., & Hofmann, S. G. (2006). Effects of
suppression and acceptance on emotional responses of individuals with anxiety and mood
disorders. Behaviour Research and Therapy, 44, 1251–1263.
Carson, J. W., Keefe, F. J., Lynch, T. R., Carson, K. M., Goli, V., Fras, A. M., & Thorpe, S. R.
(2005). Loving-kindness meditation for chronic low back pain: Results from a pilot trial.
Journal of Holistic Nursing, 23, 287–304.
Chambers, R., Lo, B. C. Y., & Allen, N. B. (2008). The impact of intensive mindfulness training
on attentional control, cognitive style, and affect. Cognitive Therapy and Research, 32,
303–322.
Cisler, J. M., & Koster, E. H. W. (2010). Mechanisms of attentional biases towards threat in
anxiety disorders: An integrative review. Clinical Psychology Review, 30, 203–216.
Cloitre, M., Koenen, K. C., Cohen, L. R., & Han, H. (2002). Skills training in affective and
interpersonal regulation followed by exposure: A phase-based treatment for PTSD related
to childhood abuse. Journal of Consulting and Clinical Psychology, 70, 1067–1074.
Craig, A. D. (2009). How do you feel—now? The anterior insula and human awareness.
Nature Reviews Neuroscience, 10, 59–70.
Cunningham, W. A., Johnson, M. K., Gatenby, J. C., Gore, J. C., & Banaji, M. R. (2003).
Neural components of social evaluation. Journal of Personality and Social Psychology, 85,
639–649.
Damasio, A. R. (1999). The feeling of what happens: Body and emotion in the making of
consciousness. New York, NY: Harcourt.
Davidson, R. J., Pizzagalli, D., Nitschke, J. B., & Putnam, K. (2002). Depression: Perspectives
from affective neuroscience. Annual Review of Psychology, 53, 545–574.
Davis, J. I., Gross, J. J., & Ochsner, K. N. (2011). Psychological distance and emotional
experience: What you see is what you get. Emotion, 11, 438–444.
Eifert, G. H., & Forsyth, J. P. (2005). Acceptance and commitment therapy for anxiety disorders:
A practitioner’s treatment guide to using mindfulness, acceptance, and values-based behavior
change strategies. Oakland, CA: New Harbinger.
Eifert, G. H., & Heffner, M. (2003). The effects of acceptance versus control contexts on
avoidance of panic-related symptoms. Journal of Behavior Therapy and Experimental
Ekman, P. (1993). Facial expressions and emotion. American Psychologist, 48, 384–392.
Etkin, A., & Wager, T. D. (2007). Functional neuroimaging of anxiety: A meta-analysis of
emotional processing in post-traumatic stress disorder, social anxiety disorder, and specific
phobia. American Journal of Psychiatry, 164, 1476–1488.
Feldner, M. T., Zvolensky, M. J., Eifert, G. H., & Spira, A. P. (2003). Emotional avoidance:
An experimental test of individual differences and response suppression using biological
challenge. Behaviour Research and Therapy, 41, 403–411.
Forman, E. M., Herbert, J. D., Moitra, E., Yeomans, P. D., & Geller, P. A. (2007). A
randomized controlled effectiveness trial of acceptance and commitment therapy and
cognitive therapy for anxiety and depression. Behavior Modification, 31, 772–799.
Fredrickson, B. L. (2001). The role of positive emotions in positive psychology: The broaden-
and-build theory of positive emotions. American Psychologist, 56, 218–226.
Fresco, D. M., Moore, M. T., van Dulmen, M., Segal, Z. V., Teasdale, J. D., Ma, H., & Williams,
J. M. G. (2007). Initial psychometric properties of the Experiences Questionnaire:
Validation of a self-report measure of decentering. Behavior Therapy, 38, 284–302.
Fresco, D. M., Segal, Z. V., Buis, T., & Kennedy, S. (2007). Relationship of post treatment
decentering and cognitive reactivity to relapse of major depressive disorder. Journal of
Frijda, N. H. (1986). The emotions. Cambridge, England: Cambridge University Press.
Gaudiano, B. A., Herbert, J. D., & Hayes, S. C. (2010). Is it the symptom or the relation to it?
Investigating potential mediators of change in acceptance and commitment therapy for
psychosis. Behavior Therapy, 41, 543–554.
Gilbert, P. (2009). The compassionate mind: A new approach to life’s challenges. London,
England: Constable-Robinson.
Goldfried, M. R., Castonguay, L. G., Hayes, A. M., Drozd, J. F., & Shapiro, D. A. (1997). A
comparative analysis of the therapeutic focus in cognitive-behavioral and psychodynamic-
interpersonal sessions. Journal of Consulting & Clinical Psychology, 65, 740–748.
Goldin, P. R., Manber-Ball, T., Hakimi, S., Canli, T., & Gross, J. J. (2009). Neural bases of
social anxiety disorder: Emotional reactivity and cognitive regulation during social and
physical threat. Archives of General Psychiatry, 66, 170–180.
Goldin, P. R., Manber-Ball, T., Werner, K., Heimberg, R., & Gross, J. J. (2009). Neural
mechanisms of cognitive reappraisal of negative self-beliefs in social anxiety disorder.
Biological Psychiatry, 66, 1091–1099.
Goldin, P. R., Ziv, M., Jazaieri, H., Werner, K., Kraemer, H., Heimberg, R. G., &
Gross, J. J. (2012). Cognitive reappraisal self-efficacy mediates the effects of individ-
ual cognitive-behavioral therapy for social anxiety disorder. Journal of Consulting and
Gray, J. A., & McNaughton, N. (2000). The neuropsychology of anxiety: An enquiry into the
functions of the septo-hippocampal system (2nd ed.). New York, NY: Oxford University
Press.
Greenberg, L. S., & Safran, J. D. (1987). Emotion in psychotherapy: Affect, cognition, and the
process of change. New York, NY: Guilford Press.
Gross, J. J. (1998a). Antecedent- and response-focused emotion regulation: Divergent con-
sequences for experience, expression, and physiology. Journal of Personality and Social
Gross, J. J. (1998b). The emerging field of emotion regulation: An integrative review. Review
of General Psychology, 2, 271–299.
Gross, J. J. (2001). Emotion regulation in adulthood: Timing is everything. Current Directions

in Psychological Science, 10, 214–219.
Gross, J. J., & John, O. P. (2003). Individual differences in two emotion regulation processes:
Implications for affect, relationships, and wellbeing. Journal of Personality and Social
Gross, J. J., & Thompson, R. A. (2007). Emotion regulation: Conceptual foundations. In J. J.
Gross (Ed.), Handbook of emotion regulation (pp. 3–24). New York, NY: Guilford Press.
Hasenkamp, W., Wilson-Mendenhall, C. D., Duncan, E., & Barsalou, L. W. (2012). Mind
wandering and attention during focused meditation: A fine-grained temporal analysis of
fluctuating cognitive states. NeuroImage, 59, 750–760.
Hayes, S. A., Orsillo, S. M., & Roemer, L. (2010). Changes in proposed mechanisms of action
during an acceptance-based behavior therapy for generalized anxiety disorder. Behaviour
Hayes, S. C., & Smith, S. (2005). Get out of your mind and into your life: The new acceptance
and commitment therapy. Oakland, CA: New Harbinger.
Hayes, S. C., Strosahl, K., & Wilson, K. G. (1999). Acceptance and commitment therapy: An
experimental approach to behavior change. New York, NY: Guilford Press.
Hayes-Skelton, S. A., Usmani, A., Lee, J. K., Roemer, L., & Orsillo, S. M. (2012). A fresh look
at potential mechanisms of change in applied relaxation for generalized anxiety disorder:
A case series. Cognitive and Behavioral Practice, 19, 1–12.
Healy, H., Barnes-Holmes, Y., Barnes-Holmes, D., Keogh, C., Luciano, C., & Wilson, K.
(2008). An experimental test of a cognitive defusion exercise: Coping with negative and
positive self-statements. Psychological Record, 58, 623–640.
Higgins, E. T. (1997). Beyond pleasure and pain. American Psychologist, 52, 1280–1300.
Hofmann, S. G., Heering, S., Sawyer, A. T., & Asnaani, A. (2009). How to handle anxiety: The
effects of reappraisal, acceptance, and suppression strategies on anxious arousal. Behaviour
Hofmann, S. G., Moscovitch, D. A., Litz, B. T., Kim, H., Davis, L. L., & Pizzagalli, D.
A. (2005). The worried mind: Autonomic and prefrontal activation during worrying.
Emotion, 5, 464–475.
Hofmann, S. G., Sawyer, A. T., Witt, A. A., & Oh, D. (2010). The effect of mindfulness-based
therapy on anxiety and depression: A meta-analytic review. Journal of Consulting and
Izard, C. E. (1991). The psychology of emotions. New York, NY: Plenum Press.
Jensen, K. B., Kosek, E., Wicksell, R., Kemani, M., Olsson, G., Merle, J. V., … Ingvar, M.
(2012). Treatment with cognitive behavioral therapy increases pain-evoked activation of
the prefrontal cortex in patients suffering from chronic pain. Pain, 153, 1495–1503.
Johnstone, T., van Reekum, C. M., Urry, H. L., Kalin, N. H., & Davidson, R. J. (2007).
Failure to regulate: Counterproductive recruitment of top-down prefrontal-subcortical
circuitry in major depression. Journal of Neuroscience, 27 , 8877–8884.
Joormann, J., & Gotlib, I. H. (2007). Selective attention to emotional faces following recovery
from depression. Journal of Abnormal Psychology, 116, 80–85.
Kabat-Zinn, J. (1982). An outpatient program in behavioral medicine for chronic pain
patients based on the practice of mindfulness meditation: Theoretical considerations and
preliminary results. General Hospital Psychiatry, 4, 33–47.
Kabat-Zinn, J. (2005). Wherever you go, there you are: Mindfulness meditation in everyday life.
New York, NY: Hyperion.
Kalisch, R., Wiech, K., Critchley, H. D., Seymour, B., O’Doherty, J. P., Oakley, D. A.,
… Dolan, R. J. (2005). Anxiety reduction through detachment: Subjective, physiological,
and neural effects. Journal of Cognitive Neuroscience, 17 , 874–883.
Koenigsberg, H. W., Fan, J., Ochsner, K. N., Liu, X., Guise, K., Pizzarello, S., … Siever, L. J.
(2009). Neural correlates of the use of psychological distancing to regulate responses to
negative social cues: A study of patients with borderline personality disorder. Biological
Koenigsberg, H. W., Fan, J., Ochsner, K. N., Liu, X., Guise, K., Pizzarello, S., … Siever, L.
J. (2010). Neural correlates of using distancing to regulate emotional responses to social
cues. Neuropsychologia, 48, 1813–1822.
Kring, A. M., & Werner, K. H. (2004). Emotion regulation and psychopathology. In P.
Philippot & R. S. Feldman (Eds.), The regulation of emotion (pp. 359–385). Mahwah,
NJ: Erlbaum.
Kross, E., & Ayduk, Z. (2009). Boundary conditions and buffering effects: Does depres-
sive symptomology moderate the effectiveness of self-distancing for facilitating adaptive
emotional analysis? Journal of Research in Personality, 43, 923–927.
Kross, E., Gard, D., Deldin, P., Clifton, J., & Ayduk, O. (2012). “Asking why” from a
distance: Its cognitive and emotional consequences for people with major depressive
disorder. Journal of Abnormal Psychology, 121, 559–569.
Lang, P. J. (1978). Anxiety: Toward a psychophysiological definition. In H. S. Akiskal & W. L.
Webb (Eds.), Psychiatric diagnosis: Exploration of biological criteria (pp. 265–389). New
York, NY: Spectrum.
Langer, E. J., & Moldoveanu, M. M. (2000). The construct of mindfulness. Journal of Social
Issues, 56, 1–9.
Lappalainen, R., Lehtonen, T., Skarp, E., Taubert, E., Ojanen, M., & Hayes, S. C. (2007).
The impact of CBT and ACT models using psychology trainee therapists: A preliminary
controlled effectiveness trial. Behavior Modification, 31, 488–511.
Leary, M. R., Tate, E. B., Adams, C. E., Batts Allen, A., & Hancock, J. (2007). Self-
compassion and reactions to unpleasant self-relevant events: The implications of treating
oneself kindly. Journal of Personality and Social Psychology, 92, 887–904.
Levenson, R. W., & Gottman, J. M. (1983). Marital interaction: Physiological linkage and
affective exchange. Journal of Personality and Social Psychology, 45, 587–597.
Levitt, J. T., Brown, T. A., Orsillo, S. M., & Barlow, D. H. (2004). The effects of acceptance
versus suppression of emotion on subjective and psychophysiological response to carbon
dioxide challenge in patients with panic disorder. Behavior Therapy, 35, 747–766.
Linehan, M. M. (1993a). Cognitive-behavioral treatment for borderline personality disorder: The
dialectics of effective treatment. New York, NY: Guilford Press.
Linehan, M. (1993b). Skills training manual for treating borderline personality disorder. New
Mathews, A., Mogg, K., Kentish, J., & Eysenck, M. (1995). Effect of psychological treatment
on cognitive bias in generalized anxiety disorder. Behaviour Research and Therapy, 33,
293–303.
Mauss, I. B., Levenson, R. W., McCarter, L., Wilhelm, F. H., & Gross, J. J. (2005). The tie
that binds? Coherence among emotion experience, behavior, and physiology. Emotion, 5,
175–190.
McCracken, L. M., Vowles, K. E., & Eccleston, C. (2005). Acceptance-based treatment
for persons with complex, long standing chronic pain: A preliminary analysis of treat-
ment outcome in comparison to a waiting phase. Behaviour Research and Therapy, 43,
1335–1346.
Mennin, D. S., & Fresco, D. M. (2009). Emotion regulation as an integrative framework for
understanding and treating psychopathology. In A. M. Kring & D. M. Sloan, Emotion
regulation and psychopathology: A transdiagnostic approach to etiology and treatment (pp.
256–379). New York, NY: Guilford Press.
Mennin, D. S., & Fresco, D. M. (2011). Emotion regulation therapy for complex and
refractory presentations of anxiety and depression. Spotlight presentation delivered at the
annual meeting of the Association for Behavioral and Cognitive Therapies, Toronto,
Canada.
Mogg, K., Philippot, P., & Bradley, B. P. (2004). Selective attention to angry faces in clinical
social phobia. Journal of Abnormal Psychology, 113, 160–165.
Muraven, M., & Baumeister, R. F. (2000). Self-regulation and depletion of limited resources:
Does self-control resemble a muscle? Psychological Bulletin, 126, 247–259.
Ochsner, K. N., Bunge, S. A., Gross, J. J., & Gabrieli, J. D. (2002). Rethinking feelings: An
fMRI study of the cognitive regulation of emotion. Journal of Cognitive Neuroscience, 14,
1215–1229.
Orsillo, S., & Roemer, L. (2011). The mindful way through anxiety. New York, NY: Guilford
Press.
Parasuraman, R. (1998). The attentive brain. Cambridge, MA: MIT Press.
Parrott, W. G. (2001). Implications of dysfunctional emotions for understanding how emotions
function. Review of General Psychology, 5, 180–186.
Paulus, M. P., & Stein, M. B. (2006). The insular view of anxiety. Biological Psychiatry, 60,
402–409.
Peers, P. V., & Lawrence, A. D. (2009). Attentional control of emotional distraction in rapid
serial visual presentation. Emotion, 9, 140–145.
Phillips, M. L., Drevets, W. C., Rauch, S. L., & Lane, R. (2003). Neurobiology of emotion
perception I: The neural basis of normal emotion perception. Biological Psychiatry, 54,
504–514.
Pishyar, R., Harris, L. M., & Menzies, R. G. (2008). Responsiveness of measures of attentional
bias to clinical change in social phobia. Cognition and Emotion, 22, 1209–1227.
Ray, R. D., Wilhelm, F. H., & Gross, J. J. (2008). All in the mind’s eye? Anger rumination and
reappraisal. Journal of Personality and Social Psychology, 94, 133–145.
Resick, P. A., & Schnicke, M. K. (1993). Cognitive processing therapy for rape victims: A
treatment manual. Newbury Park, CA: Sage.
Roemer, L., & Orsillo, S. M. (2005). An acceptance based behavior therapy for generalized
anxiety disorder. In S. M. Orsillo & L. Roemer (Eds.), Acceptance and mindfulness-based
approaches to anxiety: Conceptualization and treatment (pp. 213–240). New York, NY:
Springer.
Rottenberg, J., Gross, J. J., & Gotlib, I. H. (2005). Emotion context insensitivity in major
depressive disorder. Journal of Abnormal Psychology, 114, 627–639.
Samoilov, A., & Goldfried, M. R. (2000). Role of emotion in cognitive-behavior therapy.
Clinical Psychology: Science and Practice, 7 , 373–385.
Sanislow, C. A., Pine, D. S., Quinn, K. J., Kozak, M. J., Garvey, M. A., Heinssen, R. K., …
Cuthbert, B. N. (2010). Developing constructs for psychopathology research: Research
domain criteria. Journal of Abnormal Psychology, 119, 631–639.
Scherer, K. R., Schorr, A., & Johnstone, T. (2001). Appraisal processes in emotion. New York,
NY: Oxford University Press.
Segal, Z. V., Williams, J. M. G., & Teasdale, J. D. (2002). Mindfulness-based cognitive therapy
for depression: A new approach for preventing relapse. New York, NY: Guilford Press.
Seres, I., Unoka, Z., Bódi, N., Aspán, N., & Kéri, S. (2009). The neuropsychology of
borderline personality disorder: Relationship with clinical dimensions and comparison
with other personality disorders. Journal of Personality Disorders, 23, 555–562.
Singer, A. R., & Dobson, K. S. (2007). An experimental investigation of the cognitive
vulnerability to depression. Behaviour Research and Therapy, 45, 563–575.
Smits, J. A., Julian, K., Rosenfield, D., & Powers, M. B. (2012). Threat reappraisal as a
mediator of symptom change in cognitive-behavioral treatment of anxiety disorders: A
systematic review. Journal of Consulting and Clinical Psychology, 80, 624–635.
Teasdale, J. D., Moore, R. G., Hayhurst, H., Pope, M., Williams, S., & Segal, Z. V. (2002).
Metacognitive awareness and prevention of relapse in depression: Empirical evidence.
Tooby, J., & Cosmides, L. (1990). The past explains the present: Emotional adaptations and
the structure of ancestral environments. Ethology and Sociobiology, 11, 375–424.
Wells, A. (2008). Metacognitive therapy for anxiety and depression. New York, NY: Guilford
Press.
Wisco, B. E., & Nolen-Hoeksema, S. (2011). Effect of visual perspective on memory and
interpretation in dysphoria. Behaviour Research and Therapy, 49, 406–412.
Witvliet, C. V. O., DeYoung, N. J., Hofelich, A. J., & DeYoung, P. A. (2011). Compassionate
reappraisal and emotion suppression as alternatives to offense-focused rumination: Impli-
cations for forgiveness and psychophysiological well-being. Journal of Positive Psychology,
6, 286–299.
Zald, D. (2003). The human amygdala and the emotional evaluation of sensory stimuli. Brain
Research Reviews, 41, 88–123.
Zettle, R. D., Rains, J. C., & Hayes, S. C. (2011). Processes of change in acceptance and
commitment therapy and cognitive therapy for depression: A mediation reanalysis of
Zettle and Rains. Behavior Modification, 35, 265–283.
6
Metacognitive Therapy
Thinking Differently about Thinking
Adrian Wells
University of Manchester, United Kingdom, and NTNU, Norway
Michael Simons
RWTH Aachen University, Germany
Metacognitive therapy (MCT) was developed by Adrian Wells in the 1990s and
is based on a self-regulatory model of human information processing, called the
self-regulatory executive function model (S-REF; Wells & Matthews, 1994). This
treatment approach has a number of similarities with cognitive behavioral therapy
(CBT) but there are important ways in which it differs greatly from the latter in its
focus and objectives. At a nonspecific level, MCT appears similar to CBT: Therapy
aims at changing the particular maintaining factors of a specific disorder. These
factors can be cognitions and maladaptive coping behaviors such as safety behaviors
and avoidance. Therapy uses collaborative empiricism and guided discovery. As in
CBT, MCT starts with an individual case formulation and the socialization to the
treatment model and it utilizes techniques such as Socratic dialogue to challenge the
patient’s beliefs and exposure (combined with response prevention or blocking of
safety behaviors).
These similarities notwithstanding, there are essential differences with respect to
theory, practice, and the mechanisms and processes that are targeted. Unlike CBT,
MCT postulates that what a person thinks is of little importance; however, how a
person thinks and how thinking is controlled is central to disorder. Thoughts and
beliefs are seen as passing experiences in the mind. Most people have thoughts like
“Life is bad,” “This is scary,” or “I’m a failure” from time to time, but this does not
lead to clinical depression or clinical anxiety. Only if they answer these thoughts with
a pattern or thinking style of excessive rumination or worrying, maladaptive coping,
and focusing of attention on threat, does an emotional disorder develop. Distorted
thoughts, cognitive schemas, abnormal feelings of anxiety, despair, shame, guilt,
and so on, are seen as products of this thinking style. This thinking style is called

DOI: 10.1002/9781118528563.wbcbt06
the cognitive attentional syndrome (CAS). The CAS arises out of the control that
metacognition exerts on thinking. Metacognitive beliefs are considered central in this
respect. In practice, MCT helps patients to stop this thinking style and to challenge
their metacognitive beliefs. This emphasis is quite different from that of the cognitive
behavioral therapist who helps the patient examine the content of the thinking style
and reality test that content or its products. The difference is exemplified by the type
of questions each therapist might ask. Whereas the cognitive behavioral therapist
would ask the depressed patient, “What is the evidence that you are a failure? Can
you find any counterevidence?”, the MCT therapist would ask, “What is the point
in analyzing your failures? Can you reduce the time you spend analyzing these?”
The difference in questions may seem subtle but it leads to very different outcomes
in terms of the mental processes and cognitive effects produced. In the CBT case the
patient is encouraged to use more thinking in the form of rational analysis to overcome
a negative thought, whereas in MCT the patient is asked to reduce or control his or
her thinking in order to overcome the thought. If psychological disorders are caused
by too much thinking (the CAS) then it follows that developing mental control and
changing beliefs about the importance of thinking should be the most effective and
economical approach.
This chapter will describe in detail the features of the metacognitive model and
therapy and illustrate how this is applied in the treatment of obsessive-compulsive
disorder and posttraumatic stress disorder. In the next section we begin this task with
a more detailed consideration of the CAS.
The Cognitive Attentional Syndrome
According to Wells and Matthews (1994, 1996) the CAS consists of perseverative or
extended thinking, usually in response to an initial negative thought. This extended
thinking occurs in a number of forms but predominantly extended verbal processing
of a theme in the form of worry and rumination (in trauma reactions it also occurs
as a preoccupation with memory and trying to fill gaps; Wells, 2009). The CAS also
consists of maladaptive attention strategies and coping behaviors.
In worrying, the individual contemplates possible danger and threats (e.g., “What
if I get ill?”). Worrying is the main feature in generalized anxiety disorder (GAD)
but also a maintaining process in other emotional disorders. In social phobia, patients
worry about blushing, their hands shaking, sweating, or stuttering in upcoming social
situations. In panic disorder, patients worry that they could faint or have a heart
attack. In obsessive-compulsive disorder (OCD), patients worry about contamination
or intrusive thoughts. The perseverative doubting (“What if I have left the door
open? Can I really be sure that I locked the door?”) is a kind of worrying. In
posttraumatic stress disorder (PTSD), patients worry that the traumatic event could
happen again and that they will be permanently damaged by the event. In separation
anxiety disorder (SAD), the child worries about being left alone and about his or her
parents having an accident. In health anxiety disorder, patients worry about having
an undetected and potentially malignant illness. In borderline personality disorder,
patients worry about being rejected. Worrying generally leads to exacerbation of fears
Metacognitive Therapy 109
and anxiety. In GAD, patients worry that they cannot stop worrying; this is called
meta-worry.
Rumination is a main thinking style in depression. This consists of analyzing the
past, questioning the reason for events, and trying to find the causes and answers to
depressed mood. In anger individuals go over the offenses they have suffered and
think about revenge. Rumination seeks answers to questions such as, “Why me, what
does it mean, how can I get revenge, if only …”
Gap filling is a perseverative metamemory process in which individuals check their
memory for special events. In obsessive checking patients try to remember if they
really locked the door; in PTSD patients try to go over every detail of the event in
their mind so that they can have a complete memory of what happened.
As well as these extended forms of meaning-based processing, extended processing
occurs at the attentional level. The maladaptive attentional strategy of maintaining
attention on threat can be found across disorders. Traumatized patients are often on
the lookout for dangerous people and situations reminding them of the traumatic
event. Individuals with social phobia focus on personal signs and symptoms of con-
spicuous anxiety and failed performance whereas people with borderline personality
focus on possible signs of rejection by others. In OCD with contamination fears the
person pays heed to who touches what. Some patients with OCD excessively monitor
their own thinking in order to detect unwanted and seemingly dangerous thoughts
(“too much thinking about thinking”; Janeck, Calamari, Riemann, & Heffelfinger,
2003). In SAD, the child often looks for signs that the parent is going to leave.
In panic, health anxiety, and somatoform disorders, individuals focus their attention
on possible signs of illness (heart rate, breathing, pain, etc.). When patients focus in
this way, negative thinking persists and may escalate as danger-related constructs are
allowed greater access to processing.
Maladaptive coping behaviors form part of the CAS and often consist of thought
control strategies, avoidance, and safety behaviors. For example, in OCD and PTSD,
patients suffer from unwanted intrusive thoughts which they want to get rid of. Thus,
they try to suppress these thoughts. Ironically, the more they suppress these thoughts,
the more these thoughts remain important. This often leads to a desperate vicious
cycle of thought suppression and preoccupation. Besides this cognitive avoidance we
often find behavioral avoidance depriving the individual of an opportunity to discover
that he or she can cope in situations and that anxiety is not dangerous. Some patients
combine cognitive and emotional avoidance; for example, in complicated grief patients
often try not to think about a deceased partner in order to avoid sadness.
Safety behaviors (such as reassurance seeking or holding onto or leaning on
something in order to prevent a collapse) prevent disconfirmation of negative thoughts
and beliefs. The nonoccurrence of feared outcomes may be mistakenly attributed to
these behaviors. Some safety behaviors exacerbate bodily symptoms; for example,
controlling one’s breathing in panic disorder can lead to hyperventilation. In social
phobia, safety behaviors, such as trying too hard to be funny, may contaminate the
social performance and affect interactions in a manner consistent with negative beliefs.
These factors can maintain negative thought content and self-discrepancies, triggering
continued self-regulatory processing and the CAS.
As these processes of the CAS cause and maintain emotional suffering, one might
ask why people utilize them or why the cognitive system does not simply self-correct.
In metacognitive theory, this is due to metacognitive beliefs and experiences.
Metacognitive Beliefs
Metacognition is cognition about cognition, a higher level of cognition that monitors,

controls, and appraises thinking. In the S-REF model of psychological disorder there
are two broad domains of beliefs that are important: positive and negative. Positive
metacognitive (PMC) beliefs motivate the person to engage in sustained thinking,
threat monitoring, and maladaptive coping in response to negative thoughts and
emotions. Examples include:
• “I have to worry in order to be prepared for any possible bad outcome.”

• “Worrying shows that I take care.”
• “Worrying helps me cope.”
• “Ruminating will help me find out why I am depressed.”
• “If I look out for any possible trouble, it will not take me by surprise.”
• “If I can recognize early signs of rejection, I can do something to prevent it.”
• “I have to fill all the gaps in my memory to know that I really locked the door.”
• “I have to wash my hands to get rid of these thoughts.”
• “I must stop my memories or I will go crazy.”
Negative metacognitive (NMC) beliefs deal with the negative meaning, importance,
and consequences of thoughts, sustained thinking, and mental experiences (e.g., urges,
memories, impulses). The most important NMC beliefs are about the uncontrollability
of perseverative thinking styles: “I can’t stop worrying/ruminating.” These beliefs
lead patients to abandon any effort to stop this counterproductive thinking, which
contributes to the persistence of the CAS. In addition, there are NMC beliefs about
the danger of thoughts, sustained thinking, and mental experiences, as in the following
examples:
• “My intrusions could make me go crazy.”

• “My obsessive thoughts tell me how I really am.”
• “If I go on worrying I could become seriously ill.”
• “My negative thoughts prove that I am not normal.”
• “Bad thoughts could make me do bad things.”
Across different disorders there is some specificity in the content of PMC and NMC
beliefs (see below in relation to OCD and PTSD).
Metacognitive Experiences
As well as the role of metacognitive beliefs in assigning importance to thinking and

contributing to the CAS, more direct metacognitive experiences play a role in MCT
theory. Metacognitive experiences are the conscious on-line way in which cognition is
experienced by a person. These experiences can occur as “feeling states”; a common
example to which most people can relate is the “tip-of the-tongue effect.” This is the
feeling that an item of information is stored in memory even though it cannot be
currently remembered. There are other specific types of experience that are relevant
to psychological disorder. In particular, because cognition can itself become the
object of thinking, there are two “modes” in which thoughts or mental events can
be experienced. Wells (2000) describes these as “object mode” and “metacognitive
mode.” Object mode is the default mode of mental experiencing in which thoughts
are indistinct from perceptions of reality; we go about our lives not being aware of
the distinction between the internal cognitive and external world. In contrast to this,
in the metacognitive mode the person can take a step back from thoughts and see
them as events in the mind separate from events in the world. An elaboration of this
state is detached mindfulness (Wells & Matthews, 1994) in which such an objective
decentered relationship with thoughts is coupled with suspension of any response. As
we will see later, changing the direct way thoughts are experienced is a feature of MCT.
Basic Treatment Model

MCT aims at removing the CAS and developing new ways of relating to thoughts. In
general, MCT is a short-term treatment of about 10 weekly sessions of normal length
(i.e., 40–60 minutes). However, in some cases treatment might last longer. We will
first describe basic treatment modules and then provide more detail as these relate to
treating OCD and PTSD.
To date, there exist four new and empirically supported treatment manuals for GAD,
PTSD, OCD, and major depressive disorder published in Wells (2009). In addition,
there are five “older” manuals (for panic disorder, hypochondriasis, social phobia,
GAD, and OCD) blending cognitive and metacognitive interventions (Wells, 1997).
It is advisable to use a new and purely metacognitive treatment model if available. In
other cases, MCT can provide a universal formulation and a transdiagnostic treatment
for which general guidelines are available (Wells, 2009). Metacognitive treatments
for psychosis and borderline personality disorder, and applications to children and
adolescents (Simons, Schneider, & Herpertz-Dahlmann, 2006; Simons, 2010), have
been recently initiated.
Case Formulation
A course of metacognitive treatment begins with a joint case formulation. First,
the therapist asks for the latest episode when the patient suffered from symptoms.
Thereafter, he or she inquires about specific triggers (cognitions), response styles
(CAS), and resulting emotions and behaviors. Specific to MCT are questions about
perseverative thinking styles (CAS), metacognitive beliefs, and attentional strategies,
and placing of cognition as the trigger for these rather than more general antecedents
being used as a trigger. In the following example the therapist interviews a young
woman with depression. Instead of focusing on the content of cognitions (as in
cognitive therapy), he asks for the patient’s responses to these cognitions.
THERAPIST: Can you tell me about the last time you felt particularly depressed?
PATIENT: That was yesterday in the evening when my boyfriend called me
on the phone.
THERAPIST: What happened?
PATIENT: Well, we wanted to go the cinema. He called to cancel our night out.
THERAPIST: How did that make you feel?
PATIENT: Well, really bad.
THERAPIST: OK, it sounds as though you didn’t feel good. Can you tell me more about
the feelings you had?
PATIENT: There was a mix of feelings. I felt disappointed, sad, and angry, and if I’m
honest, a bit suspicious.
THERAPIST: What was the first thought that you had that triggered those feelings?
PATIENT: I had the thought “he doesn’t care about me.”
THERAPIST: What did you then go on to think about?
PATIENT: That he should keep his appointments, that maybe I am not that important to
him, that maybe he’s meeting someone else. And I asked myself why this always
happens to me.
THERAPIST: Well, sounds like you’re chewing on a bunch of depressive thoughts. We
call this rumination. For how long did you go on thinking like this?
PATIENT: I don’t know, the whole evening. I didn’t have anything else to do.
THERAPIST: What happened to your feelings then?
PATIENT: I felt all alone and I cried.
THERAPIST: Did you go on ruminating?
PATIENT: I think so.
THERAPIST: That sounds like ruminating made you feel even worse.
PATIENT: Yes, so what you’re saying is that it’s my fault to feel so depressed?
THERAPIST: Sounds like that could be a trigger for rumination right now. But let me
ask you a question: What if you could find a way to stop ruminating? How would you
feel?
PATIENT: That would make me feel much better. But that would mean not dealing with
my problems.
THERAPIST: That sounds like you have the belief that analyzing or ruminating could be
of help.
PATIENT: Yes, of course, I have to find answers.
THERAPIST: OK, let me ask you a question: How long have you been thinking like this?
PATIENT: Since I got my depression, which is over two years ago.
THERAPIST: And how many answers have you found in the meantime?
PATIENT: Well, no real answer yet.
THERAPIST: Maybe the answer isn’t to continue ruminating but to stop ruminating.
PATIENT: Sure, but I’m not sure I can.
THERAPIST: Do you believe that it is uncontrollable?
PATIENT: Yes, maybe it’s the depression that makes me do it. I think my head is all
messed up.
THERAPIST: So, the first thing we should do is to find out if you can control
rumination.
Socialization
Socialization follows by presenting the case formulation. The therapist emphasizes the
consequences of the CAS for symptoms and the importance of metacognitive beliefs
in contributing to the CAS. Symptoms are destigmatized and normalized as outcomes
of normal psychological processes instead of abnormal and disease processes (as in
more medical models). For example, rather than pointing out a possible chemical
imbalance causing depression, the therapist describes a ruminative thinking style based
on metacognitive beliefs leading to prolonged emotional responses.
Besides these verbal methods (which are conducted as guided discovery) the
therapist makes use of behavioral experiments. For example, the therapist asks the
patient to start and stop ruminating in the session. In disorders such as OCD
or PTSD, where thought suppression is a main feature maintaining the disor-
der, a thought suppression experiment is often conducted. The patient is asked to
have a specific thought (e.g., “Think about a pink rabbit sitting on my head”)
and to suppress this thought for a minute. Usually, patients report that the
thought repeatedly comes back. In the second step, the patient is introduced to
the metacognitive model: “I want you to notice the thoughts that pop into your
mind. If there’s the thought of a pink rabbit sitting on my head, just watch
this thought emerging and passing without suppressing it. Just leave the thought
alone.”
After socializing to the case conceptualization, the therapist presents the treatment
rationale, emphasizing that the patient will learn to stop the perseverative thinking
styles and modify his or her attentional strategies and behavioral responses. Concor-
dant with the S-REF model, which distinguishes levels of mental control, the patient
will learn to stop trying to control what is uncontrollable (e.g., spontaneous thoughts
popping into the mind) and begin to control what is controllable (the CAS). The
former is achieved by detached mindfulness and the latter by techniques such as
postponing rumination and worrying. These new experiences are presented in a way
that modifies metacognitive beliefs.
Detached Mindfulness
Detached mindfulness (DM; Wells & Matthews, 1994; Wells, 2005) is an alternative
response and a new way of relating to automatic thoughts or mental events, and has
two features:
1. mindfulness, which refers to being aware of inner cognitive events like thoughts,
beliefs, and memories. It is effectively meta-awareness; and
2. detachment, which means seeing these inner events from a distance (as an
observer) and without reacting on them.
The individual refrains from further appraisal of or attempts to cope in response to

the inner event. This is in stark contrast to the CAS. Some patients with OCD are
very much aware of their thinking (meta-awareness), but in a “nondetached” way:
They are constantly worrying about specific thoughts and try to get rid of them.
DM comprises abandoning perseverative thinking, thought control strategies, threat

monitoring, avoidance, and safety behaviors in response to cognition. DM helps
patients to shift from the object mode to the metacognitive mode. In the object mode,
thoughts are fused with facts (e.g., “My thoughts tell me that I am in danger”).
In the metacognitive mode, thoughts are just events in the mind. They are not by
themselves important. It is up to the patient to decide if he or she wants to treat the
thought as important.
The MCT therapist typically uses metaphors to illustrate the concept of DM. Here
are some examples:
Telephone metaphor: “You do not have control over the telephone ringing. When
it rings, it rings. But you decide how to answer the phone. You could answer it
immediately, or you could let it ring until it stops. In the same manner, you cannot
prevent specific thoughts from popping into your mind, but you can decide if and
when you answer them.”
Fishhook metaphor: “Thoughts are like fishhooks. It can be helpful to notice them,
but does it help to bite and chew on them?”
The therapist also uses experiential exercises to introduce DM. For instance, the
“free-association task” is an exercise in which the patient is asked to listen to some
words without reacting to them. The aim is passively to watch the “ebb and flow” of
thoughts and memories that could be triggered spontaneously by these words, but not
control, analyze, or try to influence them. After this basic instruction, the therapist says
a series of neutral words, such as blue, house, banana, tree, clouds, friends, chocolate,
walking. The therapist then asks, “What happened to the first thought by the end
of the words?” When the patient successfully abandons any strategy of deliberate
information processing, the therapist can repeat the exercise while dropping in one of
the patient’s trigger words, such as germs or failure.
Another example is the “tiger task,” in which the patient is asked to passively
observe nonvolitional aspects of imagery. The therapist instructs the patient to close
his or her eyes and to imagine a tiger without trying to change or influence the image.
When the patient can experience spontaneous movements or changes of the image
then this is used as an example of DM and the concept that thoughts have their own
behavior and can take care of themselves if left alone.
In the beginning of therapy, patients often mention difficulties in practicing
DM, stating, “It doesn’t work, the thoughts keep coming back.” This is important
information about the patient’s metacognitive beliefs such as, “I can’t stand having
this thought in my mind.” The MCT therapist is highly attentive to this type of
response and repeatedly uses this in therapy. He or she emphasizes that DM is not
intended to get rid of thoughts; it is not an improved thought suppression technique.
On the contrary, the patient’s complaint proves that he or she gives the thoughts
too much importance: “If you knew that these thoughts are completely unimportant,
would you feel any need to get rid of them?” Further, the patient is reminded that
most thoughts come and go by themselves: “How many thoughts do you have in one
day? Thousands? So what happens to them? Do you fight them all? No, they just pass
away.”
Postponing Perseverative Thinking

DM is usually combined with postponing worrying, ruminating, gap filling, or (as
in OCD) postponing carrying out a neutralizing ritual. The patient is asked to
schedule a special time (“worry time”) in the early evening where he or she might
engage his or her ruminating or worrying thoughts. Note that this is only optional.
It is more important that the patient learns to postpone the thinking process. If
he or she does not feel like worrying or ruminating later on, the therapist asks
what that could mean about the importance of these activities. The postponement
experiment is presented as an explicit experiment to test the patient’s belief that worry
or rumination and responses to thoughts are uncontrollable. The therapist closely
monitors changes in metacognitive beliefs about uncontrollability as a result of using
such experiments.
Attention Modification Strategies

Maladaptive attention strategies are part of the CAS, especially when control of
attention becomes inflexible as attention is bound up with perseverative, self-focused,
worry-based processing and monitoring for threat. Specifically in depression, patients
show reduced meta-awareness of rumination. In order to be more aware of their
thinking processes and to practice greater attentional or executive control, a particular
technique called the attention training technique (ATT; Wells, 1990) is used. The
ATT is an auditory-based attention procedure fostering selective attention, rapid
attention switching, and divided attention. The patient is exposed to a series of
sounds on which he or she is systematically instructed to focus attention. A detailed
manual can be found in Wells (2009).
Another strategy is called situational attentional refocusing (SAR; Wells, 2000)
which is intended to enhance the processing of information that is incompatible with
the patient’s dysfunctional beliefs and counteract threat monitoring. For example,
patients with social phobia tend to turn attention inward onto themselves in social
situations and try to see themselves through the eyes of others. In SAR, they learn
to focus their attention externally on features of the environment or other people
(e.g., their hair, ears, clothing, characteristics in their speech). An example of SAR as
applied to PTSD is provided later in this chapter. The therapist has to take care that
the patient does not misuse attention modification strategies as safety or avoidance
behaviors.
Modifying Metacognitive Beliefs

Since metacognitive beliefs maintain the CAS, they have to be explored and
challenged. To challenge these beliefs, MCT makes extensive use of verbal
methods, such as Socratic dialogue (“What’s the evidence for/against …?”)
and advantages–disadvantages analysis. To prevent therapy from becoming too
theoretical, behavioral experiments are of particular importance. For example, NMC
beliefs about uncontrollability can be challenged by asking the patient to start and
stop worrying or to try and lose control of worrying. For example, people with GAD
have negative beliefs about worrying. One patient believed that worrying would
damage his body, and this led to worry about worry. The therapist challenged this
by comparing the effects of 5 minutes of rest, 5 minutes of worry, and 5 minutes
of physical exercise on the patient’s pulse-rate. The patient discovered that exercise
had the greatest effect on his heart and the therapist was able to pose the question:
“Which is the most dangerous for your body, exercise or worrying?” which weakened
the danger belief. The interventions that we have already described (thought control
experiments, DM, postponement of thinking, attentional modification) represent
ways to modify metacognitive beliefs. Further examples can be found below in the
discussions of OCD and PTSD.
Coping Behaviors
The CAS usually comprises dysfunctional behaviors such as avoidance, safety behaviors
(e.g., seeking reassurance), and self-numbing strategies such as substance abuse. Most
patients do not realize that these behaviors are being used to terminate the CAS or
deal with the emotional effects of this process. MCT aims to reduce these behaviors
by identifying and challenging the corresponding metacognitive beliefs supporting
the CAS and by introducing alternative responses.
Relapse Prevention and New Plans for Processing

Before ending therapy, the therapist and patient work together at identifying and
reducing residual CAS responses and metacognitions. A “blueprint” of the therapy,
consisting of the case formulation, a list of the patient’s metacognitive beliefs before
treatment, and his or her modification, is generated. Of special importance is the
consolidation and strengthening of alternative metacognitive plans for responding to
triggering thoughts. The original thinking style, behavior, and attentional strategies
for responding to thoughts are contrasted with a new plan of processing. For
example, a patient with health anxiety described how she became anxious when
she heard about swine flu in the media. Her old plan of processing was: “When
I hear about a new disease in the media, I used to worry a lot about having
this illness (thinking style), search for physical symptoms (attentional strategy), and
go to the doctor to have a medical examination (behavior).” Her new plan was:
“When I hear about a new disease in the media and have the thought that I could
have gotten it, I tell myself that this is just a thought and I will deal with it if
necessary. I know that searching for symptoms is a self-fulfilling prophecy and I
don’t check my body for any signs of illness. I can regularly go to my doctor
but not only at times when I’m worried about symptoms. I know my problem
is not one of being sick but one of being worried. My worries are under my
control.”
Metacognitive Therapy for Obsessive-Compulsive Disorder

People with OCD suffer from intrusive thoughts, urges, and images which are
opposed to the individual’s values (e.g., having aggressive or blasphemous thoughts)
or reasoning (e.g., “Although I know my hands are supposed to be clean, I think

they are not”). To get rid of obsessive thoughts patients try to neutralize them
by carrying out rituals (compulsions) or avoid further triggers of the obsessions.
The metacognitive model of OCD (Wells, 1997, 2009) defines the pattern of
specific processes (the CAS) and metacognitive beliefs causing and maintaining the
disorder.
The Cognitive Attentional Syndrome in Obsessive-Compulsive Disorder

The perseverative thinking style in OCD consists of rumination (e.g., about having
carried out a ritual properly), worry (e.g., about possible negative outcomes if the
ritual has not been carried out properly, or maintaining concern about germs), and
gap filling (e.g., trying hard to remember if one has really switched off the stove).
Furthermore, patients use maladaptive attentional strategies such as focusing attention
on signs of threat in the environment and in one’s mind (e.g., one patient had to
check his mind obsessively for any possible homosexual thoughts) and body (e.g.,
signs of arousal, feelings of contamination). Maladaptive coping behaviors comprise
overt and covert (i.e., mental) rituals, any kind of avoidance, and thought control
strategies (especially thought suppression).
Metacognitive Beliefs in Obsessive-Compulsive Disorder

Patients with OCD hold NMC beliefs about their intrusions in such a way that these
thoughts are equated with actions, events, and objects. Thought–action fusion (TAF)
refers to the belief that obsessional thoughts can make the person do something
he or she does not want to do; for example, one adolescent feared that having
the idea of killing his parents with a knife meant that he was in danger of doing
exactly this. Thought–event fusion (TEF) is the belief that the occurrence of an
intrusion can cause events in the future or is a sign that the event has already
happened. One patient feared that having thoughts about airplane crashes could
bring about that event. Patients with contamination concerns often believe that if
they have the thought that their hands are dirty, this must mean that they really
are. Thought–object fusion (TOF) is the belief that thoughts or feelings can be
transferred into objects; for example, one patient feared that his unwanted sexual
thoughts could be transferred into a pen with which he was writing. This was a
problem because the only way to get rid of the thought was to throw away all
contaminated writing implements and attempt to have perfect control over his mind
when writing.
In addition to these beliefs, patients with OCD hold beliefs about rituals, which
include NMC beliefs about the uncontrollability of rituals and negative beliefs about
memory (e.g., “I can’t trust my memory of really locking the door”). They also have
PMC beliefs about rituals (e.g., “the ritual helps me cope with or get rid of obsessional
thoughts”) and avoidant behaviors. Finally, patients hold PMC beliefs about when
they can end the ritual (so-called “stop signals,” e.g., “I have to wash my hands until
I feel clean”).
The Treatment Process

MCT helps patients with OCD to experience intrusive thoughts as unimportant
events. This means that fusion-related metacognitive beliefs must be challenged
and the tendency to react to intrusions with extended processing or behaviors
reduced.
Treatment begins by generating a case formulation and socializing patients to
the model. Therapist and patient jointly look at the case formulation. The therapist
emphasizes that the rituals do not contribute to the patient’s (real) safety (feeling of
control, cleanliness, etc.) but only contribute to the dysregulation of thoughts and
emotions. Further, the rituals only work in the short run but are counterproductive
in the long run (“like peeing your pants to get warm”). It is critical to help the
patient move from the object-level to the meta-level. An important question used by
the therapist is: “If you no longer believed that [NMC belief, e.g., thoughts could cause
harm], what would happen to your anxiety and need to carry out your ritual?”
Behavioral experiments such as thought suppression experiments are utilized to
demonstrate the counterproductive consequences of trying to get rid of thoughts.
This is done in two steps. In the first step, the patient is asked to suppress a specific
thought; in the second step he or she is asked to just watch his or her thoughts
without intervening. This leads to the introduction of DM for obsessional thoughts.
Exposure and Ritual Manipulation Experiments

In MCT, exposure and ritual prevention (ERP) is utilized but it is different to that
used in traditional CBT (e.g., Franklin & Foa, 2011). Whereas in CBT, ERP is used
in a prolonged format with the aim of habituation, in MCT it serves to reduce the
CAS and to challenge specific metacognitive beliefs. For instance, the patient exposes
him- or herself to the trigger thought for his or her compulsions and responds to
this with DM. The neutralizing response is then postponed for as long as possible.
This can be done in a graded fashion with the aim of carrying out the ritual in a
10-minute period in the evening. This is introduced as an experiment to challenge
the belief that the obsessional thought is dangerous or important.
Refinements to the experiment are later made and the process is repeated. An
adolescent believed he could kill someone if he held a knife in his hands and did
not carry out a mental ritual (TAF) of neutralizing a violent image. The therapist
asked him to take a sharp pen and hold it against the therapist while intensifying the
thought. Before the experiment, the adolescent held a 50% belief that he could lose
control and stab the therapist; afterwards the belief fell to 10%.
In MCT, ERP can also be done in a “bystander mode,” as illustrated in the
following example. A 14-year-old girl with contamination OCD held the belief (80%)
that she could get AIDS by touching coins. The therapist himself touched some dirty
coins and then engaged the patient in the following dialogue:
THERAPIST: How much do you believe that I will get AIDS after having touched these
coins?
PATIENT: 30%.
THERAPIST: How come you are less convinced when I touch them? Would you be more
worried if you did it?
PATIENT: Yes, that would really worry me.
THERAPIST: So is the problem about germs or the amount you worry?
PATIENT: It’s about worry.
THERAPIST: Has avoiding touching coins helped you to get rid of your worry
completely?
PATIENT: No, it’s always in the back of my mind.
THERAPIST: Would it help to look at new and better ways to reduce your worry?
In MCT it is not necessary to postpone or eliminate rituals in order to modify the

relationship a patient has with an obsessional thought or to challenge metacognitive
beliefs. A technique called exposure and response commission (ERC; Wells, 2009)
changes the rule for performing a ritual so that the ritual becomes a meta-level
change experience. In this technique the patient is asked to hold an obsessional
thought in mind while checking. In some cases adaptive checking is used. A patient
who repeatedly checked the door when leaving the house was asked to check as many
times as he wanted in response to a doubt so that he might discover that his doubts
were unimportant and could subsequently be ignored. In this way rituals were used
advantageously as a means of learning the truth about doubts rather than being used
maladaptively as a means of trying to stop doubts or control emotion.
Challenging Fusion Beliefs

Below is a list of further behavioral experiments that are utilized to challenge particular
fusion beliefs.
Thought–event fusion
• “Please try to win the lottery the next week just by thinking about it.”
• “Please think intensely about my telephone falling off the desk.”
• “In the following week I want you to think about a flat tire on my car.”
Thought–action fusion
• “Think about singing a song you dislike very much. Please try this at work/in
school.”
• “Please hold your fingers next to my throat and think about strangling me.”
• “Think about running a marathon and see if this makes you do it.”
Thought–object fusion
• “Can you contaminate this card with a thought, then pick it out of the deck
without looking?”
• “Can you transfer your thoughts onto this digital recorder just by thinking them?”
• “This old book has some interesting memories associated with it. Can you tell
what they are by touching it?”
Modifying Beliefs about Rituals

After working on fusion beliefs, behavioral experiments like ERP and verbal methods
can be used to challenge beliefs about rituals and stop signals. Helpful questions
include:
• “Maybe you use the wrong rituals. How would you know?”
• “How much more is the door locked each time you check it?”
• “Do you think your hands are cleaner when you have the right thought?”
• “How can you be sure that it is enough to check eight times?”
• “If you doubt you have to check again. But what effect does checking have on
doubting? Has it removed your doubts yet?”
• “How can you doubt and be certain at the same time? Is there a better way to be
sure?”
Helpful behavioral experiments are:
• carrying out the ritual the wrong way; for example, arranging the pens in the
wrong order;
• varying the repetitions of the ritual; and
• using the ritual more to try and get rid of OCD.
Metacognitive Therapy for Posttraumatic Stress Disorder
PTSD is characterized by symptoms of reexperiencing the traumatic event (e.g.,

intrusive thoughts about the event, flashbacks, nightmares), avoidance of trauma-
associated stimuli, emotional numbing, and autonomic hyperarousal (e.g., disorders of
sleep and concentration, increased irritability, hypervigilance). PTSD can be diagnosed
only in a minority of traumatized people. Although a broad range of symptoms such as
anxiety, disgust, sleep disturbance, and irritability can be found in the early aftermath
of a traumatic event, these symptoms usually wane within a few weeks after the event.
In the metacognitive model of PTSD (Wells, 2000, 2009) these initial symptoms are
explained as a reflexive adaptation process (RAP). They primarily involve automatic
and implicit processes. In the case of intrusions, they can be seen as adaptive in that they
interrupt ongoing processing activities and stimulate the selection and modification
of upper-level knowledge and plans for dealing with threat. For instance, the person
may run imaginal simulations of dealing with threat which serves to prepare attention
and behavior for dealing with danger. However, if the CAS becomes activated this
interferes with the RAP because the components of the CAS perpetuate the sense of
danger.
The Cognitive Attentional Syndrome in Posttraumatic Stress Disorder

The following list provides examples of each of the components of the CAS that are
commonly seen in PTSD and are included in the case formulation:
• rumination about the event (e.g., “Why did this happen to me?”), often including
wishful thinking (e.g., “If only I had taken the other way”);
• worrying that the event or similar threats could happen again, or worry-
ing that one is permanently damaged or that symptoms are a sign of losing
one’s mind;
• gap filling: going over events in memory and trying to fill in specific gaps;
• threat monitoring (hypervigilance), that is, focusing attention on potential threats
similar to the traumatic event (e.g., fast cars after a road traffic accident, groups of
young men after being attacked by such a group);
• maladaptive coping behaviors often involving thought control strategies (especially
thought suppression), avoidance of situations in which the trauma occurred,
avoidance of reminders of the trauma (e.g., violent film scenes), and self-numbing
behaviors like using drugs or alcohol or self-harm behavior (especially in complex
PTSD after repeated traumatization).
Metacognitive Beliefs in Posttraumatic Stress Disorder

The PMC beliefs focus on the positive value of worrying, ruminating, gap filling,
threat monitoring, and so on. Here are some examples:
• “I must analyze why this happened to me in order to cope better next time”
(rumination).
• “I have to worry to be prepared” (worry).
• “I have to remember all the details of what happened in order to work out if I am
to blame” (gap filling).
• “Focusing on possible threat keeps me safe” (threat monitoring).
• “I must stop thoughts about the event or I will go insane” (suppression).
• “I have to avoid particular scenes in the movies because I cannot stand it.”
The NMC beliefs focus on the uncontrollability, danger, meaning, and importance
of thoughts as illustrated in these examples:
• uncontrollability: “I can’t stop worrying/ruminating”;

• danger: “My flashbacks are a sign of going crazy”;
• meaning/importance: “Remembering my sexual arousal during the assault must
mean I wanted it to happen.”
The Treatment Process

The aim of MCT is to reduce the CAS and modify the underlying metacognitive
beliefs. Treatment does not require repeated or prolonged reliving, exposure to
memories of trauma, or challenging thoughts about the event. It is held that removal
of the CAS will enable completion of the RAP and in effect the PTSD problem will
self-correct.
First of all, a metacognitive case conceptualization is jointly developed and shared
with the patient. The therapist asks about symptoms in the last few weeks and
the attempts to cope with them. These coping responses (thought suppression,
rumination, worrying, gap filling, and selective attention to potential sources of
danger) are the CAS. For each of these responses, the PMC beliefs are elicited (e.g.,
“What good does it do to pay attention to all possible dangers? In what way does
suppressing your thoughts help?”). The NMC beliefs are identified by asking about
the uncontrollability of worry/rumination and the meaning and consequences of
cognitive symptoms (e.g., “Are there disadvantages of worrying/ruminating? Could
you do it less? How uncontrollable do you believe it is? What is the worst that could
happen if you continue to have intrusive thoughts/memories?”).
In socializing to the model, the therapist explains that the symptoms are normal
reactions to an abnormal event. Two metaphors help the patient understand symptoms
and the factors maintaining them. The first is the “computer metaphor”: “If you
want to run a program or app on your computer you have to load it first; then you
can use it. The same is true of your brain: It tries to process the traumatic event and
has to load it first. You are clearly aware that memories about the event are popping
into your mind. That is not a sign that you are crazy, but rather that your brain is
healthy and doing what it needs to do.” The second is the “healing metaphor,” in
which the therapist explains how symptoms are part of the normal emotional recovery
process and that the patient’s previous attempts to find a solution have prevented
recovery: “Recovering from a trauma is similar to recovering from a physical wound.
It heals all by itself. If you have a physical wound what is the best way to allow it
to heal? Should you try to control the healing? Sometimes it itches, but you should
not scratch it, since that would only delay the healing process. What happened to you
caused an emotional wound. It heals better if you simply leave the symptoms alone.
The healing is disturbed if you ruminate, worry, try to avoid certain thoughts, and
focus on possible dangers. The goal of therapy is to reduce these unhelpful reactions.
Then the healing process can take care of things for you.”
The therapist continues socializing with a thought suppression experiment (see
above) to illustrate the unhelpful effects of the CAS and questions the effects of
rumination on emotion (“How easy is it to move on from the trauma so long as
you keep going back over it?”). The patient is then introduced to an alternative way
to deal with memories and intrusive thoughts of the traumatic event, namely DM.
This is combined with postponing perseverative thinking (rumination, worrying, gap
filling) to a scheduled time. During that time, patients can worry or ruminate, but
should not do so if they feel it is unnecessary. DM and postponement of worry and
rumination are later generalized to all other negative thoughts, not just those related
to the traumatic event.
Modifying Metacognitive Beliefs

Belief in the uncontrollability of worry and rumination is monitored by the therapist
and success at worry postponement is used as evidence to challenge the belief. Further
experiments are conducted in the session, such as attempts to lose control of worry
and using postponement in the context of exposure to reminders of the trauma as
means of challenging the belief.
Negative beliefs about symptoms, such as the belief that intrusive thoughts are
harmful and that the trauma has caused permanent psychological damage, are chal-
lenged using verbal reattribution methods. The therapist reviews the evidence for this,
looks for counterevidence, questions the mechanism of how thoughts or memory
could be harmful, and helps the patient generate an alternative view.
Reducing Counterproductive Coping

In the next step, treatment focuses on eliminating other dysfunctional responses
(avoidance of trauma-associated situations, alcohol or drug use, etc.). In this process,
the advantages and disadvantages of these strategies are explored. The advantages are
challenged and the disadvantages weighed against them. For example, patients often
use avoidance (of situations, people, and places that remind them of the traumatic
event) as a means to forget the event or to feel safe. With avoidance, however, the
trauma is not forgotten at all, and the relevant cues remain anxiety triggers. Once the
patient has recognized the negative effects of these strategies, he or she is instructed
in how to drop them.
Attention Modification
In order to reduce hypervigilance, attention modification strategies are used. Two
kinds of attention strategies are considered problematic: focusing on internal (i.e.,
bodily sensations, feelings) and external signs of threat. The systematic modification
of attention is an important component of MCT, because attention strategies lead to
a greater awareness of danger and increase anxiety. Here is a sample dialogue about
hypervigilance to external threats:
THERAPIST What are the advantages of paying attention to all possible dangers?
PATIENT: If I have them in mind, nothing can surprise me. I’m prepared.
THERAPIST: So you play it safe. Does that actually make you feel safe?
PATIENT: Not at all, I feel anxious all the time.
THERAPIST: In other words, the strategy causes problems?
PATIENT: Yes.
THERAPIST: How can you feel safe and return your thinking to how it used to be so
long as you continue to do this?
PATIENT: I guess I can’t really. I’ve got to stop doing it.
THERAPIST: I’m also interested in how you know which are the right possible dangers
to focus on.
PATIENT: I suppose I don’t know for sure.
THERAPIST: That means you have to concentrate on all possible dangers. How possible
is that?
PATIENT: It isn’t possible. So how do I stop myself doing this?
Once the patient has understood the negative effects of threat monitoring, he or she
is instructed to try and notice the activity and ban it. In some cases the therapist gives
more detailed instructions on how to modify the focus of attention. For example, the
patient can be asked to practice focusing on neutral aspects of the environment or on
safety signals such as the behavior of other people that suggests the situation is safe.
One patient who had been involved in a road accident was asked to switch attention
when crossing the road away from looking at the speed of vehicles to looking at
the gap between them. The patient was instructed to practice the new strategy for
homework and apply it in situations that served as reminders of the trauma. In some
cases, if it is safe to do so, the patient is asked to return to the site of the traumatic
event and to practice focusing externally on all aspects of the environment and to
notice the signals that the situation is safe.
Before the therapy ends, the CAS should be eliminated as completely as possible.
At the conclusion, a summary is jointly worked out that describes how the patient
previously reacted to stressful thoughts and memories (plan A), and a summary of the
new alternative plan (plan B) is compiled.
Empirical Evidence for Metacognitive Therapy
The strongest evidence for the efficacy of a particular treatment comes from random-
ized controlled trials (RCTs). There are several such trials of MCT along with case
series and uncontrolled treatment studies. To date, there are two RCTs supporting the
efficacy of MCT in GAD. MCT was superior to applied relaxation (AR) (Wells et al.
2010). Standardized recovery rates for MCT at posttreatment were 80% on measures
of worry and trait-anxiety compared with 10% and 20% for AR. At 6- and 12-month
follow-ups, improvements and the superiority of MCT were sustained. In another
RCT, both MCT and intolerance-of-uncertainty therapy (IUT) produced significant
pre- to posttreatment reductions in GAD and comorbid symptoms that were superior
to a delayed treatment control condition (van der Heiden, Muris, & van der Molen,
2012). Treatment effects were maintained at follow-up 6 months after completion
of therapy. MCT was superior to IUT using a measure of worry (Penn State Worry
Questionnaire; PSWQ). After treatment, 72% of patients treated with MCT were
recovered with a further 21% improved, whereas after IUT, 48% were recovered and
33% improved. RCTs of MCT for PTSD (Wells & Colbear, 2012; Proctor, 2008)
have demonstrated a superiority of MCT to wait-list or imaginal exposure treatment.
Standardized recovery rates across MCT studies of PTSD have been 78–90%.
Nordahl (2009) explored the effectiveness of brief MCT in a general outpatient
setting. In this RCT patients with a heterogeneous range of comorbid disorders,
many of whom had failed to respond to medication, were randomly assigned to MCT
or treatment as usual (CBT). Improvements in anxiety, depression, and worry were
seen in both treatments and patients who received MCT showed significantly greater
improvements in anxiety and worry than did those who received treatment as usual.
Rabiei, Mulkens, Kalantari, Molavi, and Bahrami (2012) randomly assigned 20
patients with body dysmorphic disorder (BDD) either to eight sessions of a modifi-
cation of the metacognitive treatment manual for OCD (Wells, 2000) or to wait-list
control group. MCT significantly reduced symptoms of BDD and thought fusion.
Aside from the RCTs, there have been case series studies of depression (Wells
et al., 2009), PTSD (Wells & Sembi, 2004), and OCD (Fisher & Wells, 2008). In
addition, group treatments of OCD (Rees & van Koesveld, 2008) and comparative
evaluations against CBT in adolescents suffering from OCD (Simons et al., 2006)
have been reported. Open trials of chronic PTSD (Wells et al., 2008) and GAD
(Wells & King, 2006) have also been published. The posttreatment effect sizes and
standardized recovery rates in these studies suggest that MCT is highly effective. In
GAD, effect sizes (Cohen’s d) at posttreatment were 2.8 (Wells & King, 2006) in
trait-anxiety and 1–1.5 in worry (Wells & King, 2006), whereas in PTSD they have
been reported as 3.5 (Wells & Sembi, 2004) and 2.9 (Wells et al., 2008) in measures
of PTSD symptom severity. Effect sizes of 3.1 were reported in a preliminary study
of depressed patients based on the Beck Depression Inventory (Wells et al., 2009).
An independent analysis of data from a randomized trial of MCT versus applied
relaxation for GAD returned standardized recovery rates of 80% following MCT
based on trait-anxiety scores. These posttreatment recovery rates are similar to rates
of 75% for GAD reported by Wells and King (2006).
Wells et al. (2012) conducted a platform study evaluating the effects of eight
sessions of treatment in clinically depressed patients who had not responded to
antidepressant medication and previous psychological therapy. Using a range of
criteria for establishing recovery, 60–90% of treatment completers were deemed
recovered at posttreatment and at 12-month follow-up.
In addition to studies of the effects of full MCT treatment, some studies have tested
the effects of individual treatment strategies. Attention training technique (ATT) has
been evaluated as a single intervention or as one module in a treatment package.
At first, ATT was found helpful in single cases of panic disorder, social phobia,
hypochondriasis, and recurrent major depressive disorder (Papageorgiou & Wells,
1998, 2000; Wells, 1990; Wells, White, & Carter, 1997). ATT has been shown to
be effective in a controlled study of the treatment of hypochondriasis (Cavanagh &
Franklin, 2000). Siegle, Ghinassi, and Thase (2007) also incorporated ATT into
a training package for depressed patients. These authors found that an attention
plus treatment as usual condition was superior to treatment as usual in improving
depression and rumination. Siegle et al. (2007) provided additional preliminary data
that the attention manipulation was associated with pre- to posttreatment changes in
subcortical (amygdala) activity in response to positive and negative stimuli.
Fisher and Wells (2005) asked patients to listen to a loop tape of their obsessional
thoughts under a habituation exposure condition or a condition that emphasized
metacognitive change. This latter condition is analogous to the metacognitively-
focused behavioral experiments used in MCT. The metacognitive condition was
superior at reducing distress, urges to neutralize, and negative beliefs.
Evidence for Metacognitive Theory
There is a large volume of evidence for the importance of perseverative thinking styles
and metacognitions across different disorders. Space does not allow for reference to
the majority of these studies but some recent additions are summarized here.
Aldoa, Nolen-Hoeksma, and Schweizer (2010) conducted a meta-analysis examin-
ing the relationships between six emotion regulation strategies (acceptance, avoidance,
problem solving, reappraisal, rumination, and suppression) and symptoms of four psy-
chopathologies (anxiety, depression, eating, and substance-related disorders). These
researchers found large effect sizes only for rumination, medium to large effect sizes
for avoidance, problem solving, and suppression, and small to medium for reappraisal
and acceptance. Ruscio, Seitchik, Gentes, Jones, and Hallion (2011) found that neg-
ative, repetitive thinking was a robust predictor of response to emotional challenge
in GAD and major depressive disorder. Yılmaz, Gençöz, and Wells (2011) found
evidence that negative metacognitive beliefs about uncontrollability and danger of
worry significantly predicted residual change in anxiety and depression.
In OCD, the MCT model postulates that fusion beliefs, beliefs about rituals, and
stop signals are central in maintaining the disorder. Myers, Fisher, and Wells (2009)
examined the longitudinal relationship between metacognitive beliefs and obsessive-
compulsive symptoms in college students. Beliefs about the power and meaning of
thoughts measured at time 1 were significant predictors of symptoms of obsessive-
compulsive distress 3 months later. In this study, “cognitive” beliefs (schemas)
concerning perfectionism and responsibility did not independently contribute to
distress. Solem, Myers, Fisher, Vogel, and Wells (2010) replicated and extended these
findings in an OCD sample compared to a community control group.
Using a different measure of metacognitive beliefs, Sica, Steketee, Ghisi, Chiri,
and Franceschini (2007) found that beliefs about the uncontrollability and danger
of thoughts predicted obsessive-compulsive symptoms over a 3-month period. Wahl,
Ertle, Bohne, Zurowski, and Kordon (2011) found common features between a
ruminative response style and obsessive rumination. Solem, Håland, Vogel, Hansen,
and Wells (2009) showed that change in metacognitive beliefs predicted improvement
in symptoms in patients with OCD who received exposure therapy; change in
cognition did not have the same effect.
The metacognitive model for PTSD emphasizes the role of thought suppression,
perseverative thinking, and maladaptive attentional strategies in maintaining the
disorder. Metacognitive thought control strategies prospectively predict PTSD
symptoms. Roussis and Wells (2008) measured stress symptoms, thought control
strategies, and worry in college students on two occasions separated by approximately
3 months. A greater tendency to endorse the use of worry to control thoughts at
time 1 was positively associated with PTSD symptoms at time 2 when level of stress
exposure, worry assessed as an anxiety symptom, and PTSD symptoms measured at
time 1 were controlled.
Holeva, Tarrier, and Wells (2001) examined the predictors of PTSD following
motor-vehicle accidents. The use of worry to control thoughts positively predicted the
subsequent development of PTSD 4–6 months later. Further studies account for the
relationship between thought suppression and intrusive trauma memories (S. A. Ben-
nett, Beck, & Clapp, 2009; Geraerts, Merckelbach, Jelicic, & Smeets, 2006; Nixon,
Cain, Nemy, & Seymour, 2009), rumination and PTSD psychopathology (Ehring,
Fuchs, & Kläsener, 2009; Michael, Halligan, Clark, & Ehlers, 2007), and attentional
bias and PTSD psychopathology (Pineles, Shipherd, Mostoufi, Abramovitz, & Yovel,
2009). H. Bennett and Wells (2010) found that rumination mediated the relation-
ship between beliefs about the trauma memory and PTSD symptoms. Moreover, the
researchers found that beliefs about memory correlated with PTSD symptoms but that
actual memory performance did not when they were treated as concurrent predictors.
In social phobia the threat monitoring component of the CAS is marked by excessive
self-focus on performance and embarrassing symptoms. Wells and Papageorgiou
(2001) tested the effects of exposure on individuals with social phobia when it
was presented under two conditions. One condition asked patients to shift to an
external attention focus (counteracting threat monitoring) whereas the other used a
habituation rationale and asked patients to stay in the situation for the same “planned
period” of time. The metacognitive condition involving attention refocusing was
superior to the comparison condition in reducing anxiety and negative beliefs.
Bouman and Meijer (1999) found that hypochondriasis was associated with
metacognitive beliefs concerning the uncontrollability of health worry and cog-
nitive self-consciousness. Buwalda, Bouman, and Van Duijn (2008) conducted a
psychoeducational course on hypochondriacal metacognition and found significant
reductions in questionnaires regarding health anxiety. Kaur, Butow, and Thewes
(2011) found that negative beliefs about worry (concerning uncontrollability and
danger) were associated with an attentional bias for health-related words.
Spada and Wells (2005) tested for relationships between metacognitive beliefs and
problem drinking. They found that positive beliefs about worry and beliefs concerning
uncontrollability and danger were positively associated with a measure of the quantity
and frequency of alcohol consumed in the last 30 days. Low cognitive confidence and
beliefs about the need to control thoughts were also predictors. Beliefs about the need
to control thoughts significantly predicted alcohol use even when anxiety and depres-
sion were controlled. Spada, Caselli, and Wells (2009) found that metacognitive beliefs
predicted drinking status across follow-up after a course of CBT in problem drinkers.
In a sample of 300 college students metacognition fostered emotion and moderated
the relationship between emotion and alcohol dependence (Moneta, 2011).
Conclusion
In this chapter we have presented an outline of the metacognitive model and treatment
and illustrated its features and techniques. This approach is based on a novel way of
thinking about thinking in psychological disorder. MCT is based on the principle that
recovery from disorder depends on regulating thinking in new ways. MCT does not
necessarily require the reevaluation or reality testing of negative thoughts or schemas
about the social self, physical self, or world. However, MCT does also deal with the
content of thoughts and beliefs but only in one domain—that of metacognition.
We have illustrated how this emphasis has implications for the focus of treatment
efforts, the type of therapeutic dialogue the therapist undertakes, and the nature of
the change techniques used.
There is a large body of evidence supporting the theory and model behind MCT,
and evidence of treatment effectiveness is beginning to accumulate. The results
of controlled clinical trials suggest that the treatment is brief and associated with
large effects. There is some preliminary indication that the treatment could be more
effective than other active treatment types. However, the small number of studies and
their preliminary nature signal the need for sustained caution in drawing any firm
conclusions about relative efficacy at this time.
References
Aldoa, A., Nolen-Hoeksma, S., & Schweizer, S. (2010). Emotion-regulation strate-
gies across psychopathology: A meta-analytic review. Clinical Psychology Review, 30,
217–237.
Bennett, H., & Wells, A. (2010). Metacognition, memory disorganization and rumination in
posttraumatic stress symptoms. Journal of Anxiety Disorders, 24, 318–325.
Bennett, S. A., Beck, J. G., & Clapp, J. D. (2009). Understanding the relationship between
posttraumatic stress disorder and trauma cognitions: The impact of thought control
strategies. Behaviour Research and Therapy, 47 , 1018–1023.
Bouman, T. K., & Meijer, K. J. (1999). A preliminary study of worry and metacognitions in
hypochondriasis. Clinical Psychology and Psychotherapy, 6, 96–101.
Buwalda, F. M., Bouman, T. K., & Van Duijn, M. A. J. (2008). The effect of a psychoedu-
cational course on hypochondriacal metacognition. Cognitive Therapy and Research, 32,
689–701.
Cavanagh, M., & Franklin, J. (2000, July). Attention training and hypochondriasis: Preliminary
results of a controlled treatment trial. Paper presented at the World Congress of Cognitive
and Behavioral Therapy, Vancouver, Canada.
Ehring, T., Fuchs, N., & Kläsener, I. (2009). The effects of experimentally induced rumination
versus distraction on analogue posttraumatic stress symptoms. Behavior Therapy, 40,
403–413.
Fisher, P. L., & Wells, A. (2005). Experimental modification of beliefs in obsessive-compulsive
disorder: A test of the metacognitive model. Behaviour Research and Therapy, 43,
821–829.
Fisher, P. L., & Wells, A. (2008). Metacognitive therapy for obsessive-compulsive disorder: A
case series. Journal of Behavior Therapy and Experimental Psychiatry, 39, 117–132.
Franklin, M., & Foa, E. (2011). Treatment of obsessive compulsive disorder. Annual Review
of Clinical Psychology, 7 , 229–243.
Geraerts, E., Merckelbach, H., Jelicic, M., & Smeets, E. (2006). Long term consequences of
suppression of intrusive anxious thoughts and repressive coping. Behaviour Research and
Therapy, 44, 1451–1460.
Holeva, V., Tarrier, N., & Wells, A. (2001). Prevalence and predictors of acute PTSD following
road traffic accidents: Thought control strategies and social support. Behavior Therapy,
32, 65–83.
Janeck, A. S., Calamari, J. E., Riemann, B. C., & Heffelfinger, S. K. (2003). Too much thinking
about thinking?: Metacognitive differences in obsessive-compulsive disorder. Journal of
Anxiety Disorders, 17 , 181–195.
Kaur, A., Butow, P., & Thewes, B. (2011). Do metacognitions predict attentional bias in
health anxiety? Cognitive Therapy and Research, 35, 575–580.
Michael, T., Halligan, S. L., Clark, D. M., & Ehlers, A. (2007). Rumination in posttraumatic
stress disorder. Depression and Anxiety, 24, 307–317.
Moneta, G. B. (2011). Metacognition, emotion, and alcohol dependence in college students:
A moderated mediation model. Addictive Behaviors, 36, 781–784.
Myers, S. G., Fisher, P. L., & Wells, A. (2009). An empirical test of the metacognitive model
of obsessive-compulsive symptoms: Fusion beliefs, beliefs about rituals, and stop signals.
Journal of Anxiety Disorders, 23, 436–442.
Nixon, R. D., Cain, N., Nehmy, T., & Seymour, M. (2009). The influence of thought
suppression and cognitive load on intrusions and memory processes following an analogue
stressor. Behavior Therapy, 40, 368–379.
Nordahl, H. M. (2009). Effectiveness of brief metacognitive therapy versus cognitive-behavioral
therapy in a general outpatient setting. International Journal of Cognitive Psychotherapy,
2, 152–159.
Papageorgiou, C., & Wells, A. (1998). Effects of attention training in hypochondriasis: A brief
case series. Psychological Medicine, 28, 193–200.
Papageorgiou, C., & Wells, A. (2000). Treatment of recurrent major depression with attention
training. Cognitive and Behavioral Practice, 7 , 407–413.
Pineles, S. L., Shipherd, J. C., Mostoufi, S. M., Abramovitz, S. M., & Yovel, I. (2009).
Attentional biases in PTSD: More evidence for interference. Behaviour Research and
Therapy, 47 , 1050–1057.
Proctor, D. (2008). A randomised controlled trial of metacognitive therapy versus exposure
therapy for post-traumatic stress disorder (Unpublished doctoral dissertation). University
of Manchester, Manchester, England.
Rabiei, M., Mulkens, S., Kalantari, M., Molavi, H., & Bahrami, F. (2012). Metacognitive
therapy for body dysmorphic disorder patients in Iran: Acceptability and proof of concept.
Journal of Behavior Therapy and Experimental Psychiatry, 43, 724–729.
Rees, C. S., & van Koesveld, K. E. (2008). An open trial of group metacognitive therapy for
obsessive-compulsive disorder. Journal of Behavior Therapy and Experimental Psychiatry,
39, 451–458.
Roussis, P., & Wells, A. (2008). Psychological factors predicting stress symptoms: Metacogni-
tion, thought control, and varieties of worry. Anxiety, Stress & Coping, 21, 213–225.
Ruscio, A. M., Seitchik, A. E., Gentes, E. L., Jones, J. D., & Hallion, L. S. (2011). Perseverative
thought: A robust predictor of response to emotional challenge in generalized anxiety
disorder and major depressive disorder. Behaviour Research and Therapy, 49, 867–874.
Sica, C., Steketee, G., Ghisi, M., Chiri, L. R., & Franceschini, S. (2007). Metacognitive
beliefs and strategies predict worry, obsessive-compulsive symptoms and coping styles:
A preliminary prospective study on an Italian non-clinical sample. Clinical Psychology &
Psychotherapy, 14, 258–268.
Siegle, G. J., Ghinassi, F., & Thase, M. E. (2007). Neurobehavioral therapies in the 21st
century: Summary of an emerging field and an extended example of cognitive control
training for depression. Cognitive Therapy and Research, 31, 235–262.
Simons, M. (2010). Metacognitive therapy and other cognitive-behavioral treatments for
posttraumatic stress disorder. Verhaltenstherapie, 20, 86–92.
Simons, M., Schneider, S., & Herpertz-Dahlmann, B. (2006). Metacognitive therapy versus
exposure and response prevention for pediatric obsessive-compulsive disorder: A case
series with randomized allocation. Psychotherapy and Psychosomatics, 75, 257–264.
Solem, S., Håland, A. T., Vogel, P. A., Hansen, B., & Wells, A. (2009). Change in metacog-
nitions predicts outcome in obsessive-compulsive disorder patients undergoing treatment
with exposure and response prevention. Behaviour Research and Therapy, 47 , 301–307.
Solem, S., Myers, S. G., Fisher, P. L., Vogel, P. A., & Wells, A. (2010). An empirical test of
the metacognitive model of obsessive-compulsive symptoms: Replication and extension.
Spada, M. M., Caselli, G., & Wells, A. (2009). Metacognitions as a predictor of drinking
status and level of alcohol use following CBT in problem drinkers: A prospective study.
Behaviour Research and Therapy, 47 , 882–886.
Spada, M. M., & Wells, A. (2005). Metacognitions, emotion and alcohol use. Clinical
Psychology and Psychotherapy, 12, 150–155.
van der Heiden, C., Muris, P., & van der Molen, H. T. (2012). Randomized controlled trial
on the effectiveness of metacognitive therapy and intolerance-of-uncertainty therapy for
generalized anxiety disorder. Behaviour Research and Therapy, 50, 100–109.
Wahl, K., Ertle, A., Bohne, A., Zurowski, B., & Kordon, A. (2011). Relations between a
ruminative thinking style and obsessive-compulsive symptoms in non-clinical samples.
Anxiety, Stress & Coping, 24, 217–225.
Wells, A. (1990). Panic disorder in association with relaxation induced anxiety: An attentional
training approach to treatment. Behavior Therapy, 21, 273–280.
guide. Chichester, England: John Wiley & Sons, Ltd.
Wells, A. (2000). Emotional disorders and metacognition: Innovative cognitive therapy. Chich-
ester, England: John Wiley & Sons, Ltd.
Wells, A. (2005). The metacognitive model of GAD: Assessment of meta-worry and relationship
with DSM-IV generalized anxiety disorder. Cognitive Therapy and Research, 29, 107–21.
Press.
Wells, A., & Colbear, J. S. (2012). Treating posttraumatic stress disorder with metacognitive
therapy: A preliminary controlled trial. Journal of Clinical Psychology, 68, 373–381.
Wells, A., Fisher, P., Myers, S., Wheatley, J., Patel, T., & Brewin, C. R. (2009). Metacognitive
therapy in recurrent and persistent depression: A multiple-baseline study of a new
treatment. Cognitive Therapy and Research, 33, 291–300.
Wells, A., Fisher, P., Myers, S., Wheatley, J., Patel, T., & Brewin, C. R. (2012). Metacogni-
tive therapy in treatment-resistant depression: A platform trial. Behaviour Research and
Therapy, 50, 367–373.
Wells, A., & King, P. (2006). Metacognitive therapy for generalized anxiety disorder: An open
trial. Journal of Behavior Therapy and Experimental Psychiatry, 37 , 206–212.
Wells, A., & Matthews, G. (1994). Attention and emotion: A clinical perspective. Hove,
England: Erlbaum/Psychology Press.
Wells, A., & Matthews, G. (1996). Modelling cognition in emotional disorder: The S-REF
model. Behaviour Research and Therapy, 34, 881–888.
Wells, A., & Papageorgiou, C. (2001). Brief cognitive therapy for social phobia: A case series.
Wells, A., & Sembi, S. (2004). Metacognitive therapy for PTSD: A preliminary investigation
of a new brief treatment. Journal of Behavior Therapy and Experimental Psychiatry, 35,
307–318.
Wells, A., Welford, M., Fraser, J., King, P., Mendel, E., Wisely, J., … Rees, D. (2008). Chronic
PTSD treated with metacognitive therapy: An open trial. Cognitive and Behavioral
Practice, 15, 85–92.
Wells, A., Welford, M., King, P., Papageorgiou, C., Wisely, J., & Mendel, E. (2010). A pilot
randomized trial of metacognitive therapy vs applied relaxation in the treatment of adults
with generalized anxiety disorder. Behaviour Research and Therapy, 48, 429–434.
Wells, A., White, J., & Carter, K. (1997). Attention training: Effects on anxiety and beliefs in
panic and social phobia. Clinical Psychology and Psychotherapy, 4, 226–232.
Yılmaz, A. E., Gençöz, T., & Wells, A. (2011). The temporal precedence of metacognition
in the development of anxiety and depression symptoms in the context of life-stress: A
prospective study. Journal of Anxiety Disorders, 25, 389–396.
7
Mindfulness and Acceptance
Techniques
James D. Herbert and Evan M. Forman
Drexel University, United States
This being human is a guest house

Every morning a new arrival.
A joy, a depression, a meanness,
some momentary awareness comes
as an unexpected visitor.
Welcome and entertain them all!
Even if they’re a crowd of sorrows,
who violently sweep your house
empty of its furniture,
still, treat each guest honorably.
He may be clearing you out
for some new delight…
Rumi, “The Guest House”
One of the most prominent trends in the field of cognitive behavioral therapy (CBT)
over the past couple of decades has been the dramatic increase in theories and clinical
strategies that highlight psychological acceptance and mindfulness. Indeed, hardly
a week goes by that CBT clinicians do not receive multiple solicitations for books,
journals, workshops, or webinars based on these themes. This trend is reflected in
serious clinical innovation, scholarship, and careful research. As seen in Figure 7.1,
for example, there has been an exponential growth in scholarly publications on
mindfulness and psychological acceptance over the past decade. At the same time,
there has been no shortage of pseudoscience that has capitalized on the increasing
prominence of this work. Although interesting in its own right, a review of mindfulness
pseudoscience is beyond the scope of this chapter; we focus instead on developments
that are scientifically grounded.

DOI: 10.1002/9781118528563.wbcbt07
800
Treatment
Mechanisms
700
600
500
400
300
200
100
0
2000 2005 2010
Figure 7.1 Number of non-overlapping publications on mindfulness and acceptance,

2000–2011. Unique PsychInfo citations. “Treatment” keywords include acceptance and
commitment therapy, dialectical behavior therapy, integrative behavioral couple therapy, func-
tional analytic psychotherapy, mindfulness-based stress reduction, mindfulness-based cognitive
therapy, and acceptance-based behavior therapy. “Mechanisms” keywords include mindfulness,
meditation, defusion, experiential acceptance, psychological acceptance, experiential avoidance,
and distress tolerance. “Mechanism” citations meeting the criteria for the “treatment” search
were not counted among the mechanism publications.
Compared with the behavioral tradition more generally, the discourse on mind-
fulness and acceptance suffers from a lack of clear consensus regarding the meaning
of various terms, including the term mindfulness itself. An advantage of technical
terminology in any scientific discipline is that such terms avoid the baggage of folk
language that can contribute to confusion when used in a technical context. In CBT,
concepts such as “conditioned stimulus” or “cognitive heuristic” are more likely to
have clear and precise meanings than are concepts derived from folk psychology such
as “fear” or “motivation.” In the case of mindfulness, the term was originally used
in Hindu and Buddhist spiritual traditions, and only recently made its way into the
lexicon of Western psychology. As a consequence, it lacks a precise technical meaning,
and consensus has yet to emerge regarding how best to understand it. Many CBT
clinicians, scholars, and researchers clearly believe that there is something of value
represented by the concept, even if they have yet to agree on exactly what that is
(Herbert & Forman, 2011a).
In this chapter, we briefly review the growth of psychological acceptance and
mindfulness in CBT, including the various reactions these ideas have prompted
within the field. We discuss the conceptualizations of these terms as commonly used
within CBT, and suggest trends toward emerging consensus. We then review the
major psychotherapy models within the broad CBT family that emphasize mindfulness
and psychological acceptance. We summarize the research to date on outcomes and
Mindfulness and Acceptance Techniques 133
mechanisms of mindfulness-based interventions within CBT. We then discuss the most

common clinical strategies and techniques used to target these processes, including
clinical case examples to illustrate their use. We conclude by suggesting directions for
future clinical innovations and research directions.
The Rise of Mindfulness and Psychological Acceptance

in Cognitive Behavioral Therapy
In the West, the concept of mindfulness has been most closely associated with
Buddhism, which was brought to the United States by nineteenth-century Asian
(and especially Chinese) immigrants (Seager, 1999). Buddhist concepts and practices
initially had little impact on either mainstream culture or the field of psychology.
Beginning in the middle of the twentieth century, psychoanalysts began discussing
meditative practices in relation to psychotherapy (Smith, 1986); this interest was
subsequently picked up by existential and humanistic psychologists (Kumar, 2002).
The concept of mindfulness was introduced to academic psychology through the work
of the social psychologist Ellen Langer (1989a, 1989b). She described mindfulness as
a “limber state of mind” (Langer, 1989a, p. 70), which involves a sensitivity to context
and an openness to new information. Mindfulness meditation became increasingly
popular in mainstream American culture during the 1970s and 1980s, and began to
impact the field of behavior therapy by the early 1990s.
Hayes (2004) provides a useful description of the emergence and growth of
mindfulness and related concepts and practices within behavior therapy. According to
this analysis, the field can be understood as three overlapping historical generations
or “waves.” The first generation reflects the seeds of the behavior therapy movement
in the 1950s, including the contributions of Skinner (1953), Wolpe (1958), and
Eysenck (1952), and the formal birth of the discipline in the 1960s. The approach
was clearly revolutionary, marking a distinct break from the dominant psychoanalytic
model of the time. It was marked by close connections between basic laboratory
research and applied technologies, especially with respect to classical and operant
conditioning principles.
The second generation was born of the perceived limitations of the first-generation
behavior modification principles and technologies that did not sufficiently account for
the role of language and cognition in psychopathology and its treatment. Reflecting
the larger “cognitive revolution” in psychology more broadly, this approach gained
traction in the 1970s and continues through to the present day. The second gen-
eration saw the “C” added to “BT,” as cognitive factors came to be emphasized.
Approaches developed by luminaries such as Albert Ellis (Ellis & Grieger, 1977;
Ellis & Harper, 1975) and Aaron Beck (Beck, Rush, Shaw, & Emery, 1979) priori-
tized one’s cognitive interpretation of the world as determining emotional reactions
and subsequent behavior. Emphasis also shifted to clinical innovations derived from
the consultation room rather than the research laboratory, and to research meth-
ods favoring clinical trials of multicomponent treatment packages for psychiatric
syndromes.
Although its roots can be traced to earlier developments, the third generation
of CBT began in earnest in the 1990s, and is gaining increasing momentum up
to the present. The focus on language and cognition in the genesis and treatment
of psychopathology remains, but with a different emphasis. Instead of trying to
change the content of cognition, the emphasis is more on fostering a nonjudgmental,
accepting stance with respect to distressing experiences, including disturbing thoughts
and dysfunctional beliefs. In addition, there is renewed interest in linking clinical
technologies to basic theoretical principles and laboratory research.
O’Donohue (2009) similarly demarcates the field into three generations, the first
two of which correspond closely to those described by Hayes (2004). However,
O’Donohue’s third generation, which he describes as more aspirational than realized,
involves a renewed focus on basic principles derived from modern learning theory.
These would include basic concepts related to acceptance and mindfulness (e.g.,
rule-governed behavior, stimulus equivalence), but would also include recent findings
from related fields such as behavioral economics.
Interestingly, there are parallels in the way each of these developments has been
received by the dominant paradigm of the time. When early behavior therapy pioneers
challenged the psychoanalytic establishment, the initial reaction was simply to ignore
the work as insignificant. As it began to gain traction, and ignoring was no longer an
option, it was greeted with hostility and disdain. As the work continued to develop,
it was coopted with pronouncements that it represented nothing that was not already
part of the established paradigm. Finally, the developments were gradually accepted
into the mainstream, and a new equilibrium was established. This same pattern of
reactions can be seen in the reaction of first-generation clinicians and theorists to the
cognitive revolution of the second generation, and in the more recent reaction of
many in the second generation to the growth of mindfulness and acceptance within
CBT (Goldfried, 2011).
We should note that Hayes’s (2004) historical analysis should not be taken to
reflect the only “true” account of the history of behavior therapy; rather, it is simply
one useful narrative to help organize the development of the field over the past
half-century. There are undoubtedly other ways of describing this history that may be
equally (or perhaps more) useful. Moreover, the fact that one can track developments
across time in this way does not by itself necessarily imply that later developments are
superior to earlier ones. Whether cognitive concepts add value to purely behavioral
ones, or whether acceptance and mindfulness concepts likewise have incremental
value, are questions that must be resolved scientifically and should not be simply
assumed. Regardless of one’s perspective on this historical narrative, there is no doubt
that the concepts of psychological acceptance and mindfulness have become quite
popular within CBT, and are destined to play an increased role in the coming years.
What Is Mindfulness?
As noted above, there has yet to emerge a full consensus around a single understanding
of the concept of mindfulness. The term derives from ancient Buddhist and even
earlier Hindu teachings and practices. In Buddhist traditions, human suffering is
believed to result from excessive attachment to transient objects and mental states.
Contemplative meditative practices are undertaken in an effort to undermine this
excessive attachment, fostering a sense of detached awareness of experience and
ultimately spiritual enlightenment. Similar ideas have also played a role in Western
traditions, including Hellenic philosophies and monastic Christian practices.
Concepts similar to mindfulness can also be found in psychology—and especially
its applied wings—since near the time of the formal founding of the discipline over a
century ago (Hofmann et al., 2011). J. C. Williams and Lynn (2010) trace the theme
of acceptance beginning with the writings of Freud and continuing throughout the
twentieth century. Both the psychoanalysts and subsequently humanistic psychol-
ogists stressed the importance of self-acceptance to well-being. Beginning in the
1990s, attention shifted to psychological or experiential acceptance, that is, the open
acceptance of the totality of one’s ongoing stream of experience, especially distressing
experience. It was during this time that a number of clinical innovations were devel-
oped within CBT that focus specifically on psychological acceptance. Although some
of these developments were genuinely novel, others involved borrowing liberally from
earlier work (e.g., from experiential psychotherapies), and still others consisted of
reconceptualizing existing behavioral procedures (e.g., exposure).
This increased emphasis on the goal of psychological acceptance and technologies to
promote it led to efforts to describe and define the concept of mindfulness. The most
frequently cited definition was offered by Jon Kabat-Zinn (1994): “paying attention
in a particular way: on purpose, in the present moment, and nonjudgmentally”
(p. 4). There are several noteworthy aspects of this definition. First, it highlights
the idea that mindfulness is an active process involving intentional embracing of
experience, rather than simply passive observation. Second, it emphasizes a sense of
heightened awareness of one’s ongoing stream of experience as it unfolds. And third,
it underscores the critical idea of nonjudgment, or the acceptance of one’s experience
as it is, rather than how one wishes it would be. Kabat-Zinn described mindfulness
as a verb, which is reflected in its common use as a synonym for the practice of
mindfulness meditation.
Following Kabat-Zinn’s discussion, several groups developed scales to address
mindfulness. Each of these efforts involves a somewhat different conceptualization
of mindfulness. K. W. Brown and Ryan (2003) developed the Mindful Attention
Awareness Scale, which is based on a unidimensional construct emphasizing “present-
centered attention-awareness.” These researchers believe that a distinct assessment of
psychological acceptance is unnecessary. The Toronto Mindfulness Scale (Lau et al.,
2006) similarly emphasizes present-moment attention to and awareness of ongoing
experience, especially in relation to contemplative meditation practices. This scale was
designed as a state, rather than a trait, measure. Based on an intervention model known
as dialectical behavior therapy (discussed later in the chapter), Baer and colleagues
developed the Kentucky Inventory of Mindfulness Skills (Baer, Smith, & Allen, 2004)
and the Five-Facet Mindfulness Scale (Baer, Smith, Hopkins, Krietemeyer, & Toney,
2006), both of which deconstruct the concept into multiple factors.
Herbert and Cardaciotto (2005) proposed a middle ground between the unifactorial
model of K. W. Brown and Ryan and the five-factor model of Baer and colleagues.
We suggested that mindfulness could be conceptualized as being comprised of two
distinct factors: “(a) enhanced awareness of the full range of present experience,
and (b) an attitude of nonjudgmental acceptance of that experience” (Herbert &
Cardaciotto, 2005, p. 198). Cardaciotto, Herbert, Forman, Moitra, and Farrow
(2008) subsequently developed the Philadelphia Mindfulness Scale (PHLMS) to
assess these two dimensions. A number of studies support this two-factor structure
(Blacker, Herbert, Forman, & Kounios, 2012; L. A. Brown et al., 2011; Myers et al.,
2012; Silpakit, Silpakit, & Wisajun, 2011).
Although unanimity has not emerged—and in fact may never emerge—on a
single definition of mindfulness, consensus is building around a few themes. First,
the dual concepts of enhanced present-moment attention to one’s experience, and
psychological acceptance of that experience, feature in most conceptualizations of
the construct. It is important to note that acceptance in this context does not
mean the acceptance of the status quo in one’s life. To the contrary, acceptance
refers to an embracing of the totality of one’s subjective experience, e.g., thoughts,
feelings, sensations, and memories. Importantly, this includes not only letting go of
the struggle with distressing experiences, but also abandoning the tendency to cling
tightly to positive experiences, which are invariably transient. Second, most agree
that mindfulness is a psychological state, rather than any particular practice designed
to foster that state. In other words, although some may achieve a heightened
state of mindfulness through formal meditative practices, the state itself is not
synonymous with those practices. One may become more mindful while working,
eating, exercising, or any other life activity. Finally, in the context of psychotherapy,
enhancing mindfulness is not a goal in and of itself, but rather is a means to an end
(Herbert, Forman, & England, 2009). Mindfulness- and acceptance-based therapeutic
strategies and techniques aim to enhance one or more aspects of this psychological
state, in the service of some larger goals related to living a more fulfilling life. We
explore these themes further below in the context of specific interventions.
Clinical Models within Cognitive Behavioral Therapy

Highlighting Mindfulness and Acceptance
Strategies aimed at enhancing mindfulness and acceptance have become central to

a variety of novel CBT models. These various approaches can be divided along
two orthogonal dimensions: the range of pathology targeted, and the broader
theoretical framework in which they are situated. Regarding the first dimension,
some models reflect comprehensive frameworks that are not specific to any particular
pathology, whereas others are more focused in their targets. The latter includes
techniques that have increasingly found their way into traditional, mainstream CBT
approaches. As for the second dimension, the various models are derived from
different theoretical paradigms within the larger CBT family. These differences are
reflected both in the nature of the theories underlying the respective clinical models,
including the theoretical and technological terminology they employ, as well as the
specific interventions they prescribe. Some approaches are derived from traditional
cognitive meditational traditions such as cognitive therapy, whereas others are rooted
in behavior analysis. Despite these distinctions, all of these approaches share an
emphasis on fostering nonjudgmental awareness and psychological acceptance of

distressing subjective experience.
Mindfulness-Based Stress Reduction

The first modern model to bring a mindfulness sensitivity to mainstream applied psy-
chology was mindfulness-based stress reduction (MBSR), developed by Kabat-Zinn
and colleagues at the University of Massachusetts Medical Center. Interestingly,
unlike all of the other approaches discussed below, MBSR did not originally develop
within the context of CBT, although it is now often associated with the broad CBT
tradition. Rather, the approach stemmed from Kabat-Zinn’s personal interest in Zen
Buddhism combined with his scientific sensibilities developed through professional
training in molecular biology and his work with medical patients (Kabat-Zinn, 2005).
MBSR is a structured program for patients with chronic pain and other medical
conditions, and emphasizes the formal practice of mindfulness meditation as well
as Hatha Yoga (a set of postures, breathing techniques, and meditation designed to
induce a healthy mind and body). It is typically delivered in a group format over eight
consecutive weekly sessions. Consistent with its Buddhist origins, MBSR is based
on the idea that much suffering results from wanting things to be different than they
actually are, particularly in the context of chronic medical problems. The approach
fosters comfort with simply “being” rather than always “doing” as a complement to
the action and goal orientation of Western medicine.
Dialectical Behavior Therapy

Like MBSR, dialectical behavior therapy (DBT) developed in part from the interest
of its founder Marsha Linehan in Buddhism, but unlike MBSR, DBT developed from
within the traditional behavior therapy tradition (Linehan & Dimeff, 2001). The
impetus for the development of DBT was Linehan’s frustration with standard CBT
programs for the treatment of chronically suicidal patients, many of whom qualify for
a diagnosis of borderline personality disorder. The “dialectic” in the program’s name
reflects various tensions inherent in the program, including that between acceptance
of intense emotional experiences on the one hand and behavior change on the other.
DBT emphasizes a therapeutic relationship in which the therapist is considered a
committed ally rather than an adversary. The therapist acknowledges the intensity of
the patient’s emotional distress while at the same time advocating for, and creating
behavioral contingencies that favor, change. Treatment is typically delivered through
a combination of weekly individual psychotherapy sessions, supplemented by weekly
group therapy sessions. Various skills, including distress tolerance, interpersonal,
and mindfulness skills, are taught during the group sessions, and then applied and
reinforced during the individual sessions (Linehan, Armstrong, Suarez, Allmon, &
Heard, 1991).
Unlike MBSR and DBT, metacognitive therapy (MCT) developed as an extension of
the cognitive therapy model of Beck and colleagues (Beck, 1976). MCT holds that
some individuals have difficulty regulating their internal experience, and overreact to
transient negative thoughts and feelings, leading to a pattern of intense rumination,
worry, and self-focused attention. This dysregulation is thought to be due to biases in
executive cognitive processes that monitor and control thinking, known as metacog-
nition (Wells & Matthews, 1994). Biases are found in both positive metacognitive
beliefs, which refer to the presumed benefits of monitoring and controlling negative
thoughts, and negative metacognitive beliefs, referring to beliefs about the danger of
certain thoughts and the uncontrollability of experience. MCT targets these metacog-
nitive factors in order to restore adaptive control over cognitive processes (Wells,
2000, 2008, 2011). Importantly, it is believed that metacognition cannot be changed
by directly challenging negative automatic thoughts. Treatment focuses instead on
restructuring maladaptive metacognitive beliefs (e.g., the belief that worrying will
prevent damaging consequences) as well as a variety of additional strategies designed
to foster “detached mindfulness,” and “cognitive decentering.”
Mindfulness-Based Cognitive Therapy

Like MCT, mindfulness-based cognitive therapy (MBCT) developed out of the Beck-
ian cognitive therapy tradition, and remains firmly rooted in a cognitive theoretical
framework. Using a structured interview, Teasdale and colleagues (2002) pursued
a line of research in which they studied the way in which individuals responded to
mildly depressive situations. They found that those with no history of depression
tended to describe the events from a more detached, mindful perspective (which
they term “metacognitive awareness”) relative to those with a history of depression.
Those susceptible to depressive episodes tended to experience a vicious cycle in
which dysphoria activated negative thinking patterns, in turn exacerbating negative
affect. MBCT is designed to interrupt this cycle by teaching patients to “decenter”
from negative thoughts primarily through mindfulness exercises, including medita-
tion training and practice derived from MBSR (Segal, Williams, & Teasdale, 2001).
In addition, lower levels of metacognitive awareness also predicted relapse among
depressed individuals. Although the approach was developed specifically to prevent
depression relapse, recent efforts have employed it with currently depressed patients
(e.g., Barnhofer et al., 2009), bipolar disorder (Deckersbach et al., 2012; Miklowitz
et al., 2009; Stange et al., 2011; Weber et al., 2010; J. Williams et al., 2008), anxiety
disorders (Craigie, Rees, Marsh, & Nathan, 2008; Evans et al., 2008; Felver, 2011;
Kim et al., 2009; Semple & Lee, 2008; Wong et al., 2011), hypochondriasis (Lovas
& Barsky, 2010; McManus, Surawy, Muse, Vazquez-Montes, & Williams, 2012; M.
J. Williams, McManus, Muse, & Williams, 2011; Yook et al., 2008), and insomnia
(Heidenreich, Tuin, Pflug, Michal, & Michalak, 2006; Yook et al., 2008).
Functional Analytic Psychotherapy

Developed by Kohlenberg and Tsai (1991), functional analytic psychotherapy (FAP)
developed out of the theoretical school of behavior analysis, which is rooted in radical
behaviorism and Skinner’s (1957) analysis of verbal behavior. FAP focuses on the
therapeutic relationship as the vehicle of change. There is less focus on explicit skills
building relative to DBT, and reduced emphasis on meditative practices relative to

MBSR or MCT. Rather, the focus is on the identification, analysis, and modification of
“clinically relevant behaviors,” which refer to the individual’s problems as manifested
in the therapy session itself. Moreover, as in the other models discussed here, there
is an emphasis on accepting distressing experience rather than trying to change it.
The approach defies the stereotype of applications of radical behaviorism, and in fact
resembles in some ways modern forms of psychodynamic therapy in practice. Although
FAP can be used as a stand-alone treatment, it is often integrated with another CBT
approach, such as DBT or acceptance and commitment therapy (Callaghan, Gregg,
Marx, Kohlenberg, & Gifford, 2004; Kanter, Tsai, & Kohlenberg, 2010).
Acceptance and Commitment Therapy

Of the various mindfulness and acceptance forms of CBT, acceptance and commitment
therapy (ACT) has attracted the most attention from researchers and clinicians
alike. ACT was developed by Hayes and colleagues (Hayes, Strosahl, & Wilson,
2011), and was originally known as “comprehensive distancing” due to the focus on
achieving psychological distance from one’s distressing subjective experiences. Like
FAP, ACT developed from within a behavior analytic tradition. It represents the
primary application of a scientific paradigm known as contextual behavioral science,
which is also comprised of a behavioristic theory of language and cognition as
well as a pragmatic philosophy of science. The central tenet of the ACT model is
that attempts to control the content of distressing subjective experiences, although
arising through normal, culturally-sanctioned psychological (and especially language)
processes, are often ineffective, counterproductive, and even harmful. Like the other
models discussed here, ACT fosters mindful awareness and acceptance of one’s
distressing experience. However, ACT is in a sense more radical (and arguably more
theoretically consistent) than some of the other models in that direct efforts to change
the content or frequency of thoughts, feelings, sensations, memories, and so on, are
explicitly disavowed. Instead, the focus is on articulating personal values and associated
goals, and then behaving consistently with those values regardless of one’s internal
experiences at any given moment. Intervention strategies include some distinctive
techniques, as well as many others borrowed from other approaches, including
experiential exercises derived from humanistic and existential psychotherapies. The
ACT model allows for any number of delivery formats, ranging from single-session
group intervention to traditional individual psychotherapy. It is broadly applicable,
having been used with a wide range of psychopathology, medical conditions, and
other problems.
Behavioral Activation
Like ACT and FAP, behavioral activation (BA) is rooted in behavior analysis. One
of the foundational developments within CBT was Beck’s cognitive therapy of
depression (Beck et al., 1979). Beck’s program consists of two broad interventions:
one focused on concrete behavior change aimed at reengagement with activities that
have come to be avoided, and another focused on cognitive restructuring. However,
component analysis studies suggest cognitive restructuring adds no incremental

benefit to the behavioral component (Dimidjian et al., 2006; Jacobson et al., 1996).
These findings led some scholars to focus on developing the behavioral component as
an intervention in its own right. In this process, they incorporated earlier behavioral
work on depression by Ferster (1973) and Lewinsohn (Lewinsohn, 1974; Lewinsohn,
Biglan, & Zeiss, 1976; Lewinsohn, Youngren, & Grosscup, 1979). BA aims to
increase the overall amount of positive reinforcement in the depressed person’s life,
while also countering avoidance and withdrawal behaviors maintained by negative
reinforcement. The approach utilizes scheduling of graded activities and mindful
acceptance of distressing thoughts and feelings (Kanter et al., 2010). BA has recently
been explored as a treatment for anxiety (Hopko, Robertson, & Lejuez, 2006) and
for chronic medical conditions (Lundervold, Talley, & Buermann, 2006).
Integrated Behavioral Couples Therapy

Developed by Andrew Cristensen at the University of California and Neil Jacobson
at the University of Washington, integrated behavioral couples therapy (IBCT) is
another program rooted in behavior analysis (Christensen et al., 2004; Jacobson,
Christensen, Prince, Cordova, & Eldridge, 2000). It is “integrative” in the sense
that it integrates both acceptance and change among distressed couples. Although
couples are encouraged to make some changes to accommodate one another’s wishes,
there is a major emphasis on abandoning chronic battles and accepting differences,
as well as accepting one’s emotional reactions to these differences, in the service
of enhancing intimacy. IBCT begins with a formal assessment period, in which the
partners are seen both as a couple and individually, in order to elucidate patterns in the
couple’s struggles and to develop a case formulation. In the active treatment phase,
couples discuss recent events that relate to these larger themes, with the therapist
encouraging more effective communication and, when appropriate, concrete behavior
change. Themes of emotional intimacy and mutual acceptance are stressed throughout
treatment.
Integration of Mindfulness Principles into Other

Cognitive Behavioral Therapy Programs
Finally, a number of clinical innovators have incorporated acceptance- and
mindfulness-enhancing strategies with traditional CBT programs. Roemer and
Orsillo (2008) and Mennin and Fresco (2009) have both developed multicomponent
acceptance-based treatments for generalized anxiety disorder. Similarly, Herbert and
colleagues have combined exposure-based treatments for social anxiety disorder with
ACT to create an acceptance-based behavior therapy for that condition (Dalrymple
& Herbert, 2007; Herbert & Cardaciotto, 2005; Herbert & Forman, in press).
Acceptance-based behavioral treatments for obesity have also been developed
(Forman, Butryn, Hoffman, & Herbert, 2009; Forman et al., in press; Niemeier,
Leahey, Palm Reed, Brown, & Wing, 2012). The sensitivities of acceptance
and mindfulness-based CBT are also increasingly reflected in the work of other
well-known traditional CBT scholars, including Barlow (Barlow & Craske, 2006;
Barlow et al., 2011), Foa (Foa et al., 2005), Marlatt (Bowen, Chawla, & Marlatt,
2011; Marlatt & Donovan, 2005), Borkovec (Behar & Borkovec, 2005), Leahy
(2002, 2011), and even Beck himself (Dozois & Beck, 2011).
Research on Mindfulness and Psychological Acceptance
There has been a veritable explosion of research over the past decade on various
aspects of mindfulness and psychological acceptance. This work can be grouped
broadly into three categories: (a) cross-sectional examination of the relationship
between these constructs and psychopathology, psychosocial functioning, and quality
of life, (b) assessment of treatment processes and mechanisms, and (c) evaluation of
the effectiveness of mindfulness- and acceptance-based interventions.
Relationship with Psychopathology

The Acceptance and Action Questionnaire (AAQ; Bond et al., 2011; Hayes, Luoma,
Bond, Masuda, & Lillis, 2006; Hayes et al., 2004) is the most widely used measure of
psychological acceptance, especially in terms of one’s ability to behave flexibly in spite
of difficult internal experiences. A multisample study of over 2,400 participants (Hayes
et al., 2004) and a meta-analysis of 32 studies with over 6,500 participants (Hayes
et al., 2006) both demonstrated strong inverse associations between psychological
acceptance and various measures of psychopathology.
As discussed above, a number of well-validated measures of mindfulness have been
developed. A comprehensive review of dozens of studies using these scales concluded
that there is a great deal of converging evidence, albeit cross-sectional, that mindfulness
is correlated with various dimensions of psychological health, including quality of
life, positive affect, self-esteem, depression, anxiety, ability to sustain attention, and
self-control (Keng, Smoski, & Robins, 2011). Moreover, functional neuroimaging
has suggested that higher mindfulness levels are associated with a stronger ability to
regulate emotional responses via prefrontal cortical inhibition of the amygdala (Keng
et al., 2011).
Treatment Mechanisms
A substantial literature supports the mechanisms postulated to drive acceptance and
mindfulness-based treatments, including variables such as experiential acceptance and
metacognitive distancing (Hayes et al., 2006). One source of this evidence is a group
of outcome studies that have obtained evidence for the mediating role of changes in
experiential avoidance in treatments of test anxiety (Zettle, 2003), trichotillomania
(Woods, Wetterneck, & Flessner, 2006), worksite stress (Bond & Bunce, 2000),
chronic pain (McCracken, Vowles, & Eccleston, 2005), nicotine addiction (Gifford
et al., 2004; Hayes, 2005), psychosis (Bach, Gaudiano, Hayes, & Herbert, 2013;
Gaudiano, Herbert, & Hayes, 2010), and obesity (Forman et al., 2009). A trial
that tracked changes in mediators and outcomes over time revealed somewhat
differing mediators between ACT and traditional CBT (Forman, Chapman, et al.,
2012). Hayes, Levin, Yadavaia, and Vilardaga (2007) conducted a meta-analysis of

mediational findings in 12 outcome studies of ACT and obtained support for the
mediating role of cognitive defusion, experiential avoidance, and mindfulness.
In a review of the research on behavioral activation, Kanter et al. (2010) concluded
that there is strong support for the components of activity scheduling, relaxation, and
skills training interventions. Other common components of behavioral activation pro-
grams (e.g., values clarification, procedures targeting verbal behavior) have received
support as part of multicomponent packages, but have not yet been shown to have
specific effectiveness independently.
Mindfulness training has also been linked to various positive states of mind, and
even neuropsychological abilities. A systematic review of 23 such studies provides pre-
liminary support that mindfulness training improves attentional and working memory
capacity and executive functions, though methodological flaws reduce confidence
in these findings (Chiesa, Calati, & Serretti, 2011). Laboratory-based component
studies offer an experimental method of investigating mechanisms of action. A
recent meta-analysis of 66 such studies (Levin, Hildebrandt, Lillis, & Hayes, 2012)
concluded that acceptance, defusion, present-moment awareness, values, and mind-
fulness are all independently efficacious over and above comparison components. For
example, acceptance strategies outperformed control strategies for people suffering
from chronic lower back pain (Vowles et al., 2007) and for coping with food cravings
(Forman et al., 2007). Interestingly, the findings on acceptance- and mindfulness-
based mechanisms contrast with the literature on cognitive mechanisms of treatment
effects, and of the effects of direct cognitive change strategies. Despite the continued
popularity of CBT intervention models emphasizing these components, there is in
fact limited evidence to support their specific effects (Longmore & Worrell, 2007).
Efficacy of Mindfulness- and Acceptance-Based Interventions

Most meta-analyses and qualitative reviews have obtained robust evidence for the
efficacy of mindfulness- and acceptance-based interventions. ACT, in particular, has
accumulated a relatively large empirical basis though it still lags compared to the
enormous database in support of traditional CBT (Beck & Dozois, 2011; Butler,
Chapman, Forman, & Beck, 2006). Based on their meta-analysis of 24 studies,
Hayes and colleagues (2006) concluded that ACT was highly effective for treating a
wide range of psychopathology, and outperformed comparison treatments. Another
meta-analysis, carried out by an independent investigator, examined 13 randomized
controlled trials (RCTs) in which ACT was compared to a control group and
obtained similar results, though the methodological rigor of many of the analyzed
studies was judged to be problematic and inversely related to effect size (Öst,
2008). However, Powers, Zum Vorde Sive Vording, and Emmelkamp’s (2009)
meta-analysis of 18 studies concluded that ACT had only a small and insignificant
advantage over other established treatments. A reanalysis of the same dataset by
Levin and Hayes (2009) concluded that ACT, in fact, was somewhat more efficacious
than comparison treatments. A number of studies have examined the effect of ACT
(and related approaches) for chronic pain, and a recent meta-analysis of 22 studies
(N = 1,235) suggested modest efficacy (Veehof, Oskam, Schreurs, & Bohlmeijer,
2011). However, a large longitudinal study provides support for robust longer-
term effects of ACT for chronic pain (Vowles, McCracken, & O’Brien, 2011). A
number of ACT trials have been criticized for small samples, lack of randomization,
absence of a strong comparison condition, shorter-term assessments, and possible
experimenter allegiances. In one trial without these particular shortcomings, patients
with depression or anxiety who received ACT demonstrated equivalent gains at
posttreatment, but greater regression to baseline at 18-month follow-up, compared
to those who received traditional CBT (Forman, Shaw, et al., 2012). A particularly
rigorous trial of anxiety disorder patients demonstrated that, at 12-month follow-up,
ACT patients had better clinical severity ratings but CBT patients reported greater
quality of life (Arch et al., 2012).
Mindfulness-based therapies (MBSR, MBCT) also have documented efficacy. For
instance, a meta-analysis of 39 studies (N = 1,140) revealed that these treatments
produce moderate to large effects among patients with cancer, generalized anxiety
disorder, depression, and other conditions (Hofmann, Sawyer, Witt, & Oh, 2010).
Three meta-analyses of randomized clinical trials for major depressive disorder (con-
sisting of 6, 10, and 21 trials) produced evidence that MBT reduces the risk of
subsequent depressive episodes (Chiesa & Serretti, 2011; Fjorback, Arendt, Ornbol,
Fink, & Walach, 2011; Piet & Hougaard, 2011). Preliminary evidence also exists for
the efficacy of MBTs for treating eating disorders, according to a systematic review
(Wanden-Berghe, Sanz-Valero, & Wanden-Berghe, 2011). A recent meta-analysis of
22 studies (N = 1,403) concluded that MBTs are efficacious in the treatment of anxi-
ety and depression among cancer patients, though the uneven quality of these studies
was noted (Piet, Wurtzen, & Zachariae, 2012). MBSR also appears to moderately
improve anxiety, depression, and psychological distress among those with a chronic
medical condition, according to another meta-analysis (Bohlmeijer, Prenger, Taal, &
Cuijpers, 2010).
DBT has had an enthusiastic reception from clinicians and psychiatric treatment
centers, but currently rests on a relatively modest basis of empirical support. Given
that DBT was developed specifically to treatment borderline personality disorder
(BPD), Kliem, Kröger, and Kosfelder (2010) identified and meta-analyzed the 16
extant studies (including 8 RCTs) that examined DBT for BPD. DBT was equally
(i.e., moderately) effective as other BPD-specific treatments in reducing suicidality
and other BPD-related symptoms, and resulted in equivalent attrition rates. A more
general review of BPD for various conditions identified 11 RCTs that supported
the efficacy of DBT and DBT-based treatments in reducing hospitalization rates,
suicidality, self-harm, substance use, binge eating, and depression (Chiesa et al.,
2011). An analysis of open trials provides preliminary support of DBT for eating
disorders, but not for emotion regulation as a mechanism of action (Bankoff, Karpel,
Forbes, & Pantalone, 2012). Limited evidence also exists that the effects of DBT
persist for up to a year posttreatment (Keng et al., 2011; Kliem et al., 2010).
Several meta-analyses have been conducted on trials of behavioral activation (Cui-
jpers, van Straten, & Warmerdam, 2007; Mazzucchelli, Kane, & Rees, 2009, 2010).
One of these evaluated 34 RCTs (with a total sample size of 2,055 patients) that
compared BA to another treatment (Mazzucchelli et al., 2009). Pooling all results,
BA demonstrated a large and significant advantage over comparison treatments, both
for those with symptoms of depression and for those who met criteria for major
depressive disorder. A separate meta-analysis of 20 studies (N = 1,353) also obtained
evidence for the efficacy of BA for enhancing well-being among those who were not
depressed (Mazzucchelli et al., 2010).
Other mindfulness- and acceptance-based approaches have received less empirical
support, but show considerable promise overall. Acceptance-based behavioral treat-
ments that borrow from the approaches discussed above appear to show solid efficacy.
Examples include acceptance-based behavior treatments for generalized anxiety disor-
der (Roemer, Orsillo, & Salters-Pedneault, 2008), social anxiety disorder (Dalrymple
& Herbert, 2007; Yuen et al., 2013), and obesity (Forman et al., 2009; Forman et al.,
in press; Niemeier et al., 2012). A review by Öst in 2007 identified only two studies
evaluating IBCT (Öst, 2008). These studies found that IBCT was equally effective as
traditional behavioral couple therapy. We could identify no later evaluations of IBCT
other than a follow-up study of a previous trial that obtained evidence that IBCT was
more effective than traditional behavioral couple therapy at 2 years posttreatment,
but that the treatments reconverged at 5 years posttreatment (Christensen, Atkins,
Baucom, & Yi, 2010). Given that FAP does not lend itself to manualized treatment
protocols, it is more difficult to research using conventional methods. What research
has been conducted on the approach, however, is largely supportive (Garc ı́a, 2008;
Maitland & Gaynor, 2012). For example, FAP added to the effectiveness of standard
cognitive therapy when combined with it (Kohlenberg, Kanter, Bolling, Parker, &
Tsai, 2002); similar results were obtained in a small study of depressed adolescents
(Gaynor & Lawrence, 2002). An RCT of smoking cessation concluded that the
medication bupropion plus a combined FAP–ACT therapy outperformed bupropion
alone (Gifford et al., 2011).
In sum, the growing database of outcomes studies strongly suggests that
mindfulness- and acceptance-based interventions are effective treatments for a variety
of psychological conditions. At the same time, systematic reviews have highlighted
most of these treatments are supported by studies that vary in number, sample size,
methodological rigor, and laboratory independence. Thus, more conclusive evidence
for efficacy awaits future study. There is also a growing literature supporting the
theorized mechanisms of these interventions.
Clinical Strategies and Techniques
The various mindfulness- and acceptance-based treatment models, although distinc-

tive in some respects, also share a number of common elements. As such, they utilize
a number of overlapping treatment techniques. These techniques can be grouped
into four overlapping groups: (a) those that facilitate an awareness of one’s current
perceptual, somatic, cognitive, and emotional experience, (b) those that encourage
cognitive distancing or “defusion” from one’s thoughts and other internal events, (c)
those that foster nonjudgmental acceptance of subjective experiences, and (d) those
that aim to foster clarity with respect to one’s values, and goals that are consistent with
those values. Although these foci may be conceptually distinct, in practice specific
intervention techniques typically target more than a single area at a time. For example,
an acceptance technique will likely also contribute to cognitive distancing, and vice
versa. Moreover, any mindfulness-based CBT treatment plan will almost certainly
also incorporate various “nonspecific” techniques (e.g., rapport building), as well as
traditional behavior therapy techniques (e.g., psychoeducation, skills training). Given
that these are shared across all CBT approaches, however, they are not reviewed here.
Awareness Strategies
One of the most commonly used strategies for increasing awareness of one’s ongo-
ing stream of experience is mindfulness meditation. The patient is instructed to
focus entirely on his or her present-moment perceptual, physiological, emotional,
and cognitive experience. Often the patient is instructed to “just notice” these
experiences, though variations include naming the experiences, categorizing them
(as thoughts, feelings, sensations, etc.), or imaginally placing the experience on a
visualization (e.g., leaves floating down a stream). In addition, the patient is taught
to notice when his or her attention has shifted away from current experiences and
gently to return attention to the present moment as often as necessary. Concen-
trative meditation involves instruction to direct one’s full attention to a particular
sensation or perception, such as one’s breath or a candle flame, again with instruc-
tions to return to this focus as soon as the mind drifts. Thus, this type of training
is focused on intentionally narrowing one’s awareness. Compassion meditation and
loving kindness meditation involve contemplations involving loving and kind con-
cern for the well-being of all forms of life. Exercises may involve directing feelings
of compassion and warm feelings toward oneself or others, and active contempla-
tion on the need to take care of oneself and be free from suffering (Hofmann,
Grossman, & Hinton, 2011). A number of somatic awareness techniques are uti-
lized by MBSR in particular, including yoga (stretches and postures designed to
enhance awareness and strength of the musculoskeletal system) and the body scan
(a systematic movement of the focus of attention on sensations throughout the
body).
Although awareness exercises are undoubtedly helpful for many, clinicians will
want to be cognizant that empirical research has yielded inconsistent results regard-
ing the relationship between awareness and psychopathology. For example, Baer
et al. (2006) found that, among nonmeditators, greater awareness (a factor they
termed “observe”) was positively correlated with dissociation, absentmindedness,
psychological symptoms, and thought suppression. Cardaciotto et al. (2008) found
no correlations between awareness and various measures of psychopathology. In
contrast, in both of these studies measures of psychological acceptance were inversely
correlated with psychopathology. These somewhat paradoxical findings may be related
to the fact that certain conditions (e.g., anxiety, depression, pain, hypochondriasis)
are associated with excessive self-focused attention and hyperawareness of bodily
experiences (e.g., Ingram, 1990; Mor & Winquist, 2002). This underscores the
importance of pairing awareness training with a focus on psychological acceptance.
That is, heightened awareness per se is not the goal, but rather nonjudgmental
awareness characterized by an attitude of openness and acceptance with respect to
one’s experience.
Cognitive Distancing
Closely related to the idea of enhanced awareness is the concept of achieving distance
from one’s experience, and particularly one’s thoughts. In fact, cognitive distancing
is a core step in cognitive restructuring, the distinctive feature of cognitive therapy.
Cognitive self-monitoring, in which one’s thoughts are recorded on paper or by some
other means, can help the patient see that thoughts are distinct from the self, and
may not be “true.” More commonly, mindfulness-based therapies encourage patients
to visualize thoughts from a distance; for example, as passing by on a crawler on
a television news broadcast. In ACT, patients are trained in various strategies that
enable distancing, which is referred to as cognitive defusion. For example, patients are
instructed to insert the prefix “I am having the thought that …” before problematic
thoughts, to sing thoughts in a silly voice, and to visualize thoughts as leaves floating
down a stream or as signs held by soldiers in a parade. Another ACT technique,
borrowed from an exercise developed by Titchener (1916), involves rapidly repeating
a key word from a distressing thought (e.g., “fat, fat, fat, fat, fat …”) until the
emotional associations of the word begin to fade.
Acceptance Strategies
Arguably the interventions most central to mindfulness and acceptance CBTs are those
aimed at fostering an open, accepting, nonjudgmental, even welcoming attitude with
respect to the full range of subjective experience. Most mindfulness exercises also
emphasize psychological acceptance in that patients are instructed to be aware of,
but not to judge or attempt to alter, their internal experiences. ACT in particular
makes frequent use of metaphors and experiential exercises to help the patients grasp
the unworkability of attempts to control rather than accept internal experiences.
For example, patients are asked to imagine being in a stalemate in a tug-of-war
with a monster, which metaphorically illustrates the futility and cost of continued
struggle against (attempts to control) the monster (one’s unwanted experiences),
versus a more successful strategy of dropping the rope altogether (accepting one’s
experiences) despite the fact that the monster remains. Another acceptance exercise
involves the therapist throwing toward the patient index cards labeled with the
patient’s most aversive internal experiences while he or she maintains a conversation
with the therapist. Patients are first instructed to block the cards from landing on
them, and subsequently are instructed to allow the cards to settle wherever they
naturally would. Patients quickly notice that the first strategy requires a great deal
of effort and results in impairments to the task at hand (the conversation), whereas
the second strategy frees one’s cognitive resources to attend to the conversation.
In processing the exercise, the therapist helps the patient see that one need not
eliminate negative thoughts (represented by the cards) in order to move forward
toward the chosen goal (the conversation in this case). Various exposure exercises can
also be conceptualized as acceptance strategies. These include traditional behavioral
exposures, as well as exposure exercises framed as “opposite action” (a strategy in DBT
involving behavior that is opposite from the action tendencies of one’s emotions).
Notably, the purpose of exposure is not framed as anxiety reduction per se, but
rather as helping achieve distance from and acceptance of distressing experiences, and
enhancing willingness to move forward behaviorally even with negative subjective
experiences.
Values Clarity Exercises

ACT, in particular, emphasizes the importance of clarifying and articulating one’s
chosen values. From this perspective, values are “qualities of action that can be
instantiated in behavior but not possessed like an object,” and they give meaning to
one’s life (Hayes, 2004, p. 656). Values are viewed as an integral part of establishing
the direction of therapy and for helping the patient see the ultimate purpose of
accepting aversive internal experiences and for committing to difficult behavioral
changes. As such, clarification of one’s values is an essential ingredient in developing
and sustaining motivation for change. Values differ from goals in the sense that the
former are more general and are not directly attainable, whereas the latter reflect
things that can be achieved. By analogy, if values are a sense of direction (like “going
east”), goals would be mileposts along the road heading eastward. An important
aspect of values work is not assuming that the focus of treatment would be solely
(or even primarily) on the initial presenting problem, but rather casting a wider net
and conducting an inquiry into the patient’s broader goals, aspirations, and dreams.
Exercises include posing existential questions such as, “What do you want your life
to stand for?” and imagining the eulogy one would hear at one’s own funeral and
comparing it with the most honest rendition based on one’s recent life.
In addition to these intervention strategies, each mindfulness- and acceptance-
based model employs a variety of additional treatment concepts and techniques.
For example, some programs (e.g., ACT) contain a variety of additional treatment
components not directly related to psychological acceptance and mindfulness per se.
Conclusions and Future Directions
As a technology firmly rooted in scientific values, the field of CBT is continuously

evolving. Among the most prominent evolutions over the past decade has been
the focus on theories and associated techniques that stress mindful acceptance of
distressing subjective experiences in the service of behavior change. As little as 10
years ago, these concepts were still viewed with skepticism by many established
behavior therapists, and mindfulness- and acceptance-based therapies were commonly
seen as situated on the fringes of the field. But that has changed. A rapidly growing
scientific literature supports not only the effectiveness of these approaches for a wide
range of problems, but also many of their proposed theoretical mechanisms, and these
approaches now increasingly find themselves within the mainstream of the field.
But that too will change, as it should. As science advances our understanding of
these approaches, some theories and related technologies will be shown not to be
useful, and will be cut by the knife of scientific parsimony. Others will go through
further refinement, and still others will emerge. Just as the mindful practitioner aims
to avoid excessive attachment to his or her transient subjective experiences, so too
must scientists and practitioners avoid becoming overly attached to today’s theories
and technologies. They too are ephemeral, and destined for change.
References
Arch, J. J., Eifert, G. H., Davies, C., Vilardaga, J. C., Rose, R. D., & Craske, M. G. (2012).
Randomized clinical trial of Cognitive Behavioral Therapy (CBT) versus Acceptance and
Commitment Therapy (ACT) for mixed anxiety disorders. Journal of Consulting and
Clinical Psychology. Advance online publication. doi:10.1037/a0028310
Bach, P., Gaudiano, B. A., Hayes, S. C., & Herbert, J. D. (2013). Reduced believability
of positive symptoms mediates improved hospitalization outcomes of Acceptance and
Commitment Therapy for psychosis. Psychosis: Psychological, Social, and Integrative Aspects,
5, 166–174.
Baer, R. A., Smith, G. T., & Allen, K. B. (2004). Assessment of mindfulness by self-report:
The Kentucky Inventory of Mindfulness Skills. Assessment, 11, 191–206.
Baer, R. A., Smith, G., Hopkins, J., Krietemeyer, J., & Toney, L. (2006). Using self-
report assessment methods to explore facets of mindfulness. Assessment, 13, 27–45.
doi:10.1177/1073191105283504
Bankoff, S. M., Karpel, M. G., Forbes, H. E., & Pantalone, D. W. (2012). A systematic review
of dialectical behavior therapy for the treatment of eating disorders. Eating Disorders: The
Journal of Treatment & Prevention, 20, 196–215. doi:10.1080/10640266.2012.668478
Barlow, D. H., & Craske, M. G. (2006). Mastery of your anxiety and panic: Therapists’ guide
Barlow, D. H., Farchione, T. J., Fairholme, C. P., Ellard, K. K., Boisseau, C. L., Allen, L. B.,
& Ehrenreich-May, J. (2011). Unified protocol for transdiagnostic treatment of emotional
disorders: Therapist guide. New York, NY: Oxford University Press.
Barnhofer, T., Crane, C., Hargus, E., Amarasinghe, M., Winder, R., & Williams, J.
M. G. (2009). Mindfulness-based cognitive therapy as a treatment for chronic
depression: A preliminary study. Behaviour Research Therapy, 47 , 366–373. doi:
10.1016/j.brat.2009.01.019
Beck, A. T. (1976). Cognitive therapy and the emotional disorders. New York, NY: International
Universities Press.
Beck, A. T., & Dozois, D. J. A. (2011). Cognitive therapy: Current status and future directions.
Annual Review of Medicine, 62, 397–409.
Behar, E., & Borkovec, T. D. (2005). The nature and treatment of generalized anxiety disorder.
In B. O. Rothbaum (Ed.), The nature and treatment of pathological anxiety: Essays in
honor of Edna B. Foa (pp. 181–196). New York, NY: Guilford Press.
Blacker, K. J., Herbert, J. D., Forman, E. M., & Kounios, J. (2012). Acceptance-versus change-
based pain management: The role of psychological acceptance. Behavior Modification, 36,
37–48. doi:10.1177/0145445511420281
Bohlmeijer, E., Prenger, R., Taal, E., & Cuijpers, P. (2010). The effects of mindfulness-
based stress reduction therapy on mental health of adults with a chronic med-
ical disease: A meta-analysis. Journal of Psychosomatic Research, 68, 539–544.
doi:10.1016/j.jpsychores.2009.10.005
Bond, F. W., & Bunce, D. (2000). Mediators of change in emotion-focused and problem-
focused worksite stress management interventions. Journal of Occupational Health
Bond, F. W., Hayes, S. C., Baer, R. A., Carpenter, K. M., Guenole, N., Orcutt, H. K.,
& Zettle, R. D. (2011). Preliminary psychometric properties of the acceptance and
action questionnaire–II: A revised measure of psychological inflexibility and experiential
avoidance. Behavior Therapy, 42, 676–688. doi:10.1016/j.beth.2011.03.007
Bowen, S., Chawla, N., & Marlatt, G. A. (2011). Mindfulness-based relapse prevention for
addictive behaviors. New York, NY: Guilford Press.
Brown, K. W., & Ryan, R. M. (2003). The benefits of being present: Mindfulness and its role
in psychological well-being. Journal of Personality and Social Psychology, 84, 822–848.
Brown, L. A., Forman, E. M., Herbert, J. D., Hoffman, K. L., Yuen, E. K., & Goetter,
E. M. (2011). A randomized controlled trial of acceptance-based behavior therapy and
cognitive therapy for test anxiety: A pilot study. Behavior Modification, 35, 31–53.
doi:10.1177/0145445510390930
Butler, A. C., Chapman, J. E., Forman, E. M., & Beck, A. T. (2006). The empirical status of
cognitive-behavioral therapy: A review of meta-analyses. Clinical Psychology Review, 26,
17–31. doi:10.1016/j.cpr.2005.07.003
Callaghan, G. M., Gregg, J. A., Marx, B. P., Kohlenberg, B. S., & Gifford, E. (2004).
FACT: The utility of an integration of Functional Analytic Psychotherapy and Acceptance
and Commitment Therapy to alleviate human suffering. Psychotherapy: Theory, Research,
Practice, Training, 41, 195–207.
Cardaciotto, L., Herbert, J. D., Forman, E. M., Moitra, E., & Farrow, V. (2008). The
assessment of present-moment awareness and acceptance: The Philadelphia Mindfulness
Scale. Assessment, 15, 204–223.
Chiesa, A., Calati, R., & Serretti, A. (2011). Does mindfulness training improve cognitive
abilities? A systematic review of neuropsychological findings. Clinical Psychology Review,
31, 449–464. doi:10.1016/j.cpr.2010.11.003
Chiesa, A., & Serretti, A. (2011). Mindfulness based cognitive therapy for psychiatric dis-
orders: A systematic review and meta-analysis. Psychiatry Research, 187 , 441–453.
doi:10.1016/j.psychres.2010.08.011
Christensen, A., Atkins, D. C., Baucom, B., & Yi, J. (2010). Marital status and satisfaction
five years following a randomized clinical trial comparing Traditional versus Integrative
Behavioral Couple Therapy. Journal of Consulting and Clinical Psychology, 78, 225–235.
doi:10.1037/a0018132
Christensen, A., Atkins, D. C., Berns, S., Wheeler, J., Baucom, D. H., & Simpson, L. E.
(2004). Traditional versus Integrative Behavioral Couple Therapy for significantly and
chronically distressed married couples. Journal of Consulting and Clinical Psychology, 72,
176–191.
Craigie, M. A., Rees, C. S., Marsh, A., & Nathan, P. (2008). Mindfulness-based cognitive
therapy for generalized anxiety disorder: A preliminary evaluation. Behavioural and
Cognitive Psychotherapy, 36, 553–568. doi:10.1017/S135246580800458X
Cuijpers, P., van Straten, A., & Warmerdam, L. (2007). Behavioral activation treat-
ments of depression: A meta-analysis. Clinical Psychology Review, 27 , 318–326.
doi:10.1016/j.cpr.2006.11.001
Dalrymple, K. L., & Herbert, J. D. (2007). Acceptance and commitment therapy for gen-
eralized social anxiety disorder: A pilot study. Behavior Modification, 31, 543–568.
doi:10.1177/0145445507302037
Deckersbach, T., Holzel, B. K., Eisner, L. R., Stange, J. P., Peckham, A. D., Dougherty,
D. D., & Nierenberg, A. A. (2012). Mindfulness-based cognitive therapy for nonremit-
ted patients with bipolar disorder. CNS Neuroscience & Therapeutics, 18, 133–141.
doi:10.1111/j.1755-5949.2011.00236.x
Dimidjian, S., Hollon, S. D., Dobson, K. S., Schmaling, K. B., Kohlenberg, R. J., Addis, M. E.,
& Jacobson, N. S. (2006). Randomized trial of behavioral activation, cognitive therapy,
and antidepressant medication in the acute treatment of adults with major depression.
Dozois, D. D., & Beck, A. T. (2011). Cognitive therapy. In J. D. Herbert & E. M. Forman
(Eds.), Acceptance and mindfulness in cognitive behavior therapy (pp. 26–56). Hoboken,
NJ: John Wiley & Sons, Inc.
Ellis, A., & Grieger, R. (1977). Handbook of Rational-Emotive Therapy. New York, NY:
Springer.
Ellis, A., & Harper, R. A. (1975). A new guide to rational living. Chatsworth, CA: Wilshire
Books.
Evans, S., Ferrando, S., Findler, M., Stowell, C., Smart, C., & Haglin, D. (2008). Mindfulness-
based cognitive therapy for generalized anxiety disorder. Journal of Anxiety Disorders, 22,
716–721. doi:10.1016/j.janxdis.2007.07.005
Eysenck, H. (1952). The effects of psychotherapy: An evaluation. Journal of Consulting
Felver, J. C. (2011). Review of Mindfulness-based cognitive therapy for anxious children: A
manual for treating childhood anxiety. [Review of the book Mindfulness-based cognitive
therapy for anxious children: A manual for treating childhood anxiety, by R. J. Semple &
J. Lee] . Mindfulness, 2, 289–291. doi:10.1007/s12671-011-0077-y
Ferster, C. B. (1973). A functional analysis of depression. American Psychologist, 28, 857–870.
Fjorback, L., Arendt, M., Ornbol, E., Fink, P., & Walach, H. (2011). Mindfulness-based stress
reduction and mindfulness-based cognitive therapy: A systematic review of randomized
controlled trials. Acta Psychiatrica Scandinavica, 124, 102–119. doi:10.1111/j.1600-
0447.2011.01704.x
Foa, E. B., Liebowitz, M. R., Kozak, M. J., Davies, S., Campeas, R., Franklin, M. E., &
Tu, X. (2005). Randomized, placebo-controlled trial of exposure and ritual prevention,
clomipramine, and their combination in the treatment of obsessive-compulsive disorder.
American Journal of Psychiatry, 162, 151–161.
Forman, E. M., Butryn, M. L., Hoffman, K. L., & Herbert, J. D. (2009). An open trial of
an acceptance-based behavioral intervention for weight loss. Cognitive and Behavioral
Practice, 16, 223–235. doi:10.1016/j.cbpra.2008.09.005
Forman, E. M., Butryn, M. L., Juarascio, A. S., Bradley, L. E., Lowe, M. R., Herbert, J. D.,
& Shaw, J. A. (in press). The Mind Your Health Project: A randomized controlled trial
of an innovative behavioral treatment for obesity. Obesity.
Forman, E. M., Chapman, J. E., Herbert, J. D., Goetter, E. M., Yuen, E. K., & Moitra,
E. (2012). Using session-by-session measurement to compare mechanisms of action
for acceptance and commitment therapy and cognitive therapy. Behavior Therapy, 43,
341–354. doi:10.1016/j.beth.2011.07.004
Forman, E. M., Hoffman, K. L., McGrath, K. B., Herbert, J. D., Brandsma, L. L., & Lowe,
M. R. (2007). A comparison of acceptance- and control-based strategies for coping
with food cravings: An analog study. Behaviour Research and Therapy, 45, 2372–2386.
doi:10.1016/j.brat.2007.04.004
Forman, E. M., Shaw, J. A., Goetter, E. M., Herbert, J. D., Park, J. A., & Yuen, E. K.
(2012). Long-term follow-up of a randomized controlled trial comparing acceptance and
commitment therapy and standard cognitive behavior therapy for anxiety and depression.
Behavior Therapy. Advance online publication. doi:10.1016/j.beth.2012.04.004
Garc ı́a, R. F. (2008). Recent studies in functional analytic psychotherapy. International Journal
of Behavioral Consultation and Therapy, 4, 239–249.
Gaudiano, B. A., Herbert, J. D., & Hayes, S. C. (2010). Is it the symptom or the relation to
it? Investigating potential mediators of change in acceptance and commitment therapy for
psychosis. Behavior Therapy, 41, 543–554.
Gaynor, S. T., & Lawrence, P. (2002). Complementing CBT for depressed adolescents with
Learning through In Vivo Experience (LIVE): Conceptual analysis, treatment description,
and feasibility study. Behavioral and Cognitive Psychotherapy, 30, 79–101.
Gifford, E. V., Kohlenberg, B. S., Hayes, S. C., Antonuccio, D. O., Piasecki, M. M., Rasmussen-
Hall, M. L., & Palm, K. M. (2004). Acceptance-based treatment for smoking cessation.
Gifford, E. V., Kohlenberg, B. S., Hayes, S. C., Pierson, H. M., Piasecki, M. P., Antonuccio,
D. O., & Palm, K. M. (2011). Does acceptance and relationship focused behavior therapy
contribute to bupropion outcomes? A randomized controlled trial of functional analytic
psychotherapy and acceptance and commitment therapy for smoking cessation. Behavior
Therapy, 42, 700–715.
Goldfried, M. (2011). Mindfulness and acceptance in cognitive behavior therapy: What’s new?
In J. D. Herbert & E. M. Forman (Eds.), Acceptance and mindfulness in cognitive behavior
therapy (pp. 109–131). Hoboken, NJ: John Wiley & Sons, Inc.
Hayes, S. C. (2004). Acceptance and commitment therapy, relational frame theory, and the
third wave of behavioral and cognitive therapies. Behavior Therapy, 35, 639–665.
Hayes, S. C. (2005, July). State of the ACT Evidence. Paper presented at the ACT Summer
Institute, Philadelphia, PA.
Hayes, S. C., Levin, M., Yadavaia, J. E., & Vilardaga, J. C. (2007). ACT: Model and processes
of change. Paper presented at the Association for Behavioral and Cognitive Therapies,
Philadelphia, PA.
Hayes, S. C., Luoma, J. B., Bond, F. W., Masuda, A., & Lillis, J. (2006). Acceptance and
commitment therapy: Model, processes and outcomes. Behaviour Research and Therapy,
44, 1–25. doi:10.1016/j.brat.2005.06.006
Hayes, S. C., Strosahl, K. D., & Wilson, K. G. (2011). Acceptance and Commitment Therapy:
The process and practice of mindful change (2nd ed.). New York, NY: Guilford Press.
Hayes, S. C., Strosahl, K., Wilson, K. G., Bissett, R. T., Pistorello, J., Toarmino, D., & McCurry,
S. M. (2004). Measuring experiential avoidance: A preliminary test of a working model.
Psychological Record, 54, 553–578.
Heidenreich, T., Tuin, I., Pflug, B., Michal, M., & Michalak, J. (2006). Letters to the editor:
Mindfulness-based cognitive therapy for persistent insomnia: A pilot study [Letter].
Psychotherapy and Psychosomatics, 75, 188–189. doi:10.1159/000091778
Herbert, J. D., & Cardaciotto, L. (2005). A mindfulness and acceptance-based perspective on
social anxiety disorder. In S. Orsillo & L. Roemer (Eds.), Acceptance and mindfulness-
based approaches to anxiety: Conceptualization and treatment (pp. 189–212). New York,
NY: Springer.
Herbert, J. D., & Forman, E. M. (Eds.) (2011a). Acceptance and mindfulness in cognitive
behavior therapy: Understanding and applying the new therapies. Hoboken, NJ: John Wiley
& Sons, Inc.
Herbert, J. D., & Forman, E. M. (2011b). The evolution of cognitive behavior therapy: The
rise of psychological acceptance and mindfulness. In J. D. Herbert & E. M. Forman
(Eds.), Acceptance and mindfulness in cognitive behavior therapy: Understanding and
applying the new therapies (pp. 3–25). Hoboken, NJ: John Wiley & Sons, Inc.
Herbert, J. D., & Forman, E. M. (in press). Acceptance and mindfulness-based therapies for
social anxiety disorder: Current findings and future directions. In J. W. Weeks (Ed.),
The Wiley-Blackwell handbook of social anxiety disorder. Hoboken, NJ: John Wiley & Sons,
Inc.
Herbert, J. D., Forman, E. M., & England, E. L. (2009). Psychological acceptance. In W.

O’Donohue & J. E. Fisher (Eds.), General principles and empirically supported techniques
of cognitive behavior therapy (pp. 77–101). Hoboken, NJ: John Wiley & Sons, Inc.
Hofmann, S. G., Grossman, P., & Hinton, D. E. (2011). Loving-kindness and compassion
meditation: Potential for psychological interventions. Clinical Psychology Review, 31,
1126–1132. doi:10.1016/j.cpr.2011.07.003
Hofmann, S. G., Sawyer, A. T., Witt, A. A., & Oh, D. (2010). The effect of mindfulness-based
therapy on anxiety and depression: A meta-analytic review. Journal of Consulting and
Clinical Psychology, 78, 169–183. doi:10.1037/a0018555
Hopko, D. R., Robertson, S. M. C., & Lejuez, C. W. (2006). Behavioral activation for anxiety
disorders. Behavior Analyst Today, 7 , 212–224.
Ingram, R. E. (1990). Self-focused attention in clinical disorders: Review and a conceptual
model. Psychological Bulletin, 107 , 156–176. doi:10.1037/0033-2909.107.2.156
Jacobson, N. S., Christensen, A., Prince, S. E., Cordova, J., & Eldridge, K. (2000). Integrative
behavioral couple therapy: An acceptance-based, promising new treatment for couple
discord. Journal of Consulting and Clinical Psychology, 68, 351–355.
Jacobson, N. S., Dobson, K. S., Truax, P. A., Addis, M. E., Koerner, K., Gollan, J. K.,
& Prince, S. E. (1996). A component analysis of cognitive-behavioral treatment for
Kabat-Zinn, J. (1994). Wherever you go, there you are: Mindfulness meditation in everyday life.
Kabat-Zinn, J. (2005). Coming to our senses: Healing ourselves and the world through mindfulness.
Kanter, J. W., Manos, R. C., Bowe, W. M., Baruch, D. E., Busch, A. M., & Rusch, L.
C. (2010). What is behavioral activation? A review of the empirical literature. Clinical
Psychology Review, 30, 608–620. doi:10.1016/j.cpr.2010.04.001
Kanter, J., Tsai, M., & Kohlenberg, R. J. (Eds.). (2010b). The practice of functional analytic
psychotherapy. New York, NY: Springer.
Keng, S. L., Smoski, M. J., & Robins, C. J. (2011). Effects of mindfulness on psycholog-
ical health: A review of empirical studies. Clinical Psychology Review, 31, 1041–1056.
doi:10.1016/j.cpr.2011.04.006
Kim, Y. W., Lee, S.-H., Choi, T. K., Suh, S. Y., Kim, B., Kim, C. M., & Yook, K.H. (2009).
Effectiveness of mindfulness-based cognitive therapy as an adjuvant to pharmacotherapy
in patients with panic disorder or generalized anxiety disorder. Depression and Anxiety,
26, 601–606. doi:10.1002/da.20552
Kliem, S., Kröger, C., & Kosfelder, J. (2010). Dialectical behavior therapy for borderline
personality disorder: A meta-analysis using mixed-effects modeling. Journal of Consulting
and Clinical Psychology, 78, 936–951. doi:10.1037/a0021015
Kohlenberg, R. J., Kanter, J. W., Bolling, M. Y., Parker, C., & Tsai, M. (2002). Enhanc-
ing cognitive therapy for depression with functional analytic psychotherapy: Treat-
ment guidelines and empirical findings. Cognitive and Behavioral Practice, 9, 213–
229.
Kohlenberg, R., & Tsai, M. (1991). Functional analytic psychotherapy. New York, NY: Plenum.
Kumar, S. M. (2002). An introduction to Buddhism for the cognitive-behavioral therapist.
Cognitive and Behavioral Practice, 9, 40–43.
Langer, E. J. (1989a). Mindfulness. New York, NY: Addison-Wesley.
Langer, E. J. (1989b). Minding matters: The consequences of mindlessness-mindfulness. In L.
Berkowitz (Ed.), Advances in experimental social psychology (Vol. 22, pp. 137–173). New
York, NY: Academic Press.
Lau, M. A., Bishop, S. R., Segal, Z. V., Buis, T., Anderson, N. D., Carlson, L., & Devins, G.
(2006). The Toronto Mindfulness Scale: Development and validation. Journal of Clinical
Psychology, 62, 1445–1467. doi:10.1002/jclp.20326
Leahy, R. L. (2002). A model of emotional schemas. Cognitive and Behavioral Practice, 9,
177–190.
Leahy, R. L. (2011). Emotional schema therapy: A bridge over troubled waters. In J. D.
Herbert & E. M. Forman (Eds.), Acceptance and mindfulness in cognitive behavior therapy
(pp. 109–131). Hoboken, NJ: John Wiley & Sons, Inc.
Levin, M. E., & Hayes, S. C. (2009). Is Acceptance and Commitment Therapy superior to
established treatment comparisons? [Comment/Reply]. Psychotherapy and Psychosomatics,
78, 380. doi:10.1159/000235978
Levin, M. E., Hildebrandt, M. J., Lillis, J., & Hayes, S. C. (2012). The impact of treatment com-
ponents suggested by the psychological flexibility model: A meta-analysis of laboratory-
based component studies. Behavior Therapy, 43, 741–756. doi:10.1016/j.beth.2012.
05.003
Lewinsohn, P. M. (1974). A behavioral approach to depression. In R. J. Friedman & M. M.
Katz (Eds.), Psychology of depression: Contemporary theory and research (pp. 157–185).
Oxford, England: John Wiley & Sons, Ltd.
Lewinsohn, P. M., Biglan, A., & Zeiss, A. M. (1976). Behavioral treatment for depression.
In P. O. Davidson (Ed.), Behavioral management of anxiety, depression and pain (pp.
91–146). New York, NY: Brunner/Mazel.
Lewinsohn, P. M., Youngren, M. A., & Grosscup, S. J. (1979). Reinforcement and depression.
In R. A. Dupue (Ed.), The psychobiology of depressive disorders: Implications for the effects of
stress (pp. 291–316). New York, NY: Academic Press.
Linehan, M. M., Armstrong, H. E., Suarez, A., Allmon, D., & Heard, H. L. (1991). Cognitive-
behavioral treatment of chronically parasuicidal borderline patients. Archives of General
Psychiatry, 48, 1060–1064.
Linehan, M. M., & Dimeff, L. (2001). Dialectical behavior therapy in a nutshell. California
Psychologist, 34, 10–13.
Longmore, R. J., & Worrell, M. (2007). Do we need to challenge thoughts in cognitive behavior
therapy? Clinical Psychology Review, 27 , 173–187. doi:10.1016/j.cpr.2006.08.001
Lovas, D. A., & Barsky, A. J. (2010). Mindfulness-based cognitive therapy for hypochondriasis,
or severe health anxiety: A pilot study. Journal of Anxiety Disorders, 24, 931–935.
doi:10.1016/j.janxdis.2010.06.019
Lundervold, D. A., Talley, C., & Buermann, M. (2006). Effect of behavioral activation
treatment on fibromyalgia-related pain anxiety and cognition. International Journal of
Behavioral Consultation and Therapy, 2, 73–78.
Maitland, D. W. M., & Gaynor, S. T. (2012). Promoting efficacy research on functional analytic
psychotherapy. International Journal of Behavioral Consultation and Therapy, 7 , 63–71.
Marlatt, G. A., & Donovan, D. M. (2005). Relapse prevention: Maintenance strategies in the
treatment of addictive behaviors. New York, NY: Guilford Press.
Mazzucchelli, T. G., Kane, R., & Rees, C. (2009). Behavioral activation treatments for
depression in adults: A meta-analysis and review. Clinical Psychology: Science and Practice,
16, 383–411. doi:10.1111/j.1468-2850.2009.01178.x
Mazzucchelli, T. G., Kane, R. T., & Rees, C. S. (2010). Behavioral activation inter-
ventions for well-being: A meta-analysis. Journal of Positive Psychology, 5, 105–121.
doi:10.1080/17439760903569154
McCracken, L. M., Vowles, K. E., & Eccleston, C. (2005). Acceptance-based treatment
for persons with complex, long standing chronic pain: A preliminary analysis of
treatment outcome in comparison to a waiting phase. Behavior Research and Therapy, 43,
1335–1346. doi:10.1016/j.brat.2004.10.003
McManus, F., Surawy, C., Muse, K., Vazquez-Montes, M., & Williams, J. (2012). A random-
ized clinical trial of mindfulness-based cognitive therapy versus unrestricted services for
health anxiety (hypochondriasis). Journal of Consulting and Clinical Psychology. Advance
online publication. doi:10.1037/a0028782
Mennin, D., & Fresco, D. M. (2009). Emotion regulation as an integrative framework for
understanding and treating psychopathology. In A. M. Kring & D. M. Sloan (Eds.), Emo-
tion regulation and psychopathology: A transdiagnostic approach to etiology and treatment
Miklowitz, D. J., Alatiq, Y., Goodwin, G. M., Geddes, J. R., Fennell, M. J., Dimid-
jian, S., & Williams, J. (2009). A pilot study of mindfulness-based cognitive ther-
apy for bipolar disorder. International Journal of Cognitive Therapy, 2, 373–382.
doi:10.1521/ijct.2009.2.4.373
Mor, N., & Winquist, J. (2002). Self-focused attention and negative affect: A meta-analysis.
Psychological Bulletin, 128, 638–662. doi:10.1037/0033-2909.128.4.638
Myers, S. B., Sweeney, A. C., Popick, V., Wesley, K., Bordfeld, A., & Fingerhut, R. (2012). Self-
care practices and perceived stress levels among psychology graduate students. Training
and Education in Professional Psychology, 6, 55–66. doi:10.1037/a0026534
Niemeier, H. M., Leahey, T., Palm Reed, K., Brown, R. A., & Wing, R. R. (2012). An
acceptance-based behavioral intervention for weight loss: A pilot study. Behavior Therapy,
43, 427–435. doi:10.1016/j.beth.2011.10.005
O’Donohue, W. (2009). A brief history of cognitive behavior therapy: Are there troubles ahead?
In W. O’Donohue & J. E. Fisher (Eds.), General principles and empirically supported
techniques of cognitive behavior therapy (pp. 1–14). Hoboken, NJ: John Wiley & Sons,
Inc.
Öst, L.-G. (2008). Efficacy of the third wave of behavioral therapies: A system-
atic review and meta-analysis. Behaviour Research and Therapy, 46, 296–321.
doi:10.1016/j.brat.2007.12.005
Piet, J., & Hougaard, E. (2011). The effect of mindfulness-based cognitive therapy for
prevention of relapse in recurrent major depressive disorder: A systematic review and meta-
analysis. Clinical Psychology Review, 31, 1032–1040. doi:10.1016/j.cpr.2011.05.002
Piet, J., Wurtzen, H., & Zachariae, R. (2012). The effect of mindfulness-based therapy on
symptoms of anxiety and depression in adult cancer patients and survivors: A systematic
review and meta-analysis. Journal of Consulting and Clinical Psychology. Advance online
publication. doi:10.1037/a0028329
Powers, M. B., Zum Vorde Sive Vording, M. B., & Emmelkamp, P. M. (2009). Acceptance
and commitment therapy: A meta-analytic review. Psychotherapy and Psychosomatics, 78,
73–80. doi:10.1159/000190790
Roemer, L., & Orsillo, S. M. (2008). Mindfulness- and acceptance-based behavioral therapies in
practice. New York, NY: Guilford Press.
Roemer, L., Orsillo, S. M., & Salters-Pedneault, K. (2008). Efficacy of an acceptance-
based behavior therapy for generalized anxiety disorder: Evaluation in a random-
ized controlled trial. Journal of Consulting and Clinical Psychology, 76, 1083–1089.
doi:10.1037/a0012720
Seager, R. H. (1999). Buddhism in America. New York, NY: Columbia University Press.
for depression: A new approach to preventing relapse. New York, NY: Guilford Press.
Semple, R. J., & Lee, J. (2008). Treating anxiety with mindfulness: Mindfulness-based cognitive
therapy for children. In Greco, L. A. & Hayes, S. C. (Eds.), Acceptance and mindfulness
treatments for children and adolescents: A practitioner’s guide (pp. 63–87). Oakland, CA:
New Harbinger Publications.
Silpakit, C., Silpakit, O., & Wisajun, P. (2011). The validity of Philadelphia Mindfulness Scale
Thai version. Journal of Mental Health of Thailand, 19, 140–147.
Smith, J. C. (1986). Meditation: A sensible guide to a timeless discipline. Chicago, IL: Research
Press.
Skinner, B. F. (1953). Science and human behavior. New York, NY: Macmillan.
Skinner, B. F. (1957). Verbal behavior. Acton, MA: Copley.
Stange, J. P., Eisner, L. R., Holzel, B. K., Peckham, A. D., Dougherty, D. D., Rauch,
S. L., & Deckersbach, T. (2011). Mindfulness-based cognitive therapy for bipolar dis-
order: Effects on cognitive functioning. Journal of Psychiatric Practice, 17 , 410–419.
doi:10.1097/01.pra.0000407964.34604.03
Teasdale, J. D., Moore, R. G., Hayhurst, H., Pope, M., Williams, S., & Segal, Z. V. (2002).
Metacognitive awareness and prevention of relapse in depression: Empirical evidence.
Titchener, E. B. (1916). A text-book of psychology. New York, NY: Macmillan.
Veehof, M. M., Oskam, M.-J., Schreurs, K. M. G., & Bohlmeijer, E. T. (2011). Acceptance-
based interventions for the treatment of chronic pain: A systematic review and meta-
analysis. Pain, 152, 533–542. doi:10.1016/j.pain.2010.11.002
Vowles, K. E., McCracken, L. M., & O’Brien, J. Z. (2011). Acceptance and values-based action
in chronic pain: A three-year follow-up analysis of treatment effectiveness and process.
Behaviour Research and Therapy, 49, 748–755. doi:10.1016/j.brat.2011.08.002
Vowles, K. E., McNeil, D. W., Gross, R. T., McDaniel, M. L., Mouse, A., Bates, M., &
McCall, C. (2007). Effects of pain acceptance and pain control strategies on physical
impairment in individuals with chronic low back pain. Behavior Therapy, 38, 412–425.
doi:10.1016/j.beth.2007.02.001
Wanden-Berghe, R. G., Sanz-Valero, J., & Wanden-Berghe, C. (2011). The application of
mindfulness to eating disorders treatment: A systematic review. Eating Disorders: The
Journal of Treatment & Prevention, 19, 34–48. doi:10.1080/10640266.2011.533604
Weber, B., Jermann, F., Gex-Fabry, M., Nallet, A., Bondolfi, G., & Aubry, J. (2010).
Mindfulness-based cognitive therapy for bipolar disorder: A feasibility trial. European
Psychiatry, 25, 334–337. doi:10.1016/j.eurpsy.2010.03.007
Wells, A. (2000). Emotional disorders and metacognition: Innovative cognitive therapy. Chich-
Wells, A. (2008). Metacognitive therapy: A practical guide. New York, NY: Guilford Press.
Wells, A. (2011). Metacognitive therapy. In J. D. Herbert & E. M. Forman (Eds.), Acceptance
and mindfulness in cognitive behavior therapy (pp. 83–108). Hoboken, NJ: John Wiley &
Sons, Inc.
Wells, A., & Matthews, G. (1994). Attention and emotion: A clinical perspective. Hove,
England: Erlbaum.
Williams, J., Alatiq, Y., Crane, C., Barnhofer, T., Fennell, M., Duggan, D., Goodwin, G.
(2008). Mindfulness-based cognitive therapy (MBCT) in bipolar disorder: Preliminary
evaluation of immediate effects on between-episode functioning. Journal of Affective
Disorders, 107 , 275–279. doi:10.1016/j.jad.2007.08.022
Williams, J. C., & Lynn, S. J. (2010). Acceptance: An historical and conceptual review.
Imagination, Cognition and Personality, 30, 5–56.
Williams, M. J., McManus, F., Muse, K., & Williams, J. (2011). Mindfulness-based cognitive
therapy for severe health anxiety (hypochondriasis): An interpretative phenomenological
analysis of patients’ experiences. British Journal of Clinical Psychology, 50, 379–397.
doi:10.1111/j.2044-8260.2010.02000.x

Press.
Wong, S. Y., Mak, W. W., Cheung, E. Y., Ling, C. Y., Lui, W. W., Tang, W., & Ma, H. S.
(2011). A randomized, controlled clinical trial: The effect of mindfulness-based cognitive
therapy on generalized anxiety disorder among Chinese community patients: Protocol for
a randomized trial. BMC Psychiatry, 11, 187. doi:10.1186/1471-244X-11-187
Woods, D. W., Wetterneck, C. T., & Flessner, C. A. (2006). A controlled evalua-
tion of acceptance and commitment therapy plus habit reversal for trichotilloma-
nia. Behavior Research and Therapy, 44, 639–656. doi:S0005-7967(05)00126-9 [pii]
10.1016/j.brat.2005.05.006
Yook, K., Lee, S.-H., Ryu, M., Kim, K.-H., Choi, T. K., Suh, S. Y., & Kim, M. J. (2008).
Usefulness of mindfulness-based cognitive therapy for treating insomnia in patients with
anxiety disorders: A pilot study. Journal of Nervous and Mental Disease, 196, 501–503.
doi:10.1097/NMD.0b013e31817762ac
Yuen, E. K., Herbert, J. D., Forman, E. M., Goetter, E. M., Comer, R., & Bradley, J. (2013).
Treatment of social anxiety disorder using online virtual environments in Second Life.
Zettle, R. D. (2003). Acceptance and commitment therapy (ACT) vs. systematic desensitization
in treatment of mathematics anxiety. Psychological Record, 53, 197–215.
8
Therapeutic Relaxation
Melissa A. Day, Joshua C. Eyer,
and Beverly E. Thorn
University of Alabama, United States
Over the last several decades, the acceptance and use of relaxation techniques for
the management and treatment of an array of illnesses and disorders has expanded
greatly. These approaches are now a common treatment for hypertension, irritable
bowel syndrome, headache, chronic pain, insomnia, anxiety, and depression, among
many other disorders. An evidence base now exists for a range of approaches that
differ in their theoretical bases and methodology of implementation. Fundamentally,
however, all relaxation techniques are cognitive behavioral therapeutic approaches
that emphasize the patient’s role as an active participant in his or her treatment,
rather than simply a passive recipient of health care. In essence, relaxation techniques
represent a foundation upon which many other coping skills may be built.
Our review of relaxation techniques in this chapter is divided into three major
sections. In the first part of the chapter, we define and articulate what relaxation is and
also discuss proposed theoretical mechanisms to explain how relaxation is thought to
produce its beneficial effects. In the second section, we describe the underlying theory,
clinical implementation, and research regarding the most commonly implemented
relaxation techniques, providing both broad and technique-specific clinical indications
and contraindications. In the final section, we provide a commentary on the current
state of the evidence regarding the efficacy of relaxation approaches and discuss areas
for potential future advancement.
It should be noted that the focus of this chapter is intended for the therapeutic
application of relaxation in adult populations; discussion of the clinical application of
relaxation to children is beyond the scope of this chapter. The reader is referred to
http://www.effectivechildtherapy.com for up-to-date information on current empiri-
cally supported treatments for children, a service of the Association for Behavioral and
Cognitive Therapies and the Society of Clinical Child and Adolescent Psychology.
Furthermore, we will not cover all extant relaxation interventions nor provide an

DOI: 10.1002/9781118528563.wbcbt08
exhaustive documentation of the huge volume of research dedicated to this topic.

We hope this chapter will spark intellectual curiosity and, in support of that, we offer
references to more in-depth discussions where the interested reader may locate more
detailed, technique-specific information.
Definition and Mechanism of Relaxation
What Is Relaxation?
In the general public there is an unspoken idea of what constitutes relaxation and
personal preferences dictate the nuances of that idea. For example, one person may
think of relaxation as going for a run in the crisp morning air, having coffee with a
friend, or easing back into a comfortable recliner to listen to a favorite CD. Another
person may have a more specific view, and may think of relaxation as his or her
meditation time each morning. Yet another individual may think of relaxation as
taking his or her daily anxiolytic medication. Needless to say, there are a large number
of ways in which one may relax.
However, the National Institutes of Health (NIH) Technology Assessment Panel
(1996) defined therapeutic relaxation techniques as a specific set of behavioral inter-
ventions that share two basic components: (a) repetitive focus on a word, phrase,
prayer, sound, bodily sensation, or muscular activity, and (b) the adoption of a passive
attitude toward any arising thought and a return to the focus. Additionally, as defined
by the National Center for Complementary and Alternative Medicine (NCCAM;
a center within NIH), all relaxation therapies are a form of mind–body medicine
designed to enhance the mind’s capacity to affect bodily function and symptoms
(NCCAM, 2013). The advantage of these broad definitions is that they capture most,
if not all, of the diverse relaxation techniques under one overarching framework.
Other classifications exist that use different organizational strategies, such as cogni-
tive versus somatic (Freeman, 2008) or deep versus brief methods (NIH Technology
Assessment Panel, 1996). Both of these definitions have drawbacks. Under the cogni-
tive versus somatic conceptualization, techniques that primarily emphasize relaxation
of the mind (e.g., meditation) are considered “cognitive,” whereas techniques that
hold relaxation of the body as the primary focus (e.g., progressive muscle relaxation)
are considered “somatic.” This differentiation recalls the mind–body dualism underly-
ing the traditional biomedical model. Given the well-accepted biopsychosocial model
(Engel, 1977), defining relaxation interventions as either cognitively or somatically
focused may be an arbitrary and, ultimately, unhelpful distinction. Under the deep
versus brief distinction, “deep” is intended to refer to more in-depth methods of
relaxation that allegedly require more time to master, whereas “brief” refers to a
shorter form of one of the deep methods. Since there is little evidence that “deep”
(longer) techniques achieve relaxation states that are distinct from “brief” techniques,
this division also may not be particularly useful.
A unifying aspect of most current definitions of therapeutic relaxation is that the
primary goal is to elicit the psychophysiological relaxation response and, thereby,
reduce the stress response (Benson, Greenwood, & Klemchuk, 1975). Reduction
Therapeutic Relaxation 159
in the stress response has, in turn, been shown to lead to reductions in symptoms
associated with a variety of stress-related physical and psychological disorders (e.g.,
Astin, Shapiro, Eisenberg, & Forys, 2003; Esch, Fricchione, & Stefano, 2003;
Stefano, Fricchione, & Esch, 2006). Some techniques are employed primarily to
induce a reduction in the stress response (e.g., imagery-assisted relaxation), whereas
other techniques may not have relaxation as the primary goal (e.g., meditation) but
result in a relaxation response nonetheless. In some cases, there is evidence that
certain techniques provide added benefits beyond a relaxed state (e.g., hypnosis for
habit control, meditation for insight). However, in this chapter we have limited our
discussion to these techniques as relaxation therapies.
In the second part of the chapter, within the context of describing the theory,
practice, and research of the most commonly used relaxation techniques, we have
separately described the defining features of each given intervention. We consider a
clear operational definition of the technique utilized as indispensable and we have
sought to identify and make reference to standardized protocols wherever possible.
How Does Relaxation Elicit Therapeutic Effects?

That relaxation techniques produce reliable therapeutic effects is well established.
However, the mechanisms involved in these processes and the exact pathways by
which they occur are less clear. The difficulty in determining the pathway from a
relaxation exercise to its therapeutic effects arises naturally from the involvement of
multiple interacting biological systems. Despite this complexity, one may say that
relaxation is the product of an important physiological process that balances the body’s
stress response.
Typically, equilibrium in one’s level of arousal is achieved by balancing the activity
of two complementary systems, an activating network that increases arousal and
a calming network that promotes restfulness (Benson et al., 1975; Jacobs, 2001).
To do this, the hypothalamus regulates the activity of the two main branches of
the autonomic nervous system: the parasympathetic nervous system, which produces
the relaxation response, and the sympathetic nervous system, which produces the
stress response (Brodal, 2010; Esch et al., 2003; McEwen, 2007). The physiological
pathway leading to the relaxation response is the generally accepted mechanism by
which most relaxation techniques produce a relaxed state. In contrast, activation of
the stress response generates periods of heightened arousal.
The stress response evolved before the time of board meetings and traffic jams,
at a time when the world was primitive and unforgiving. Survival depended on fast
reactions to daily occurrences of deadly threats. The options were to freeze, run,
fight, or, as a last resort, play dead (Bracha, 2004). One poor reaction meant that
one’s genes could not be passed along to the next generation. Thus, the human
stress response evolved for life-preserving action. Unfortunately, this adaptation is
one of the least practical aspects of the human body for humans in the developed
world because few of us experience daily life-threatening situations. The physiological
response to outrunning an avalanche can be essentially the same as the response to
going on a first date or asking for a raise; like an on–off switch, the body tends to
respond with a rapid, all-or-nothing reaction.
Physiologically, the stress response occurs through the action of the hypothalamic-
pituitary-adrenal (HPA) axis (Brodal, 2010; Esch et al., 2003; McEwen, 2007).
The hypothalamus initiates the acute stress response by stimulating the sympathetic
nervous system to coordinate internal organ activity; this activation increases heart
rate, blood pressure, respiration, muscle tone, and body temperature, opens up airways
and pupils, and triggers sweating and piloerection (goose bumps). The hypothalamus
also signals the pituitary to activate the adrenal gland to release endocrine compounds
related to high arousal, especially epinephrine, norepinephrine, and cortisol. Cognitive
changes associated with acute stress include focused attention on the potential stressor
and heighted concentration. In the short term, this physiological state is perfect for
escaping from a stressor.
However, when associated with prolonged or repeated unresolved stressors, the
stress response can lead to a breakdown of the system (Esch et al., 2003; McEwen,
2007). Chronic stress leads to wide-ranging negative effects for the body includ-
ing increases in blood pressure, blood sugar dysregulation, greater abdominal fat,
hormone imbalances, reduced neurological and immune function, chronic systemic
inflammation, and reduced muscle strength. Associated cognitive and affective changes
include reduced ability to focus attention and concentrate, and increased feelings of
helplessness and depressed affect. These changes, in turn, contribute to poor health
in a number of domains. As might be expected, chronic stress has been linked to
a wide range of health conditions including heart attack, stroke, respiratory disease,
autoimmune conditions, and depression. However, inducing the relaxation response
reduces the negative impacts of chronic stress and can help restore the body to
homeostasis (Esch et al., 2003; Stefano et al., 2006).
Described nearly 40 years ago by Benson (Benson et al., 1975), the relaxation
response is a biological process that both decreases and moderates the stress response
and triggers strong recuperative processes. In the relaxation response the hypotha-
lamus stimulates the parasympathetic nervous system to coordinate internal organ
activity to decrease heart rate, blood pressure, muscle tension, and respiration, and
promote digestion and body temperature regulation (Benson et al., 1975; Bro-
dal, 2010; Stefano et al., 2006). Associated cognitive and affective changes include
reduced cortical arousal and self-reported feelings of positive affect (Benson et al.,
1975). These identifiable signs of relaxation are important for two reasons. First, they
support the idea that the relaxation response does not function as simply the absence
of stress, but rather it serves as a balancing system that produces a characteristic relaxed
state. Second, this distinction is clinically important because it suggests that relaxation
carries physiological characteristics that can be recognized by clinicians and clients
to identify and track success at achieving the relaxation response during therapy. In
fact, the stress and relaxation responses are fairly accessible to assessment using visual
evaluation or a rating scale such as the Behavioral Rating Scale (Poppen, 1998);
physiologically using body temperature, heart rate, or brain activity; or subjectively
by patient self-report. These physiological sequelae have also been linked to a number
of microbiological changes in the body and associated brain changes (Stefano et al.,
2006). It is important to note that changes in brain activity (e.g., cognition or affect)
likely have a bidirectional effect on the bodily changes noted above. Although Benson
et al. (1975) suggested that when the body relaxes, the mind follows—implying that
body changes “cause” the mind to change—it is likely that it proceeds equally as well
in the other direction—changes in the mind lead to changes in the body. Thus, the
benefits of relaxation therapies arise through complex interactions among a number
of physiological, muscular, and cognitive/affective processes functioning within the
context of the social environment.
Relaxation Techniques
This section reviews the most commonly used relaxation techniques. Within the
context of each technique we discuss key aspects related to theory, clinical practice, and
research. The relaxation techniques we will discuss in this section include breathing
techniques, guided imagery, progressive muscle relaxation (in both its extended
and abbreviated forms), biofeedback, autogenic training, hypnosis, and meditation.
Clinical considerations and contraindications are broadly discussed within a summary
subsection that follows the descriptions of the various relaxation techniques.
Breathing Techniques
Historical roots and theory. It is difficult to pinpoint the exact origin of therapeutic
breathing techniques as a form of relaxation. For well over 5,000 years, various
meditation and yogic practices have used the breath as a primary focus of awareness.
Many therapists often begin with some form of breathing exercise prior to more in-
depth relaxation training, and most relaxation techniques incorporate some variation
on breath focus. Breathing techniques are relatively quick to master and often elicit
immediate (albeit modest) reductions in autonomic arousal and skeletal muscle
tension (Smith, 2005). Everly and Lating (2002) go so far as to state that “controlled
respiration is one of the oldest and certainly the single most efficient acute intervention
for the mitigation and treatment of excessive stress” (p. 215). Fundamentally, the
distinguishing characteristic of relaxed breathing techniques is that the focus of
attention is attempting to slow down and deepen the breath to mimic respiration rate
and rhythm in a naturally relaxed state.
Clinical practice. In general, the goal of relaxed breathing exercises is to engage the
diaphragm more fully to cultivate deep, slow respiration (Fried, 1993). The work
of the lungs and the intercostal (chest) and trapezius (shoulder) muscles is reduced
as these areas are associated with more active, forced, shallow breathing. Often it
is useful to demonstrate diaphragmatic breathing to patients by having them place
one hand on their abdomen and the other on their chest while asking them to
maximize the movement of the lower hand while minimizing the movement of the
upper hand. The goal in relaxed breathing is for patients to extend the outbreath
and to make it slow and even, with exhalation taking approximately twice as long (6
seconds) as inhalation (3 seconds). Other forms of breathing exercises include slight
variations on this procedure. For example, in deep breathing, the patient takes several
deep breaths, holding each breath for 5 seconds before slowly exhaling; in paced
respiration, patients are taught to maintain slow breathing via the use of a metronome
or some other external pacing device. In breathing retraining (Craske & Barlow,
2006), patients are led to hyperventilate first to demonstrate the physiological effects
of fast, shallow breathing compared to slow, deep breathing. It is of note that these
techniques are very portable, and patients are typically encouraged to practice them
frequently throughout the day both at predetermined intervals and particularly in
response to stressful situations.
Research. Fried (1993) detailed the link between deep, diaphragmatic breathing and
the relaxation response, particularly in opposition to hyperventilation, and provided a
technical account of breathing techniques and their psychophysical effects. Decades
of studies on breathing exercises (e.g., deep breathing, diaphragmatic breathing,
abdominal breathing, breathing retraining) suggest that long, slow breaths produce
reliable autonomic activation consistent with the relaxation response (Benson et al.,
1975; Busch, Magerl, Kern, Haas, Hajak, & Eichhammer, 2012; Pal, Velkumary,
& Madanmohan, 2004). Support for the efficacy of breathing relaxation has been
found for a number of stress-related health conditions, such as hypertension (Mourya,
Mahajan, Singh, & Jain, 2009), pain (Busch et al., 2012), and psychological conditions
(Kim & Kim, 2005), especially panic (Schmidt et al., 2000).
Guided Imagery
Historical roots and theory. Guided imagery (GI) has a long history and may be traced
back to Ancient Greece as well as Native American and other indigenous cultures, var-
ious religious groups, and Chinese medicine. The origins of GI are extremely diverse,
potentially explaining why definitions of this technique are inconsistent across helping
disciplines (Menzies & Taylor, 2004). Many current therapies, including various
forms of meditation, biofeedback, autogenic training, and hypnosis, incorporate GI
techniques. As an overarching concept, imagery has been described as “any thought
representing a sensory quality” (Joseph, 2004, p. 12), though other definitions have
also been proposed (see Menzies & Taylor, 2004). In conceptualizing GI, Ahsen
(1968) theorized that personality and consciousness are fundamentally made up of
images. GI is believed to elicit therapeutic change in numerous disorders by identify-
ing and changing distorted images associated with the primary characteristics of the
disease or dysfunction. In this respect, Ahsen’s theory is similar to Beck’s cognitive
model (Beck, Rush, Shaw, & Emery, 1979). Hence, perhaps the defining feature of
GI lies in creating a vivid image in the mind of some desired place/state that as closely
as possible mirrors how that place/state would actually be experienced in real life.
Clinical practice. In GI, the therapist encourages the patient to engage in visualizing
images using all the senses (visual, auditory, olfactory, tactile, and gustatory). The
rationale behind inclusion of all the senses is that it will render the imagery more
vivid and real. Usually, the content of the GI session is determined by the patient’s
own description of his or her symptoms. For example, a patient may describe her
chronic headache symptoms to her therapist by saying that the muscles in her neck
area feel like a tightly coiled rope. The therapist may then include imagery within the
session that guides the patient to visualize the muscles in her neck as a coiled rope
that is slowly uncoiling, lengthening, and smoothening out. GI is also used to assist
patients to relax by creating personalized, mental images of a passive, relaxing setting
or activity, often accompanied by a repetitive self-statement or relaxing words. Pairing
the scene with a relaxing word provides a cue for the patient which, after sufficient
pairings, may be used to bring the relaxing scene to mind quickly during stressful
times.
Research. The flexibility and variability of GI leads it to suffer from poor standard-
ization across research implementations. However, GI has been shown to reduce
stress and increase immunity (Trakhtenberg, 2008; Watanabe et al., 2006), and
there is evidence that it is likely helpful in a wide range of disorders that include
stress-related physical conditions, such as heart surgery (Casida & Lemanski, 2010),
cancer (Kwekkeboom, Wanta, & Bumpus, 2008), and pain (Posadzki & Ernst,
2011), and psychological problems, such as anxiety and depression (Apóstolo &
Kolcaba, 2009), among many others. The reader is referred to the Academy for
Guided Imagery for more information and for an extensive list of efficacy studies
(www.academyforguidedimagery.com/).
Progressive Muscle Relaxation

Historical roots and theory. Edmund Jacobson, the pioneer of progressive muscle
relaxation (PMR), built his approach upon the fundamental premise that in order
to achieve full relaxation, a patient must first be able to differentiate between the
muscular sensations of tension (i.e., shortened/contracted muscle fibers) versus
relaxation (i.e., lengthened muscle fibers). In its original format, this version of
PMR frequently required over 100 therapy sessions to allegedly master the technique.
Consequently, this original method is rarely implemented in its full form within current
clinical practice and research. Joseph Wolpe (1958) adapted Jacobson’s protocol
to develop a more condensed, streamlined approach, referred to as abbreviated
progressive muscle relaxation (APMR) therapy, in which multiple muscle groups
undergo relaxation training simultaneously. Wolpe included therapeutic suggestions
to create strong tension in targeted muscle groups followed by release of that tension
with the rationale that this procedure would assist patients in discriminating muscular
tension from muscular relaxation. Bernstein and Carlson (1993) later labeled this
technique the tension–release cycle. Thus, the factors that distinguish APMR from
PMR are (a) multiple muscle groups are targeted simultaneously, (b) therapeutic
suggestion is commonly used, and (c) tension–release cycles are implemented with
each muscle group targeted. Öst (1987) later used APMR as the foundation for a
brief, standardized relaxation protocol named applied relaxation, which integrates
multiple relaxation theories to build rapid, reliable relaxation skills in patients. Below,
we focus on the abbreviated approach and use the term PMR to indicate APMR,
which is also consistent with the present literature.
Clinical practice. First standardized by Bernstein and Borkovec (1973) and

updated by Andrasik (1986), basic PMR teaches a patient to engage in a series of
tension–release cycles with each tension phase lasting approximately 5–7 seconds
and each release/relaxation phase lasting 20–30 seconds. Once the patient obtains
the sensation of the muscle group fully relaxed, then the next muscle group is
targeted. The sequence of muscle groups moves from the hands to the head, and
then down to the feet. For information on the specific muscles contained in each
group targeted, the reader is referred to Rime and Andrasik (2011). Typically, two
tension–release cycles per major muscle group are all that is necessary for the patient
to report complete relaxation in that muscle group. However, therapist instructions
assert that it is clinically important that the patient report no remaining tension before
proceeding to the next muscle group; thus, in some cases more repetitions may be
needed. Patients may also report difficulty releasing their muscles after contraction,
which may necessitate switching to a different technique. In some abbreviated
protocols, guided imagery (described above) is also incorporated to assist the patient
with the relaxation process (Bernstein & Borkovec, 1973; Cautela & Gordon, 1978).
Research. PMR has been shown to reduce mental and physiological signs of stress
in a variety of populations ranging from college students (Dolbier & Rush, 2012)
to inpatients with severe psychological disturbance (Vancampfort et al., 2011). PMR
shows some evidence of efficacy with stress-related physical conditions such as pain
(Emery, France, Harris, Norman, & Van Arsdalen, 2008) and psychological condi-
tions such as anxiety and depression (Lolak, Connors, Sheridan, & Wise, 2008). In an
extensive review of PMR, Carlson and Hoyle (1993) found evidence for the efficacy
of PMR in a wide range of health conditions including chronic migraine and tension
headache, tinnitus, cancer chemotherapy symptoms, hypertension, depression, neck
pain, low back pain, stress/stress-reactions, and others. McCallie, Blum, and Hood
(2006) also reported empirical support for the use of PMR in insomnia; headache;
anxiety, depression, and distress in cancer patients; irritable bowel syndrome; and
arthritis pain; but not for chronic obstructive pulmonary disease or chronic neck
pain. The applied relaxation protocol developed by Öst (1987) has been used for the
treatment of a range of disorders including specific phobias, panic disorder, headache,
pain, epilepsy, and tinnitus. It appears particularly efficacious for anxiety disorders,
especially generalized anxiety disorder, for which it shows equivalent treatment effects
to cognitive behavioral therapy (e.g., Dugas et al., 2010).
Biofeedback
Historical roots and theory. Biofeedback is a relatively “young” relaxation approach in
that it was not examined empirically until the 1960s. Early pioneers of this approach
included Neal E. Miller and his colleagues at Yale. However, it was the work of Lee Birk
(1973) in the first medical text on biofeedback that led to the technique we know
today. Fundamentally, “biofeedback is a technique in which biologic information
about the self is used to modify, correct, or strengthen processes within the self”
(Andrasik & Lord, 2008, p. 192). Thus, the two distinguishing characteristics of
biofeedback are the use of instrumentation and the provision of feedback/information.
The overarching goal of biofeedback is to increase patient awareness of and influence
over two kinds of psychophysiological processes: (a) processes typically not under
voluntary control, and (b) processes that are ordinarily easy to regulate but that,
due to some disease process, have broken down (NIH Technology Assessment
Panel, 1996). In this way, biofeedback is able to assist patients in altering abnormal
physiological processes to engender a healthier level of function.
Clinical practice. Biofeedback interventions utilize a variety of technological monitor-

ing instruments that are used in isolation or in combination and that vary in degree of
sophistication. Examples of current technology include electromyography, electroen-
cephalography, thermometers, and galvanometry. For general relaxation purposes,
three modalities are typically used to monitor and provide feedback regarding phys-
iological manifestations of the relaxation response: (a) muscular feedback, indicating
reduced muscular tension, (b) thermal feedback, indicating increased peripheral blood
flow, and (c) skin-conductance biofeedback, indicating reduced sweat-gland activity
(Andrasik & Lord, 2008). In a standard implementation, sensors are placed on tar-
geted anatomical regions of the body to detect localized physiological activity and
transmit this information to a monitoring instrument. The monitoring instrument,
often a computer, electronically processes the input received from the sensors and
converts the bioelectrical signals to a visual or auditory cue for the patient. The cue
provides feedback on changes in the patient’s individual physiological markers. By
this means, the patient increases his or her awareness of autonomic physiological
processes and gradually learns by trial and error to influence such processes until
they come under voluntary control. A key aspect of biofeedback-aided relaxation
therapy is that patients learn to manage their stress levels through biofeedback. This
focus on individualized training reduces standardization across patients and studies
(Yucha & Montgomery, 2008), yet the approach used by biofeedback is standardized
and reinforces patient-specific relaxation signals, whether those are cognitive, as in
guided imagery, or behavioral, as in progressive muscle relaxation (see Schwartz &
Andrasik, 2003). For a more in-depth, comprehensive instruction on biofeedback,
the interested reader is encouraged to consult Chapter 13 (“Neurofeedback”), as well
as Andrasik and Lord (2008), Schwartz and Andrasik (2003), Andreassi (2007), and
Stern, Ray, and Quigley (2001). Board certification is available from the Biofeedback
Certification International Alliance for clinicians who wish to instruct in biofeedback
as a therapeutic technique (www.bcia.org).
Research. Biofeedback is a widely used clinical technique that has been recognized
by the American Psychological Association (APA) as a clinical proficiency since 1997
(APA, 2012). Biofeedback-aided relaxation techniques have been supported in a
wide range of stress-related psychological and medical conditions. In an extensive
review of the literature, the Association for Applied Psychophysiology and Biofeed-
back evaluated the empirical basis for biofeedback in a range of conditions (Yucha &
Montgomery, 2008). They concluded that there is sufficient evidence that biofeed-
back is “efficacious” for anxiety, attention-deficit/hyperactivity disorder, chronic
pain, epilepsy, headache, hypertension, motion sickness, Raynaud’s disease, and tem-
poromandibular disorder. Conditions for which biofeedback was listed as “probably
efficacious” included alcoholism/substance abuse, arthritis, diabetes mellitus, insom-
nia, traumatic brain injury, and vulvar vestibulitis. Biofeedback-aided relaxation was
not found to have specific effects for any condition. Nevertheless, some research
suggests modest additive benefits from the addition of biofeedback to relaxation, as

for tension headache (Nestoriuc, Martin, Rief, & Andrasik, 2008), whereas others
have found little evidence for the specific efficacy of biofeedback, as in hypertension
(Greenhalgh, Dickson, & Dundar, 2010) and labor pain (Barragán Loayza, Solà, &
Juandó Prats, 2011). More research is needed to determine the specific benefits of
biofeedback to treatment effects and/or maintenance.
Autogenic Training
Historical roots and theory. Developed in Berlin at the beginning of the twentieth
century, autogenic training (AT) was formally described by Johannes Schultz in the
early 1930s. Schultz proposed that guiding the patient to think key self-statements
about autonomic nervous system changes associated with relaxation could actually
elicit physiological changes related to the relaxation response. He hypothesized
that guiding patient thoughts in this way subsequently led to changes in blood flow,
feelings of warmth, a sensation of heaviness, and a promoted sense of relaxation. Thus,
the distinguishing component of AT is that it aims to focus a patient’s attention, with
or without words, on physiological sensations that lead to the desired decreases in
autonomic arousal.
Clinical practice. Schultz and Luthe (1969) later developed a sequence of basic
focusing instructions that are commonly implemented when engaging patients in
AT. Initially, patients are guided to imagine a peaceful and relaxing environment
(see GI section above); following this, therapist instruction is tailored to engender
the six following relaxing bodily sensations: heaviness in the extremities (targeting
reduced skeletal muscle tension); warmth in the extremities (targeting increased
blood flow/vasodilation); slow and regular heartbeat (targeting cardiac regulation);
smooth, even, relaxed breathing (targeting regulation of the breath); warmth in the
upper abdomen (targeting regulation of visceral organs); and coolness in the forehead
(targeting increased peripheral blood flow). As patients become more adept and
familiar with AT, it is recommended that the patient personalize the phrases that
are designed to elicit heaviness and warmth to increase their salience. Alternatively,
patients may prefer to visualize images (rather than use verbal content) that correspond
with and elicit each of the physiological sensations associated with Schultz’s formulas.
For example, patients may visualize themselves basking their arms and legs in warm
sunlight or letting cool water flow over their foreheads.
Research. Decades of investigation support AT for eliciting the physiological relax-

ation response (Schultz & Luthe, 1969), and AT has been used therapeutically for a
wide range of difficulties. In a quantitative review of 67 years of AT studies, Stetter
and Kupper (2002) found evidence for the efficacy of AT in tension or migraine
headache, hypertension, coronary heart disease, asthma, pain disorder, Raynaud’s
disease, bowel disease, fibromyalgia, eczema, anxiety, sleep disorders, alcoholism, and
depression. More recent evidence has shown the salutary effects of AT on anxiety
(Kanji, White, & Ernst, 2004), irritable bowel syndrome (Shinozaki et al., 2010),
headache and pain medication usage in migraine (Juhasz et al., 2007; Zsombok,
Juhasz, Budavari, Vitrai, & Bagdy, 2003), and insomnia, anxiety, and depression in
those with comorbid chronic illness (Bowden, Lorenc, & Robinson, 2012).
Hypnosis
Historical roots and theory. The origins of hypnosis can be traced back to times
predating written language, but Milton Erikson, often considered the father of
modern hypnosis, was one of the first to emphasize the necessity to empirically
examine the process, state, and products of hypnosis. His experimental studies
effectively established hypnosis as a bona fide therapeutic technique. In the literature,
the hypnotic state is characterized by neurophysiological changes related to deep
relaxation, focused attention, vivid imagery, reduction of discursive thought, and
most importantly, increased receptivity to therapeutic suggestion (Faymonville, Boly,
& Laureys, 2006). Debate continues as to whether hypnosis is (a) a unique form
of mental processing in which altered states of consciousness are achieved (i.e., the
neodissociation model; see Hilgard, 1986, 1992, for details), or (b) a placebo effect
that can be simply understood in terms of an individual’s suggestibility, positive
attitudes, and expectations (i.e., the social-psychological model; see Spanos & Coe,
1992). It suffices clinically to understand that the characteristic benchmark of a
hypnotic induction is an increase in the patient’s responsiveness to therapeutic
suggestions and, for our purposes, that those suggestions can generate relaxed states.
Clinical practice. Generally the hypnotic induction procedure has three components:
(a) a presuggestion phase, (b) a suggestion phase, and (c) a postsuggestion phase.
During the presuggestion phase, the therapist focuses the patient’s attention and elicits
the relaxation response, typically via the use of a combined relaxation technique such
as deep breathing or guided imagery. Deepening techniques are often used, offering
suggestions that the patient is descending a staircase with accompanying instructions to
feel progressively deeper relaxation with each downward step. During the suggestion
phase, the therapist makes individually tailored, goal-specific suggestions targeted
toward the patient’s symptom(s). It is important to note here that a patient will not
submit to a suggestion that is incompatible with his or her wishes or desires. The
postsuggestion phase is designed to promote and prolong the hypnotic suggestions
after the intervention (e.g., suggestions of maintained relaxation). Posthypnotic cues
are also sometimes prepared. For example, Patterson, Everett, Burns, and Marvin
(1992) described giving a patient with burn pain a cue for comfort and relaxation
during subsequent dressing changes that was anchored by touching the patient’s
shoulder. Following the postsuggestion phase, the therapist gradually brings the
patient back out of the deep relaxation state. In self-hypnosis practice, which is often
recommended for the patient postsession, patients guide themselves through the
hypnosis induction, generally consisting of each of the three steps noted above, and
provide their own hypnotic suggestions. Clinically, hypnosis has been used to generate
the relaxation response, both as a direct intervention and in the process of providing a
disorder-specific intervention. As a result, hypnosis usually utilizes protocols generated
for the disorder being treated (Palsson, 2006). Board certification in clinical hypnosis
is available through the American Society of Clinical Hypnosis (www.asch.net).
Research. Research provides support for the clinical use of hypnosis and self-hypnosis
in the treatment of a range of physiological and psychological disorders. In a recent
comprehensive critical review of hypnosis as an adjunct to medical care for a wide
range of conditions (the heterogeneity precluded a statistic analysis of effects),
Pinnell and Covino (2000) found evidence that hypnosis improves health-care-
related anxiety, asthma in those with high hypnotizability, dermatological diseases,
irritable bowel syndrome, hemophilia, nausea and emesis in cancer treatment, and
obstetric/gynecological treatment. More recent research supports its use in depression
(Shih, Yang, & Koo, 2009), medical distress (Schnur, Kafer, Marcus, & Montgomery,
2008), state anxiety, headache, and irritable bowel syndrome (Hammond, 2010). The
recent findings for pain conditions are particularly robust, representing an important
area of future research (M. P. Jensen, 2010), and show evidence of efficacy for pain
related to cancer treatment (Coveney, Grieve, & Kumar, 2011), labor and childbirth
(Landolt & Milling, 2011), major burns (Berger et al., 2010), multiple sclerosis
(M. P. Jensen et al., 2009), spinal cord injury (M. P. Jensen et al., 2010), chronic
widespread pain (Grøndahl & Rosvold, 2008), and temporomandibular disorder
and breast cancer pain (Nash & Tasso, 2010), among others. In addition, evidence
suggests that hypnosis may be more effective for chronic pain than other treatments
(Dillworth & Jensen, 2010) and that individuals with low susceptibility may be trained
to respond better to hypnotic interventions (Batty, Bonnington, Tang, Hawken, &
Gruzelier, 2006). However, recent evidence also suggests that hypnotherapy may not
be as effective as previously thought for some treatments such as smoking cessation
(Barnes et al., 2010).
Meditation
Historical roots and theory. Meditative relaxation techniques have historical roots
across numerous religious contexts including Christianity, Judaism, Shintoism, Tao-
ism, Sufism, and Buddhism (Benson, Kotch, Crassweller, & Greenwood, 1977).
A number of meditation techniques have been implemented clinically, including
concentration meditation, transcendental meditation, and mindfulness meditation.
Currently, the most widely used meditation technique in therapeutic settings is the
subgroup of practices falling under the umbrella of mindfulness meditation. Among
the conceptual definitions of mindfulness that have been proposed (e.g., Bishop,
2002; Shapiro, Carlson, Astin, & Freedman, 2006), Jon Kabat-Zinn, the founder of
mindfulness-based approaches within the Western (allopathic) medical community,
describes mindfulness simply as “the awareness that emerges through paying atten-
tion on purpose, in the present moment, and non-judgmentally to the unfolding
of experience, moment by moment” (Kabat-Zinn, 2003, p. 145). The theory sug-
gests that, by focusing mindful, nonjudgmental awareness on moment-to-moment
experience, one retrains attentional processes and cultivates a persistent ability to
respond with choice rather than react automatically (Kabat-Zinn, 1990), while also
generating the relaxation response (Benson et al., 1975; Mohan, Sharma, & Bijlani,
2011). Specifically, what distinguishes mindfulness meditation from other relaxation
techniques is its explicit focus on training the mind to reduce emotional and behav-
ioral reactivity theoretically linked to stress and a number of health complications.
Currently, meditation for relaxation purposes is often taught within the context of
a standardized, group-delivered, mindfulness-based stress reduction (MBSR) proto-
col (Kabat-Zinn, 1990) and instructor certification is available from the Center for
Mindfulness (http://www.umassmed.edu/cfm).
Clinical practice. Mindfulness-based therapeutic approaches typically teach patients a

variety of mindfulness meditation practices that are designed to enhance the transfer
of training to everyday life. The primary difference between each of the techniques
is the object of one’s focused attention. Patients may be instructed to be aware of
the sensation of taste, physical sensations, movements (as with yoga and walking
meditation), the breath as it enters and leaves the body, sounds, and, eventually, the
arising and passing away of thoughts. The premise of mindfulness meditation is not
necessarily to gain deep insight (although this may happen over time); rather, it is
simply to notice whatever arises without reacting with attachment or aversion. Patients
are instructed just to label the phenomenon (e.g., “thinking”), and then return to
the focus (e.g., the movements of the breath). Within any given meditation practice,
distraction in any number of forms (e.g., thoughts, sounds, painful sensations) is not
seen as a problem but is rather viewed as an opportunity to notice that the mind has
wandered and then, calmly and nonjudgmentally, return to the focal object. For more
information, see Chapter 7, “Mindfulness and Acceptance Techniques.”
Research. Although meditation in a variety of formats has been found to be clinically

useful (Chiesa & Serretti, 2010), mindfulness meditation is typically researched
within the context of MBSR. Currently, it is unclear which benefits of mindfulness
are attributable to meditation-specific cognitive effects (Chiesa & Serretti, 2010; Jha,
Krompinger, & Baime, 2007) or a generalized relaxation response. Nevertheless,
studies have supported the efficacy of MBSR in the treatment of a variety of stress-
related physiological and psychological symptoms (Chiesa & Serretti, 2009). Recent
reviews have reported efficacy for psychological conditions (Bohlmeijer, Prenger, Taal,
& Cuijpers, 2010; Keng, Smoski, & Robins, 2011), for medical conditions (Shigaki,
Glass, & Schopp, 2006), and in comorbid populations reporting an array of both
psychological and medical conditions (Baer, 2003; Grossman, Niemann, Schmidt, &
Walach, 2004).
Clinical Considerations across Techniques

Relaxation techniques are a core tool of psychotherapy and are generally considered
helpful and low in risk. They are regularly employed in a variety of approaches
to elicit a relaxation response, reduce stress, and help patients engage in adaptive
coping. However, it is important to note that the use of relaxation may not always
be beneficial. Although specific contraindications are rare, considerations related to
the characteristics of the therapist, patient, and relaxation play an important role in
the clinical implementation of relaxation across techniques. The reader is referred to
Smith (2005) and Schwartz, Schwartz, and Monastra (2003) for detailed discussions
of clinical cautions in the use of relaxation.
As with other therapeutic interventions, both evidence-based practice and ethical

standards mandate that therapists have both the skill and expertise to deliver a therapy
in a competent manner, although the preferred techniques for each therapist will likely
be different. It is therefore important that therapists become proficient in a range
of techniques to determine those that fit best within their practice. Furthermore,
in the United States, credentialing organizations exist to ensure competence for
several of the relaxation modalities (e.g., Biofeedback Certification International
Alliance), and professional organizations may also evaluate specific techniques for
special designations (e.g., the APA Commission for the Recognition of Specialties
and Proficiencies in Professional Psychology recognizes biofeedback as a professional
proficiency; APA, 2012). Although practitioners are not prohibited from using most
techniques without certification, ethical standards require practice within defined
boundaries of training and expertise (APA, 2010). Thus, practitioners who use
a technique regularly should consider credentialing as a method of ensuring and
demonstrating professional competence and ethical practice.
Despite its relatively low risk as a therapeutic technique, some patient populations
may present with factors that influence treatment; therefore, such factors should
be carefully considered prior to commencing relaxation therapy. Patient character-
istics such as low positive expectation or trust, poor motivation or engagement, or
emotional dysfunction can hinder the formation of a working alliance (Halperin,
Weitzman, & Otto, 2010). Similarly, patients with severe psychological dysfunction
or dysregulation, conditions that significantly impair cognition or attention, acute
agitation, or active substance abuse may not benefit from some or all of these tech-
niques due to difficulties engaging cognitively or managing distraction. Patients with
a trauma history may especially benefit from efforts at building safety and trust before
attempting relaxation. When medical or other physical conditions are present, the
choice between techniques—or if to use them at all—is particularly important as
some may offer lower risk to patients than others. Physician supervision is important
in cases where the patient’s health may be adversely affected by treatment. Relaxation
should be selected carefully when using deep breathing with respiratory conditions or
after chest/abdominal surgery; PMR with pain, physical conditions, or injury; or AT
following heart surgery, as examples. Patients may also express concern about specific
techniques due to cultural, religious, or personal reasons, such as concern about the
religious roots of meditation. Such negative reactions also carry the potential to erode
the therapeutic alliance and disrupt therapy permanently, emphasizing the importance
of respecting patient preference in choosing a specific relaxation technique to deliver.
Given these considerations, the choice of relaxation technique clearly involves collab-
orative, careful decision making and underscores the importance of having a range of
techniques to choose from during the selection process.
During relaxation therapy, the therapist should engage in continued assessment
of patient response as some negative patient reactions have been associated with the
practice of relaxation and thus warrant caution. Schwartz et al. (2003) identified five
categories of unpleasant phenomena linked with relaxation, including musculoskele-
tal activity (e.g., cramps), disturbing sensory experiences (e.g., depersonalization),
sympathetic nervous system activity (e.g., elevated heart rate), disturbing cognitive
and/or emotional reactions (e.g., intrusive thoughts, anxiety), and other negative
experiences (e.g., headache, sexual arousal). Schwartz et al. also noted that, for a small
number of patients, relaxation produces a paradoxical negative emotional state called
relaxation-induced anxiety, characterized by intense feelings of anxiety and associated
physical symptoms (Astin et al., 2003). Consequently, it is important to use relaxation
cautiously with patients who are highly anxious or afraid of ceding control (Braith,
McCullough, & Bush, 1988). Similarly, transient negative experiences, such as nausea
and headache, have been reported by some patients using specific relaxation therapies,
especially hypnosis (Astin et al., 2003). Relaxation therapy can produce undesirable
effects in patients with a history of trauma, dissociation, psychotic breaks, or seizures,
particularly when using techniques that emphasize internal cognitive focus such as
GI (Harding, 1996; Smith, 2005). Meditation relaxation has also been reported to
trigger psychotic or manic symptoms in vulnerable individuals (Kuijpers, van der Hei-
jden, Tuinier, & Verhoeven, 2007; Yorsten, 2001), and GI may reinforce maladaptive
coping patterns in those who use fantasy for avoidance (Smith, 2005). Some evidence
exists to suggest that relaxation interventions for severe anxiety disorders such as
panic may be linked to worse outcomes in some patients by reducing the effectiveness
of exposure interventions (Schmidt et al., 2000). This finding led Lilienfeld (2007)
to categorize relaxation training as a treatment for panic disorders that “possibly
produces harm in some individuals.” Barlow, Allen, and Choate (2004) suggest in
their unified protocol for emotional disorders that relaxation techniques used by
patients for emotional avoidance may erode the therapeutic effects of psychosocial
treatment. This is particularly noteworthy given the common use of relaxation as an
early module in cognitive behavioral therapy.
Thus far, we have described the various elements and factors that are important
to consider in relation to therapeutic relaxation, as well as providing descriptions
of the most widely used relaxation techniques. In the final section, we attempt to
make some connections between what has been discussed and provide a commentary
on the current state of the evidence in regard to therapeutic relaxation and some
needed future directions. Furthermore, singular relaxation techniques are typically
not delivered as a stand-alone treatment; thus we discuss various integrated relax-
ation treatment programs and the ways in which specific techniques are sometimes
combined.
Commentary and Conclusions
Evidence from studies evaluating a wide variety of therapeutic relaxation techniques

indicates that they are clearly efficacious in enhancing a subjective state of relaxation
and well-being and reducing the psychophysiological stress response. These outcomes,
in turn, have been shown to lead to reductions in symptoms associated with a
variety of stress-related disorders, as well as specific mental disorders. However, the
relative benefit of one relaxation technique over another has, in general, not been
substantiated. All the techniques presented in this chapter appear to engage the same
physiological pathway eliciting Benson’s relaxation response; thus, differentiating the
state achieved through deep breathing from those elicited by AT or mindfulness
may be a relatively futile exercise. Nevertheless, some have suggested that different
techniques might produce meaningful, specific differences in therapeutic effects.
In a comparative review of relaxation studies that appears not to have been repeated
since, Lehrer, Carr, Sargunaraj, and Woolfolk (1994) cited some evidence (a) for
specific therapeutic effects when a technique was matched to the desired outcome
in the domains of muscular, autonomic, or cognitive activity, and (b) for localized
effects to be greater than generalized effects at specific locations (e.g., index finger in
thermal biofeedback vs. generalized AT). This would suggest that a patient learning
relaxation to manage tension headaches would respond better to PMR than other,
more generalized relaxation interventions. Despite its intuitive logic, evidence for this
degree of specificity has minimal support. For example, in a large meta-analysis of
studies using biofeedback for headache patients, temperature biofeedback resulted in
significant improvements in migraine headache frequency when compared to wait-list
controls, but these gains were not significantly different from other forms of relaxation
(Nestoriuc et al., 2008). In the same meta-analysis, electromyographic biofeedback in
tension-type headaches produced evidence of strong efficacy compared to placebo, but
evidence of greater efficacy for biofeedback over relaxation therapies produced only a
small effect size (Nestoriuc et al., 2008). Similarly, there is little research to establish
the specificity of mindfulness training on theorized changes in cognition instead of (or
in addition to) a cumulative relaxation response (Chiesa & Serretti, 2009; Dobkin &
Zhao, 2011; Hölzel et al., 2011; Jain et al., 2007; C. G. Jensen, Vangkilde, Frøkjær,
& Hasselbalch, 2012). Further, there is no consensus in the mindfulness literature
on the necessary amount of practice needed to achieve observed effects (Carmody &
Baer, 2008, 2009; Zeidan, Johnson, Diamond, David, & Goolkasian, 2010). Thus, as
with many other biopsychosocial treatments that have been shown to be efficacious,
the process by which the desired outcomes are achieved is either quite general (i.e.,
eliciting the relaxation response) or has not yet been specified.
Nevertheless, relaxation techniques are an increasingly important part of modern
therapeutic paradigms. Cognitive behavioral therapy has long used relaxation exercises
as modular interventions that were often included in standard treatment. In programs
such as MBSR (Kabat-Zinn, 1990) and mindfulness-based cognitive therapy a variety
of meditation techniques are taught. Increasingly, variations on the general cognitive
behavioral therapy approach, such as acceptance and commitment therapy and dialec-
tical behavior therapy, present mindfulness techniques as core treatment components.
Even physical interventions, such as yoga, tai chi, qigong, exercise, and others are now
being promoted as offering health benefits associated with the relaxation response
in addition to those accrued from physical activity alone. Given that we have little
information as to what forms of relaxation work best for different types of patients
or disorders, the increase in availability of a range of relaxation techniques is both
desirable and likely beneficial to patients. Furthermore, it may be quite valuable to
offer patients experience with a variety of relaxation techniques so that they may
choose what they feel most comfortable with.
In conclusion, a large number of relaxation approaches currently exist and (as
described above) there are as many different theoretical orientations on relaxation as
there are techniques. However, it is not known whether various relaxation techniques
work for the reasons specified by the associated theory. It is possible that we are
coming full circle to Benson’s original assertion that all relaxation interventions are
efficacious simply because they each serve to elicit shared biopsychosocial changes
broadly associated with the relaxation response. If this is the case, given that we
are operating within a health care system in which resources are scarce, it may
be prudent for less involved, more time-efficient forms of relaxation (i.e., possibly
breathing techniques) to become the standard of care. In order to justify expenditure
of additional resources beyond less involved approaches, we need to be able to
show that the patient and therapist resources devoted to a complex relaxation
approach not only produce larger outcomes/deeper relaxation than a less involved
approach, but that the more complex approach works via the hypothesized specific
mechanism.
Questions of how, for whom, and how much, are in critical need of answers, and
this is not just the case for relaxation therapies; research investigating these questions is
sorely needed for all current biopsychosocial treatment approaches. Answers to these
questions will result in (a) the development of streamlined interventions that distill
the true active principles of change, (b) the ability to match patients to the specific
treatment approach that is most likely to maximize benefit efficiently for the particular
individual, and (c) knowledge necessary to tailor treatment dose to specific patient
needs such that resources are maximized. Ultimately, to demonstrate the true public
health value of relaxation interventions and to foster acceptance and dissemination
of these approaches, we must be able to verify that the available relaxation treatment
protocols produce desirable outcomes and that they do so because of the therapeutic
procedures that the specific intervention entails.
References
Ahsen, A. (1968). Basic concepts in eidetic psychotherapy. New York, NY: Brandon House.
American Psychological Association. (2012). Recognized specialties and proficien-
cies in professional psychology. Retrieved from http://www.apa.org/ed/graduate/
specialize/recognized.aspx
American Psychological Association. (2010, June 1). Ethical principles of psychologists and
code of conduct: 2010 amendments. Retrieved from http://www.apa.org/ethics/code/
Andrasik, F. (1986). Relaxation and biofeedback for chronic headaches. In A. D. Holtzman &
D. C. Turk (Eds.), A handbook of psychological treatment approaches (pp. 213–239). New
York, NY: Pergamon.
Andrasik, F., & Lord, A. O. (2008). Biofeedback. In L. Freeman (Ed.), Mosby’s complementary
and alternative medicine: A research-based approach (3rd ed., pp. 189–214). Philadelphia,
PA: Mosby Elsevier.
Andreassi, J. L. (2007). Psychophysiology: Human behavior and physiological response (5th ed.).
Mahwah, NJ: Erlbaum.
Apóstolo, J. L. A., & Kolcaba, K. (2009). The effects of guided imagery on comfort, depression,
anxiety, and stress of psychiatric inpatients with depressive disorders. Archives of Psychiatric
Nursing, 23, 403–411. doi:10.1016/j.apnu.2008.12.003
Astin, J. A., Shapiro, S. L., Eisenberg, D. M., & Forys, K. L. (2003). Mind-body medicine:
State of the science, implications for practice. JABFM: Journal of the American Board of
Family Medicine, 16, 131–147. doi: 10.3122/jabfm.16.2.131
Baer, R. A. (2003). Mindfulness training as a clinical intervention: A conceptual and empi-

rical review. Clinical Psychology: Science and Practice, 10, 125–143. doi:10.1093/
clipsy.bpg015
disorders. Behavior Therapy, 35, 205–230. doi:10.1016/S0005-7894(04)80036-4
Barnes, J., Dong, C. Y., McRobbie, H., Walker, N., Mehta, M., & Stead, L. F. (2010).
Hypnotherapy for smoking cessation (Art. No.: CD001008). Cochrane Database of
Systematic Reviews, 10. doi:10.1002/14651858.CD001008.pub2
Barragán Loayza, I. M., Solà, I., & Juandó Prats, C. (2011). Biofeedback for pain management
during labour (Art. No.: CD006168). Cochrane Database of Systematic Reviews, 6.
doi:10.1002/14651858.CD006168.pub2
Batty, M. J., Bonnington, S., Tang, B.-K., Hawken, M. B., & Gruzelier, J. H. (2006).
Relaxation strategies and enhancement of hypnotic susceptibility: EEG neurofeedback,
progressive muscle relaxation and self-hypnosis. Brain Research Bulletin, 71, 83–90.
doi:10.1016/j.brainresbull.2006.08.005
Benson, H., Greenwood, M. M., & Klemchuk, H. (1975). The relaxation response: Psy-
chophysiologic aspects and clinical applications. International Journal of Psychiatry in
Medicine, 6, 87–98.
Benson, H., Kotch, J. B., Crassweller, K. D., & Greenwood, M. M. (1977). Historical and
clinical considerations of the relaxation response. American Scientist, 65, 441–445.
Berger, M. M., Davadant, M., Marin, C., Wasserfallen, J.-B., Pinget, C., Maravic, P., …
Chiolero, R. L. (2010). Impact of a pain protocol including hypnosis in major burns.
Burns, 36, 639–646. doi:10.1016/j.burns.2009.08.009
Bernstein, D. A., & Borkovec, T. D. (1973). Progressive relaxation training: A manual for the
helping professions. Champaign, IL: Research Press.
Bernstein, D. A., & Carlson, C. R. (1993). Progressive relaxation: Abbreviated methods. In
P. M. Lehrer & R. L. Woolfolk (Eds.), Principles and practice of stress management (2nd
ed., pp. 53–85). New York, NY: Guilford Press.
Birk, L. (1973). Biofeedback: Behavioral medicine. New York, NY: Grune and Stratton.
Bishop, S. R. (2002). What do we really know about mindfulness-based stress reduction?
Psychosomatic Medicine, 64, 71–83.
Bohlmeijer, E., Prenger, R., Taal, E., & Cuijpers, P. (2010). The effects of mindfulness-
based stress reduction therapy on mental health of adults with a chronic med-
ical disease: A meta-analysis. Journal of Psychosomatic Research, 68, 539–544.
doi:10.1016/j.jpsychores.2009.10.005
Bowden, A., Lorenc, A., & Robinson, N. (2012). Autogenic training as a behavioural approach
to insomnia: A prospective cohort study. Primary Health Care Research & Development,
13, 175–185. doi:10.1017/S1463423611000181
Bracha, H. S. (2004). Freeze, flight, fight, fright, faint: Adaptationist perspectives on the acute
stress response spectrum. CNS Spectrums, 9, 679–685.
Braith, J. A., McCullough, J. P., & Bush, J. P. (1988). Relaxation-induced anxiety in
a subclinical sample of chronically anxious subjects. Journal of Behavior Therapy and
Experimental Psychiatry, 19, 193–198. doi:10.1016/0005-7916(88)90040-7
Brodal, P. (2010). The central nervous system: Structure and function (4th ed.). New York, NY:
Oxford University Press.
Busch, V., Magerl, W., Kern, U., Haas, J., Hajak, G., & Eichhammer, P. (2012). The
effect of deep and slow breathing on pain perception, autonomic activity, and mood
processing: An experimental study. Pain Medicine, 13, 215–228. doi:10.1111/j.1526-

4637.2011.01243.x
Carlson, C. R., & Hoyle, R. H. (1993). Efficacy of abbreviated progressive muscle relaxation
training: A quantitative review of behavioral medicine research. Journal of Consulting &
Clinical Psychology, 61, 1059–1067. doi:10.1037/0022-006X.61.6.1059
Carmody, J., & Baer, R. A. (2008). Relationships between mindfulness practice and levels of
mindfulness, medical and psychological symptoms and well-being in a mindfulness-based
stress reduction program. Journal of Behavioral Medicine, 31, 23–33.
Carmody, J., & Baer, R. A. (2009). How long does a mindfulness-based stress deduction
program need to be? A review of class contact hours and effect sizes for psychological
distress. Journal of Clinical Psychology, 65, 627–638.
Casida, J., & Lemanski, S. A. (2010). An evidence-based review on guided imagery utilization
in adult cardiac surgery. Clinical Scholars Review, 3, 22–30. doi:10.1891/1939-
2095.3.1.22
Cautela, J. R., & Gordon, J. (1978). Relaxation: A comprehensive manual for adults, children,
and children with special needs. Champaign, IL: Research Press.
Chiesa, A., & Serretti, A. (2009). Mindfulness-based stress reduction for stress management
in healthy people: A review and meta-analysis. Journal of Alternative and Complementary
Medicine, 15, 593–600. doi:10.1089/acm.2008.0495
Chiesa, A., & Serretti, A. (2010). A systematic review of neurobiological and clin-
ical features of mindfulness meditations. Psychological Medicine, 40, 1239–1252.
doi:10.1017/S0033291709991747
Coveney, E., Grieve, M., & Kumar, B. (2011). Impact of therapeutic hypnosis on pain
and anxiety in patients undergoing breast cancer surgery. European Journal of Surgical
Oncology, 37 , 1002. doi:10.1016/j.ejso.2011.08.103
Craske, M. G., & Barlow, D. H. (2006). Mastery of your anxiety and panic: Therapist guide
Dillworth, T., & Jensen, M. P. (2010). The role of suggestions in hypnosis for chronic pain: A
review of the literature. Open Pain Journal, 3, 39–51.
Dobkin, P. L., & Zhao, Q. (2011). Increased mindfulness: The active component of the
mindfulness-based stress reduction program? Complementary Therapies in Clinical Prac-
tice, 17 , 22–27. doi:10.1016/j.ctcp.2010.03.002
Dolbier, C. L., & Rush, T. E. (2012). Efficacy of abbreviated progressive muscle relaxation
in a high-stress college sample. International Journal of Stress Management, 19, 48–68.
doi:10.1037/a0027326
Dugas, M. J., Brillon, P., Savard, P., Turcotte, J., Gaudet, A., Ladouceur, R., … Gervais,
N. J. (2010). A randomized clinical trial of cognitive-behavioral therapy and applied
relaxation for adults with generalized anxiety disorder. Behavior Therapy, 41, 46–58.
doi:10.1016/j.beth.2008.12.004
Emery, C. F., France, C. R., Harris, J., Norman, G., & Van Arsdalen, C. (2008). Effects
of progressive muscle relaxation training on nociceptive flexion reflex threshold in
healthy young adults: A randomized trial. Pain, 138, 375–379. doi:10.1016/j.pain.2008.
01.015
Engel, G. L. (1977). The need for a new medical model: A challenge for biomedicine. Science,
196, 129–136.
Esch, T., Fricchione, G. L., & Stefano, G. B. (2003). The therapeutic use of the relaxation
response in stress-related diseases. Medical Science Monitor: International Medical Journal
of Experimental and Clinical Research, 9, RA23–34.
Everly, G. S., Jr., & Lating, J. M. (2002). A clinical guide to the treatment of the human stress
response (2nd ed.). New York, NY: Kluwer.
Faymonville, M.-E., Boly, M., & Laureys, S. (2006). Functional neuroanatomy of the hyp-
notic state. Journal of Physiology-Paris, 99, 463–469. doi:10.1016/j.jphysparis.2006.
03.018
Freeman, L. (2008). Relaxation therapy. In L. Freeman (Ed.), Mosby’s complementary and
alternative medicine: A research-based approach (3rd ed., pp. 129–157). Philadelphia, PA:
Mosby Elsevier.
Fried, R. (1993). The psychology and physiology of breathing in behavioral medicine, clinical
psychology, and psychiatry. New York, NY: Plenum Press.
Greenhalgh, J., Dickson, R., & Dundar, Y. (2010). Biofeedback for hypertension:
A systematic review. Journal of Hypertension, 28, 644–652. doi:10.1097/HJH.
0b013e3283370e20
Grøndahl, J. R., & Rosvold, E. O. (2008). Hypnosis as a treatment of chronic widespread pain
in general practice: A randomized controlled pilot trial. BMC Musculoskeletal Disorders,
9, 124. doi:10.1186/1471-2474-9-124
Grossman, P., Niemann, L., Schmidt, S., & Walach, H. (2004). Mindfulness-based stress
reduction and health benefits: A meta-analysis. Journal of Psychosomatic Research, 57 ,
35–43. doi:10.1016/S0022-3999(03)00573-7
Halperin, D. M., Weitzman, M. L., & Otto, M. W. (2010). Therapeutic alliance and common
factors treatment. In M. W. Otto & S. G. Hofmann (Eds.), Avoiding treatment failures
in the anxiety disorder (pp. 51–66). doi:10.1007/978-1-4419-0612-0_4
Hammond, D. C. (2010). Hypnosis in the treatment of anxiety- and stress-related disorders.
Expert Review of Neurotherapeutics, 10, 263–273. doi:10.1586/ern.09.140
Harding, S. (1996). Relaxation: With or without imagery? International Journal of Nursing
Practice, 2, 160–162. doi: 10.1111/j.1440-172X.1996.tb00043.x
Hilgard, E. R. (1986). Divided consciousness: Multiple controls in human thought and action.
New York, NY: John Wiley & Sons, Inc.
Hilgard, E. R. (1992). Dissociation and theories of hypnosis. In E. Fromm & M. Nash (Eds.),
Contemporary hypnosis research (pp. 69–101). New York, NY: Guilford Press.
Hölzel, B. K., Carmody, J., Vangel, M., Congleton, C., Yerramsetti, S. M., Gard, T., &
Lazar, S. W. (2011). Mindfulness practice leads to increases in regional brain gray matter
density. Psychiatry Research: Neuroimaging, 191, 36–43. doi:10.1016/j.pscychresns.
2010.08.006
Jacobs, G. D. (2001). The physiology of mind-body interactions: The stress response and the
relaxation response. Journal of Alternative and Complementary Medicine, 7(Suppl. 1),
83–92. doi:10.1089/107555301753393841
Jain, S., Shapiro, S. L., Swanick, S., Roesch, S. C., Mills, P. J., Bell, I., & Schwartz, G. E.
R. (2007). A randomized controlled trial of mindfulness meditation versus relaxation
training: Effects on distress, positive states of mind, rumination, and distraction. Annals
of Behavioral Medicine, 33, 11–21. doi:10.1207/s15324796abm3301_2
Jensen, C. G., Vangkilde, S. A., Frøkjær, V. G., & Hasselbalch, S. (2012). Mindfulness training
affects attention—Or is it attentional effort? Journal of Experimental Psychology: General,
141, 106–123. doi:10.1037/a0024931
Jensen, M. P. (2010). A neuropsychological model of pain: Research and clinical implications.
Journal of Pain, 11, 2–12. doi:10.1016/j.jpain.2009.05.001
Jensen, M. P., Barber, J., Romano, J. M., Hanley, M. A., Raichle, K. A., Molton, I. R., …
Patterson, D. R. (2010). Effects of self-hypnosis training and EMG biofeedback relaxation
training on chronic pain in persons with spinal-cord injury. International Journal of

Clinical and Experimental Hypnosis, 57 , 239–268. doi:10.1080/00207140902881007
Jensen, M. P., Barber, J., Romano, J. M., Molton, I. R., Raichle, K. A., Osborne, T. L.,
… Patterson, D. R. (2009). A comparison of self-hypnosis versus progressive muscle
relaxation in patients with multiple sclerosis and chronic pain. International Journal of
Clinical and Experimental Hypnosis, 57 , 198–221. doi:10.1080/00207140802665476
Jha, A. P., Krompinger, J., & Baime, M. J. (2007). Mindfulness training modifies sub-
systems of attention. Cognitive Affective and Behavioral Neuroscience, 7 , 109–119.
doi:10.3758/CABN.7.2.109
Joseph, A. (2004). The impact of imagery on cognition and belief systems. European Journal
of Clinical Hypnosis, 5, 12–15.
Juhasz, G., Zsombok, T., Gonda, X., Nagyne, N., Modosne, E., & Bagdy, G. (2007). Effects
of autogenic training on nitroglycerin-induced headaches. Headache: The Journal of Head
and Face Pain, 47 , 371–383. doi:10.1111/j.1526-4610.2006.00718.x
Kabat-Zinn, J. (1990). Full catastrophe living: Using the wisdom of your body and mind to face
stress, pain and illness. New York, NY: Delacourt.
Kabat-Zinn, J. (2003). Mindfulness-based interventions in context: Past, present, and future.
Kanji, N., White, A. R., & Ernst, E. (2004). Autogenic training reduces anxiety after
coronary angioplasty: A randomized clinical trial. American Heart Journal, 147 , 508.
doi:10.1016/j.ahj.2003.10.011
Keng, S.-L., Smoski, M. J., & Robins, C. J. (2011). Effects of mindfulness on psychological
health: A review of empirical findings. Clinical Psychology Review, 31, 1041–1056.
doi:10.1016/j.cpr.2011.04.006
Kim, S.-D., & Kim, H.-S. (2005). Effects of a relaxation breathing exercise on fatigue in
haemopoietic stem cell transplantation patients. Journal of Clinical Nursing, 14, 51–55.
doi:10.1111/j.1365-2702.2004.00938.x
Kuijpers, H. J. H., van der Heijden, F. M. M. A., Tuinier, S., & Verhoeven, W. M. A. (2007).
Meditation-induced psychosis. Psychopathology, 40, 461–464. doi: 10.1159/000108125
Kwekkeboom, K. L., Wanta, B., & Bumpus, M. (2008). Individual difference variables
and the effects of progressive muscle relaxation and analgesic imagery interventions on
cancer pain. Journal of Pain & Symptom Management, 36, 604–615. doi:10.1016/
j.jpainsymman.2007.12.011
Landolt, A. S., & Milling, L. S. (2011). The efficacy of hypnosis as an intervention for labor
and delivery pain: A comprehensive methodological review. Clinical Psychology Review,
31, 1022–1031. doi:10.1016/j.cpr.2011.06.002
Lehrer, P. M., Carr, R., Sargunaraj, D., & Woolfolk, R. L. (1994). Stress management
techniques: Are they all equivalent or do they have specific effects? Biofeedback and
Self-Regulation, 19, 353–401.
Lilienfeld, S. O. (2007). Psychological treatments that cause harm. Perspectives on Psychological
Science, 2, 53–70. doi:10.1111/j.1745-6916.2007.00029.x
Lolak, S., Connors, G. L., Sheridan, M. J., & Wise, T. N. (2008). Effects of progressive
muscle relaxation training on anxiety and depression in patients enrolled in an outpa-
tient pulmonary rehabilitation program. Psychotherapy and Psychosomatics, 77 , 119–125.
doi:10.1159/000112889
McCallie, M. S., Blum, C. M., & Hood, C. J. (2006). Progressive muscle relaxation. Journal
of Human Behavior in the Social Environment, 13, 51–66. doi:10.1300/J137v13n03_04
McEwen, B. S. (2007). Physiology and neurobiology of stress and adaptation: Central role of
the brain. Physiological Reviews, 87 , 873–904. doi:10.1152/physrev.00041.2006
Menzies, V., & Taylor, A. L. (2004). The idea of imagination: An analysis of “Imagery”.
Advances, 20, 4.
Mohan, A., Sharma, R., & Bijlani, R. L. (2011). Effect of meditation on stress-induced changes
in cognitive functions. Journal of Alternative and Complementary Medicine, 17 , 207–212.
doi:10.1089/acm.2010.0142
Mourya, M., Mahajan, A. S., Singh, N. P., & Jain, A. K. (2009). Effect of slow-and fast-
breathing exercises on autonomic functions in patients with essential hypertension. Journal
of Alternative and Complementary Medicine, 15, 711–717. doi:10.1089/acm.2008.0609
Nash, M. R., & Tasso, A. (2010). The effectiveness of hypnosis in reducing pain and suffering
among women with metastatic breast cancer and among women with temporomandibular
disorder. International Journal of Clinical and Experimental Hypnosis, 58, 497–504.
National Center for Complementary and Alternative Medicine (2013, April). Relaxation
techniques for health: An introduction (NCCAM Pub No.: D461). Retrieved from
http://nccam.nih.gov/health/stress/relaxation.htm?nav=gsa
National Institutes of Health Technology Assessment Panel on Integration of Behavioral
and Relaxation Approaches into the Treatment of Chronic Pain and Insomnia (1996).
Integration of behavioral and relaxation approaches into the treatment of chronic pain
and insomnia. JAMA, 276, 313–318.
Nestoriuc, Y., Martin, A., Rief, W., & Andrasik, F. (2008). Biofeedback treatment for headache
disorder: A comprehensive efficacy review. Applied Psychophysiology & Biofeedback, 33,
125–140.
Öst, L.-G. (1987). Applied relaxation: Description of a coping technique and review of
controlled studies. Behaviour Research & Therapy, 25, 397–409. doi:10.1016/0005-
7967(87)90017-9
Pal, G. K., Velkumary, S., & Madanmohan. (2004). Effect of short-term practice of breathing
exercises on autonomic functions in normal human volunteers. Indian Journal of Medical
Research, 120, 115–121.
Palsson, O. S. (2006). Standardized hypnosis treatment for irritable bowel syndrome: The
North Carolina protocol. International Journal of Clinical and Experimental Hypnosis,
54, 51–64. doi:10.1080/00207140500322933
Patterson, D. R., Everett, J. J., Burns, G. L., & Marvin, J. A. (1992). Hypnosis for the
treatment of burn pain. Journal of Consulting and Clinical Psychology, 60, 713–717.
Pinnell, C. M., & Covino, N. (2000). Empirical findings on the use of hypnosis in medicine: A
critical review. International Journal of Clinical and Experimental Hypnosis, 48, 170–194.
doi:10.1080/00207140008410047
Poppen, R. (1998). Behavioral relaxation training and assessment (2nd ed.). Thousand Oaks,
CA: Sage.
Posadzki, P., & Ernst, E. (2011). Guided imagery for musculoskeletal pain: A systematic
review. Clinical Journal of Pain, 27 , 648–653. doi:10.1097/AJP.0b013e31821124a5
Rime, C., & Andrasik, F. (2011). Relaxation techniques and guided imagery. In S. D. Waldman
(Ed.), Pain management (2nd ed., pp. 967–975). Philadelphia, PA: Saunders/Elsevier.
Schmidt, N. B., Woolaway-Bickel, K., Trakowski, J., Santiago, H., Storey, J., Koselka,
M., & Cook, J. (2000). Dismantling cognitive-behavioral treatment for panic disor-
der: Questioning the utility of breathing retraining. Journal of Consulting & Clinical
Schnur, J. B., Kafer, I., Marcus, C., & Montgomery, G. H. (2008). Hypnosis to manage distress
related to medical procedures: A meta-analysis. Contemporary Hypnosis, 25, 114–128.
doi:10.1002/ch.364
Schultz, J. H., & Luthe, W. (1969). Autogenic therapy, Vol. 1: Autogenic methods. New York,
NY: Grune & Stratton.
Schwartz, M. S., & Andrasik, F. (Eds.). (2003). Biofeedback: A practitioner’s guide (3rd ed.).
Schwartz, M. S., Schwartz, N. M., & Monastra, V. J. (2003). Problems with relaxation and
biofeedback-assisted relaxation, and guidelines for management. In M. S. Schwartz & F.
Andrasik (Eds.), Biofeedback: A practitioner’s guide (3rd ed., pp. 251–264). New York,
NY: Guilford Press.
Shapiro, S. L., Carlson, L. E., Astin, J. A., & Freedman, B. (2006). Mechanisms of mindfulness.
Journal of Clinical Psychology, 62, 373–386.
Shigaki, C. L., Glass, B., & Schopp, L. H. (2006). Mindfulness-based stress reduction
in medical settings. Journal of Clinical Psychology in Medical Settings, 13, 209–216.
doi:10.1007/s10880-006-9033-8
Shih, M., Yang, Y.-H., & Koo, M. (2009). A meta-analysis of hypnosis in the treatment
of depressive symptoms: A brief communication. International Journal of Clinical &
Experimental Hypnosis, 57 , 431–442. doi:10.1080/00207140903099039
Shinozaki, M., Kanazawa, M., Kano, M., Endo, Y., Nakaya, N., Hongo, M., & Fukudo, S.
(2010). Effect of autogenic training on general improvement in patients with irritable
bowel syndrome: A randomized controlled trial. Applied Psychophysiology & Biofeedback,
35, 189–198. doi:10.1007/s10484-009-9125-y
Smith, J. C. (2005). Relaxation, meditation, and mindfulness. New York, NY: Springer.
Spanos, N., & Coe, W. (1992). A social psychological approach to hypnosis. In E. Fromm &
M. Nash (Eds.), Contemporary hypnosis research (pp. 102–130). New York, NY: Guilford
Press.
Stefano, G. B., Fricchione, G. L., & Esch, T. (2006). Relaxation: Molecular and physiological
significance. Medical Science Monitor, 12, HY21–31.
Stetter, F., & Kupper, S. (2002). Autogenic training: A meta-analysis of clinical outcome studies.
Applied Psychophysiology & Biofeedback, 27 , 45–98. doi:10.1023/A:1014576505223
Stern, R. M., Ray, W. J., & Quigley, K. S. (2001). Psychophysiological recording (2nd ed.). New
York, NY: Oxford University Press.
Trakhtenberg, E. C. (2008). The effects of guided imagery on the immune system: A
critical review. International Journal of Neuroscience, 118, 839–855. doi:10.1080/
00207450701792705
Vancampfort, D., De Herdt, M., Knapen, J., Maurissen, K., Raepsaet, J., Deckx, S., … Probst,
M. (2011). Effects of progressive muscle relaxation on state anxiety and subjective well-
being in people with schizophrenia: A randomized controlled trial. Clinical Rehabilitation,
25, 567–575. doi:10.1177/0269215510395633
Watanabe, E., Fukuda, S., Hara, H., Maeda, Y., Ohira, H., & Shirakawa, T. (2006). Differences
in relaxation by means of guided imagery in a healthy community sample. Alternative
Therapies in Health Medicine, 12, 60–66.
Press.
Yorsten, G. A. (2001). Mania precipitated by meditation: A case report and literature review.
Mental Health, Religion, & Culture, 4, 209–213. doi:10.1080/713685624
Yucha, C. B., & Montgomery, D. (2008). Evidence-based practice in biofeedback and
neurofeedback. Retrieved from http://www.dol.gov.edgekey-staging.net/ebsa/pdf/
MHPAEA258.pdf on July 13, 2013.
Zeidan, F., Johnson, S. K., Diamond, B. J., David, Z., & Goolkasian, P. (2010). Mindful-
ness meditation improves cognition: Evidence of brief mental training. Consciousness &
Cognition, 19, 597–605. doi:10.1016/j.concog.2010.03.014
Zsombok, T., Juhasz, G., Budavari, A., Vitrai, J., & Bagdy, G. (2003). Effect of autogenic
training on drug consumption in patients with primary headache: An 8-month follow-up
study. Headache: The Journal of Head and Face Pain, 43, 251–257. doi: 10.1046/j.1526-
4610.2003.03049.x
9
Attentional Bias Modification
Nader Amir and Sara Conley
San Diego State University, United States
Introduction
“Attention is the selective aspect of information-processing” (Kosslyn, Brown, &

Dror, 1999, p. 102). As this statement implies, what we attend to is what we
comprehend. Thus, it is not surprising that experimental psychopathologists have long
suspected a pivotal role for attention in different forms of psychopathology. In this
chapter we will examine basic models of attention (e.g., its components, automatic vs.
strategic attention, early vs. late attention) and the role of attentional bias in emotional
disorders. Finally, we will review attempts to use the basic knowledge gained from the
role of attentional bias in anxiety and depression to develop novel treatments for these
disorders. We will close this chapter with suggestions for future directions for the field.
Basic Models of Attention
Daily life is replete with examples of the importance of attention in our well-being.
For example, most of us have an attentional bias for our names. This biased attention
serves the basic need to be hypervigilant when information that is likely relevant to
us is present in our environment. Moreover, this bias is present both during waking
and sleep states. For example, a person’s name is more likely to wake her or him from
sleep than other words heard at similar sound volumes. This notion is supported by
experimental studies. Moray (1959) for instance, used a dichotic listening task to test
attentional bias for one’s own name. During the task participants heard two messages,
one in each ear, and were told to attend to one of the messages by repeating it out
loud and ignoring the other message. When asked to recall the message that they
were repeating, participants often remembered some information from the passage

DOI: 10.1002/9781118528563.wbcbt09
that they were told to ignore. Moray (1959) found that participants recalled their
name when it was spoken in the to-be-ignored message, revealing that participants’
goal of attending to self-relevant information was stronger than their goal to attend
to the to-be-attended-to message.
Top-Down versus Bottom-Up Processing

Our goals can influence our attention in a top-down or a bottom-up fashion (Pashler,
Johnson, & Ruthruff, 2001). Separating top-down and bottom-up influences can help
clarify the role of attention in our daily life. Top-down control of attention reflects
our intentions whereas bottom-up control of attention reflects stimuli features that
attract our attention (Pashler et al., 2001); however, our attention is guided by both
top-down and bottom-up influences. On the one hand, there are stimuli that attract
our attention, such as a flashing red light; on the other hand, we have the ability to
choose what we pay attention to, such as what types of stores are present along a
road (e.g., gas station vs. shoe store). Choosing what we pay attention to (e.g., only
paying attention to the gas stations along the road and ignoring the shoe stores when
we need to fill up our gas tank) utilizes top-down control, allowing us to guide our
attention to relevant stimuli, even when external information (i.e., exogenous cues;
Posner, 1980) competes for our attentional resources. Another drastic example of
top-down attention control is the study by Simons and Chabris (1999). Participants
were asked to monitor a basketball game. Unexpectedly during their monitoring, a
person wearing a gorilla suit, or a woman carrying an opened umbrella walked across
the court. Forty-six percent of participants who monitored the basketball game failed
to notice any unexpected event.
Automatic versus Strategic Processing

Another classification divides attention into automatic and strategic processes. Auto-
matic processes are often defined as capacity-free, outside of awareness, and not
involving volition (McNally, 1995; Shiffrin & Schneider, 1977). Automatic processes
include “direct environmental control over internal cognitive processes involved in
perception, judgment, behavior, and goal pursuits” (Bargh, 2011, p. 629). On the
other hand, strategic processing requires cognitive capacity, conscious awareness, and
voluntary control (Shiffrin & Schneider, 1977).
Early Selection versus Late Selection Processing

A third classification highlights the role of “early selection” versus “late selection”
in attention processes (e.g., Driver, 2001). The “early selection” view suggests that
focusing attention on task-relevant stimuli allows an individual to exclude distracters
from his or her perceptual processing whereas the “late selection” view suggests that
all information, including distracters, are processed, but if an individual focuses on
task-relevant information distracters are prevented from controlling behavior. More
recent theorists (e.g., Lavie, 2010) suggest that early selection is more voluntary
(strategic) in the sense that limited processing capacity allows people to perceive only
Attentional Bias Modification 183
what is necessary for the task at hand. Furthermore, late selection is automatic in the
sense that it has unlimited capacity, meaning that everything is processed, including
distracters, and mandatory in the sense that people cannot select what to attend to.
Research has expanded on the principle of early versus late selection showing the
effect of information load in processing information (Lavie, 2005, 2010). For example,
one can inhibit distracters (early selection) when the task that is being completed is
of high perceptual load (identifying an X in a set of random letters); however, if the
task being completed involves a low perceptual load (identifying an X in a set of Ns),
distracters are perceived (late selection), but their impact on behavior depends on
other types of load (e.g., load on working memory; Forster & Lavie, 2009).
Attentional Networks (Alerting, Orienting, and Executive Control)

Finally, other views state that attention is not a unitary construct; rather, attention
comprises a set of networks that are functionally and structurally independent
but work cooperatively. Posner and colleagues (Posner & Petersen 1990;
Posner, Rothbart, Sheese, & Tang, 2007) have distinguished three attentional
networks: alerting, orienting, and executive control. Alerting is involved in maintaining
an appropriate sensitivity level by which to perceive and process stimuli and has been
related to activity in the locus coeruleus and activation of right frontal and parietal
brain areas (Posner et al., 2007). The orienting network involves the selection of
information from among numerous sensory stimuli and has been associated with
activations in the superior parietal lobe, frontal eye fields, and temporoparietal
junction. The executive control network specializes in conflict resolution and
voluntary action control and is related to midline frontal areas, anterior cingulate
gyrus, and lateral prefrontal cortex (Posner et al., 2007). Fan, McCandliss, Sommer,
Raz, and Posner (2002) developed the attention network task (ANT), combining the
Ericksen f lanker tasks (Eriksen & Eriksen, 1974) and Posner’s exogenous cueing tasks
(Posner, 1980), to evaluate the efficiency of each attention network while reliably and
independently assessing the networks using a simple reaction time task. Thus, studies
that examine the role of attention in emotional disorder should consider the relative
impact of each component of the attentional network in each emotional disorder.
In summary, research suggests that attention is not a unitary construct and there
are multiple models (e.g., automatic vs. strategic; early vs. late selection, etc.) that
attempt to explain the role of attention in guiding behavior. Therefore, models
of psychopathology that attempt to use attention in anxiety or depression should
consider these models when making predictions regarding the role of attention in
maintaining these clinical conditions.
Correlational Evidence for the Relationship between

Attention and Anxiety
Cognitive models of anxiety suggest that attentional bias toward threat-relevant

information plays a role in the etiology and maintenance of anxiety disorders (Beck &
Clark, 1997; Eysenck, 1992, 1997; Williams, Watts, MacLeod, & Mathews, 1997).
More specifically, these models propose that information processing in general, and
attentional bias more specifically, is guided by anxiety-related schemas that are present
in emotional disorders. These models elaborate further that the limited capacity of
the human attentional system leads to some information in the environment being
attended to while other information is ignored; thus, incoming information must be
prioritized. Therefore, an attentional bias toward threat-relevant information can lead
to increased availability of threat, meaning that threatening information is prioritized
above other information, causing anxiety (see Ouimet, Gawronski, & Dozois, 2009).
Researchers have relied on these models of anxiety to develop testable hypotheses
regarding the role of attentional bias in anxiety. For example, a large body of research
suggests that anxiety is related to an attentional bias toward threat-relevant infor-
mation. These studies use methods borrowed from cognitive psychology to measure
attention (for reviews, see Bar-Haim, Dominique, Pergamin, Bakermans-Kranenburg,
& van Ijzendoorn, 2007; Mogg & Bradley, 1998). For example, to examine atten-
tional bias for threat-relevant information in anxious individuals, researchers have
employed interference tasks that require participants to perform a central task while
ignoring distracters (Mathews & MacLeod, 2005). Two tasks commonly used to
examine attentional bias for threat-related information in individuals suffering from
anxiety include the emotional Stroop task (Williams, Mathews, & MacLeod, 1996)
and the attentional probe detection task (MacLeod, Mathews, & Tata, 1986).
In the emotional Stroop task, participants are asked to name the colors in which
emotional words are written while ignoring the meaning of these words. Anxiety
sufferers are slower at color-naming anxiety-related words than neutral words, whereas
nonanxious controls are not (for a review, see Williams et al., 1996). This finding
suggests that the activation of threat meaning may interfere with the color-naming
task in participants with anxiety to a greater extent than it does in controls. However,
the emotional Stroop task is considered an impure measure of attention because
some versions of the paradigm (i.e., presenting a block of words on one card) may
involve postattentional processing of the stimuli (Fox, 1994), and because attention is
measured while responding to threat-related material. Therefore, the Stroop paradigm
may involve both biased attention to threat and attempts at inhibition of word
meaning.
Partly in response to the above criticism, researchers began using more direct
measures of attention to measure attentional biases for threat-relevant material (e.g.,
the probe detection paradigm; MacLeod et al., 1986). In the probe detection task
(PDT), participants are presented with two words simultaneously, one on top of the
other (or presented side by side). One of the words has a threat-relevant meaning
(e.g., death) while the other word is neutral (e.g., table). These words are then
removed from the screen after a brief time (e.g., 500 ms). Participants see a probe
(e.g., a letter “E” or “F”) that is located in place of either word and are instructed to
identify the probe by pressing a corresponding mouse button (i.e., left mouse button
for letter “E” and right mouse button for letter “F”). The letters appear with equal
frequency in the location previously occupied by the threat word and the neutral
word. Attentional bias in this task is revealed by shorter response latencies to identify
the probes that replace threat words compared to the response latency for probes that
replace a neutral word.
Bar-Haim et al. (2007) reviewed 172 studies using the emotional Stroop task
and the PDT. This meta-analysis revealed that there is a reliable association between
anxiety and attentional bias as measured by these tasks with an average effect size
(Cohen’s d) of 0.45 (confidence interval [CI]: 0.40–0.49). These studies indicate
that anxious individuals exhibit an attentional bias across a range of populations
(adults and children), stimuli (words and pictures), and stimuli presentation durations
(subliminal and supraliminal; Bar-Haim et al., 2007). Thus, the association between
anxiety and attentional bias is a reliable finding in experimental psychopathology
research. However, few studies have considered the various components of attention
when describing the relationship between anxiety and attention. For example, which
components of attention (alerting, orienting, or executive control) are involved in
anxiety (cf. Fan et al., 2002; Ouimet et al., 2009)?
In summary, there is ample evidence for the role of attentional bias in anxiety.
Moreover, this bias is present across populations, stimuli, and methods of measuring
attention. However, two issues remain regarding the relationship between attention
and anxiety. First, the direction of this relationship is not clear. That is, from these
studies, it is not clear whether attentional bias causes anxiety, or whether anxiety is
the cause of attentional bias. Second, it is not clear what component of attention is
involved in anxiety.
Correlational Evidence for the Relationship between

Attention and Depression
Depression may also be characterized by an attentional bias for depression-related

information. However, the nature and time course of this bias may differ from
what is found in anxiety. Patients with anxiety typically display an attentional bias
for threatening information rapidly, and the bias is present even during conditions
that restrict stimulus awareness (Mathews & MacLeod, 2005). On the other hand,
participants who are suffering from depression display an attentional bias only when
information is easily visible (Mathews, Ridgeway, & Williamson, 1996), and when
the stimuli is presented for longer exposures (e.g., 1,000 ms) that allow elaborative
processing to occur (Bradley, Mogg, & Lee, 1997; Eizenman et al., 2003; Mathews
& MacLeod, 2005; Mogg & Bradley, 2005; Wisco, 2009). Furthermore, attentional
bias in depressed individuals is present for depression-related stimuli rather than for
threat-relevant stimuli as is the case in anxiety (Wells & Beevers, 2010; see Mogg &
Bradley, 2005, for a review). This difference between anxiety and depression may be
attributed to biases in anxiety being automatic and biases in depression being strategic
(Mathews & MacLeod, 2005).
A larger body of research has examined the role of attentional bias in anxiety than
depression. However, researchers have used the PDT (Koster, Crombez, Verschuere,
& De Houwer, 2006; Mogg, Bradley, & Williams, 1995) the Stroop task (Bradley,
Mogg, Millar, & White, 1995; Holmes & Pizzagalli, 2008; Mogg, Bradley, Williams,
& Mathews, 1993), and a dichotic listening task (Ingram, Bernet, & McLaughlin,
1994; McCabe & Gotlib, 1993), with depressed individuals showing that there is
an attentional bias for disorder-specific stimuli when the presentation is long (e.g.,
1,000 ms or longer). However, such biases are not present when stimuli are presented
for shorter durations (i.e., 500 ms). A recent review of attentional bias for depression
suggested that depressed individuals do not show an automatic attentional bias
for depression-related information but do so once the stimuli have captured their
attention (Gotlib & Joormann, 2010). That is, these individuals may exhibit difficulties
disengaging their attention away from depression-related information. However, this
area is in need of further research, including the role that attentional biases play in
the maintenance of depression. In summary, research suggests that depression may be
characterized by an attentional bias for negative information. However, the nature of
this bias may be characterized by difficulty in disengaging attentional recourses from
negative information once the information has captured attention.
The Causal Role of Attention in Emotional Disorders
Although the studies described above suggest that anxiety and depression are associ-
ated with attentional bias toward threat-relevant information, they do not speak to
the issue of causality. Indirect evidence for the causal role of attentional bias toward
relevant information in emotional disorders comes from treatment outcome studies.
That is, if attentional bias toward threat-relevant information is a necessary condition
for anxiety, then amelioration of anxiety should be associated with a reduction of
attentional bias to threat. Empirical investigations of this question have generally
supported this hypothesis in anxious individuals using both the emotional Stroop
paradigm (e.g., Lundh & Ost, 2001; Mattia, Heimberg, & Hope, 1993) and the
PDT (e.g., Hofmann, 2000; Pishyar, Harris & Menzies, 2008).
Single Session Studies of Causal Relationship between

Attention and Anxiety
Researchers have also examined the causal relationship between attentional bias
and anxiety using experimental methods that manipulate attention to examine the
effect on anxiety. For example, in a seminal study Macleod, Rutherford, Campbell,
Ebsworthy, and Holker (2002) addressed the causal association between attentional
bias and emotional vulnerability via attentional bias modification. Participants in this
study were randomly assigned to one of two attention-training tasks conducted on
a computer. One program was designed to train the participants’ attention toward
threat-relevant information (referred to as the attend threat condition). The second
program was designed to train the participants’ attention toward neutral words
(referred to as the attend neutral condition). Both programs resembled the PDT
described above. Each program consisted of 672 trials in which pairs of words
were presented, one above the other, on a computer screen. Word pairs contained
one threat-relevant word and one neutral word. In the attend threat condition,
probes appeared in the position of the threat word on 576 training trials (93%).
The remaining 96 trials were designed to provide a measure of attentional bias to
threat words. In these test trials, threat word position and probe position were fully
crossed as in a typical PDT, thus permitting measurement of a participant’s tendency

to attend preferentially to threat-relevant or neutral words. In the attend neutral
condition, probes appeared in the position of the neutral word on 93% of the trials,
with the remaining 96 trials again providing a measure of attentional bias. After
completing a dot probe task designed to modify attention by inducing an attentional
bias toward or away from negative stimulus, participants were exposed to an anagram
stress manipulation task that was designed to influence negative mood state. During
the anagram stress tests, participants were presented with random letter strings and
were asked to solve the anagram by rearranging the letters to make an English word.
Unbeknownst to the participants, the letters in some of the anagrams could not be
rearranged to create a regular word, and those that could were very difficult to solve.
Moreover, participants received failure feedback while completing the task and were
also videotaped for what they were told was class purposes.
Emotional variability was measured by examining variation in negative mood as
a result of completing the anagram task after one of the two attention training
conditions. Results indicated that participants did gain an attentional bias toward or
away from threat consistent with their training condition and that this bias generalized
to novel stimuli. Examining the analogue mood scale data revealed that the attention
modification did not affect mood posttraining; however, it did modify emotional
vulnerability such that groups differed in negative emotional reaction to the stressful
anagram task. These results have also been replicated in independent laboratories.
For example, Van Bockstaele, Koster, Verschuere, Crombez, and De Houwer (2012)
successfully manipulated attentional bias using an exogenous cueing task. However,
they did not obtain generalization to a different interference task.
Amir, Weber, Beard, Bomyea, and Taylor (2008) administered a single session
attention training program to individuals with high levels of social anxiety. The
authors modified the dot probe procedures used by Mathews and MacLeod (2002)
to encourage participants to disengage their attention from threat stimuli (i.e., using
faces with negative and neutral expressions). Specifically, the paradigm created a
contingency between the location of the nonthreat stimuli (i.e., neutral face) and
the probe in one group (attention modification program, or AMP), and not in the
other (attention control condition, or ACC). Attentional bias was assessed before
and after training, and participants were also asked to give an impromptu speech
to determine the effect of the manipulation on anxiety. Results revealed that the
procedure effectively modified attention disengagement. Moreover, participants in
the AMP condition experienced less anxiety reactivity as a result of the speech, and
were judged as having superior speech performance relative to control participants by
independent raters.
Heeren, Lievens, and Philippot (2011) examined whether the beneficial effects of
attention training result from learning to disengage attention from threat or learning
to orient attention toward nonthreat. Individuals with social phobia were randomly
assigned to one of four training conditions: (a) disengagement from threat, (b)
engagement toward nonthreat, (c) disengagement from threat and reengagement
toward nonthreat, and (d) a control condition. Training attention to disengage from
threat reduced behavioral indices of anxiety. However, engagement toward nonthreat
faces did not have a similar effect, suggesting that difficulty in disengaging attention
from threat is a critical process in maintenance of the disorder.
Najmi and Amir (2010) examined the effect of a single AMP session on behav-
ioral approach toward feared stimuli in individuals with contamination fears. These
researchers utilized a PDT similar to the original task used by MacLeod et al. (1986)
to measure attentional bias. Participants’ attention was trained away from threatening
information, meaning that the probe replaced neutral words on the majority of the
trials in this condition. Behavioral approach was measured by the number of steps the
participant completed in a series of three different behavioral approach tests (BATs;
adapted from Cougle, Wolitzky-Taylor, Lee, and Telch (2007)), each of which
assessed avoidance of a different type of contaminant. The first BAT consisted of a pile
of dirty underwear and other clothes. Participants were told that “some of these items
may have been touched with bodily f luids.” The second BAT included a mixture of
“dirt, dead insects, and cat hair.” This mixture was made of potting soil, dead crickets,
and cat hair. The third BAT involved a toilet (with an open lid) that was made to
look unclean with blotches of potting soil on the inside of the bowl. Each BAT
comprised six steps in a graduated hierarchy. If participants were able to complete
the first item, they were asked to complete the next one on the hierarchy, and so
on, and if they refused to perform an item, the experimenter terminated that BAT.
Attention training was effective in reducing attentional bias to threat and increasing
behavioral approach toward feared stimuli in individuals with contamination-related
fears. Because groups did not differ in their level of anxiety or obsessive-compulsive
symptoms posttraining, but did differ in their level of attentional bias for threat, these
researchers concluded that the difference between the two groups posttraining reflects
the creation of differing vulnerability to the behavioral challenge.
Reese, McNally, Najmi, and Amir (2010) assigned 41 spider-fearful individuals
either to receive attention training (n = 20) or to a control condition (n = 21). A
modified dot probe discrimination paradigm with photographs of spiders and cows
was used to train attention. Training reduced attentional bias for spiders, but only
temporarily. Although both groups declined in spider fear and avoidance, reduction in
attentional bias did not produce significantly greater symptom reduction in the training
group than in the control group. However, reduction in attentional bias predicted
reduction in self-reported fear for the training group. The reduction in attentional
bias for threat may have been insufficiently robust to produce symptom reduction
greater than that produced by exposure to a live spider and spider photographs alone.
Replicating this finding, Van Bockstaele et al. (2011) also successfully changed the
attentional processing for spiders; however, there was no effect on self-reported or
physiological anxiety in response to spiders.
Although the above studies support the hypothesis that training attention away
from threat may be causally involved in amelioration of anxiety response to stress,
an alternative hypothesis is that cognitive biases in anxiety reflect a more general
cognitive deficit that may not be specific to attention disengagement difficulties (e.g.,
Bishop, 2009; Derakshan & Eysenck, 2009; Derryberry & Reed, 2002; Eysenck,
Derakshan, Santos, & Calvo, 2007; Wells, White, & Carter, 1997). As such, the
anxiety-ameliorating effects of attention training may be due to an increase in general
attentional control and not directly related to attention disengagement training away
from threat. If so, then attention training may increase top-down cognitive capacities
that in turn inhibit threat processing (e.g., Pessoa, 2009; Pessoa, McKenna, Gutierrez,
& Ungerleider, 2002).
To examine this hypothesis, Klumpp and Amir (2010) examined the effect of
attention training in moderately socially anxious undergraduate students. These
researchers included a third training condition that comprised training to attend
toward threat, similar to MacLeod et al. (2002), in addition to the standard training,
disengagement from threat, and control training conditions. The addition of the
attend threat condition allowed these researchers to test the hypothesis that enhanced
attentional control, rather than more efficient attentional disengagement from threat,
may be involved in attention training studies. The response latency data in this study
were largely inconclusive. However, participants who were trained to attend toward
threat and participants who were trained to attend away from threat faces exhibited
a relative decrease in anxiety during a speech challenge compared to participants in a
placebo control condition. No difference in anxiety scores between the two attention
training conditions was found in this moderately anxious sample. Replicating and
extending this finding, Van Bockstaele, Verschuere, De Houwer, and Crombez (2010)
found more extinction in an attend toward threat group, compared to both the attend
away from threat group and a control group in which attention was not manipulated.
In summary, these single session studies provide converging evidence from multiple
laboratories using related but distinct methodologies attesting to the causal role of
attentional bias to threat in the maintenance of anxiety and indicate that attention
modification procedures may have clinical utility.
Single Session Studies of Attention Training in Depression

Researchers have also examined the causal role of attentional bias in depression.
For example, Clasen, Wells, Ellis, and Beevers (2012) used an exogenous cuing
task developed by Posner (1980) but modified for emotional material (Amir, Elias,
Klumpp, & Przeworski, 2003) to examine bias. Images of faces were presented from a
range of emotions including happy, sad, fearful, and neutral. Bias for negative material
was more strongly associated with impairments in mood recovery for depressed and
nondepressed participants; however, biases for sad material were particularly important
in recovery impairments for depressed, but not nondepressed participants. These
authors suggested that a negative attentional bias facilitates the persistence of sad
mood; however, the single session study design did not allow for researchers to test
for temporal precedence.
Multisession and Clinical Studies of Attention Training in Anxiety

Although the studies reviewed above suggest that AMP can be used to reduce anxiety
in response to stress, it is not clear that such training can have long-lasting effects.
Moreover, it is not clear to what extent these training protocols can ameliorate clinical
levels of anxiety. In order to examine the efficacy of the protocol on clinical levels
of anxiety, they should be tested in randomized, double-blind, placebo-controlled
trials.
Li, Tan, Qian, and Liu (2008) used a PDT with pictures of positive and nega-
tive faces to modify attentional bias in individuals with high social anxiety. These
researchers assigned their participants to one of two groups. In one group, par-
ticipants received a dot probe task with the training contingency being away from
negative material. In the control group, participants received the typical PDT without
a contingency between the position of the probe and the position of the negative
material. Seven days of attentional disengagement training resulted in an increase
in focus of attention on positive faces. Their results also showed that scores on the
Social Interaction Anxiety Scale (SIAS) were reduced in the attention training group
compared to the control group. However, scores on the Social Phobia Scale (SPS)
and the Fear of Negative Evaluation Scale (FNE) did not differ between the two
groups, suggesting a limited reduction of social anxiety. The participants in this study
did not meet diagnostic criteria for an anxiety disorder; however, other researchers
have used attention training with clinical populations.
To date, five randomized, double-blind, placebo-controlled studies have examined
the effect of computerized AMP in the treatment of anxiety (Amir, Beard, Burns, &
Bomyea, 2009; Amir, Beard, Taylor, et al., 2009; Carlbring et al., 2012; Heeren,
Reese, McNally, & Philippot, 2012; Schmidt, Richey, Buckner, & Timpano, 2009)
in clinical populations. In these studies, the authors used variations of the PDT to
induce selective processing of neutral cues when these cues compete for attentional
resources with threat-relevant cues. The placebo group (attention control condition,
ACC) was identical to AMP except that the location of the probe relative to the
threatening or neutral stimuli was random (i.e., the probe replaced neutral stimuli on
50% of trials, and threatening stimuli on the other 50% of trials). In four of these
five studies, participants in the AMP group showed significantly larger reductions in
clinician- and self-rated symptoms of anxiety and functional impairment relative to
the control group.
Schmidt et al. (2009) examined the effect of attention training in 36 individuals
who sought treatment for general social phobia (GSP). Participants were randomly
assigned to either the AMP or the ACC. Patients in the AMP condition exhibited
significantly greater reductions in social anxiety and trait anxiety compared to patients
in the control condition. At termination, 72% of patients in the active treatment
condition, relative to 11% of patients in the control condition, no longer met DSM-IV
criteria for GSP. At 4-month follow-up, patients in the AMP condition continued to
maintain clinical improvement, and diagnostic differences across conditions were also
maintained. These findings further bolster confidence in the generalizability of the
AMP efficacy across sites.
Amir, Beard, Taylor, et al. (2009) tested the hypothesis that a multisession AMP
would reduce symptoms of social anxiety and associated functional impairment in
44 individuals seeking treatment for GSP. Participants met criteria for a primary
diagnosis of GSP using the Structured Clinical Interview for DSM-IV (First, Spitzer,
Gibbon, & Williams, 1994). Fifty percent of participants had co-occurring Axis I
disorders. Participants completed the AMP or ACC twice each week for 4 weeks.
Each training session was approximately 20 minutes in duration. Primary outcome
measures were interview- and self-reported social anxiety symptoms (Liebowitz Social
Anxiety Scale [LSAS]; Liebowitz, 1987; Social Phobia and Anxiety Inventory [SPAI];
Turner, Beidel, & Dancu, 1996; Turner, Beidel, Dancu, & Stanley, 1989) and
functional impairment (Sheehan Disability Scale [SDS]; Sheehan, 1983). Researchers
submitted participants’ scores on these measures to 2 (Group: AMP, ACC) X 2
(Time: pretraining, posttraining) analyses of variance with repeated measurement
on the second factor. Results revealed significant Group X Time interactions for
all measures, on the LSAS, SPAI, and SDS, respectively. Follow-up paired t tests
conducted within each group revealed that participants in the AMP group showed a
significant decrease in scores from pre- to postassessment on the LSAS. Similar analyses
in the ACC group revealed a significant decrease in scores from pre- to postassessment
on the LSAS. Analyses of covariance conducted on posttreatment scores, covarying
pretreatment scores, and using the LSAS, SPAI, and SDS as the dependent variables,
revealed that the AMP group was less socially anxious and less functionally impaired
relative to the ACC group at postassessment. Thus, consistent with prediction,
results revealed that participants who received the AMP exhibited greater decreases
in interviewer and self-report measures of social anxiety and impairment relative to
the ACC group. Patients maintained their gains at 4-month follow-up. Moreover,
data on diagnostic status after treatment revealed that 50% of participants in the AMP
group no longer met diagnostic criteria for GSP compared to 14% of participants
in the ACC group. Finally, results revealed that the AMP significantly facilitated
attention disengagement from threat from pre- to postassessment, and reduction in
interviewer-rated social anxiety symptoms was mediated by change in attentional bias
(Mackinnon, Lockwood, Hoffman, West, & Sheets, 2002). These findings provide
empirical support consistent with the hypothesized mechanism of the AMP.
In the third study, Amir et al. examined the effects of a similar eight-session AMP in
a sample of 29 treatment-seeking patients who met diagnostic criteria for generalized
anxiety disorder (GAD; Amir, Beard, Burns, et al., 2009). The interviewer measures
included the Structured Clinical Interview for DSM-IV (SCID; First et al., 1994) and
the Hamilton Rating Scale for Anxiety (HRSA; Hamilton, 1959). The self-report
measures included the State-Trait Anxiety Inventory (STAI; Spielberger, Gorsuch,
Lushene, Vagg, & Jacobs, 1983), the Beck Depression Inventory II (BDI-II; Beck,
Steer, & Brown, 1996), the Worry Domains Questionnaire (WDQ; Tallis, Eysenck,
& Mathews, 1992), and the Penn State Worry Questionnaire (PSWQ; Meyer, Miller,
Metzger, & Borkovec, 1990). Consistent with previous studies, participants in the
AMP group demonstrated significantly greater reductions on interviewer- and self-
reported anxiety symptoms. Further, a significantly larger proportion of participants in
the AMP group (50%) compared to the ACC group (13%) no longer met diagnostic
criteria for GAD after training. Finally, a mediation analysis (Mackinnon et al., 2002)
supported the hypothesis that change in attentional bias mediated the reduction in
interviewer-rated anxiety (HRSA) from pre- to posttreatment.
Heeren et al. (2012) also examined the effect of attention training on reducing the
symptoms of social anxiety, but also included behavioral and physiological measures
of anxiety reduction. Participants who were trained to attend to nonthreatening
cues demonstrated significantly greater reductions in self-reported, behavioral, and
physiological measures of anxiety than did participants from the attend to threat and
control conditions (Heeren et al., 2012).
In addition to the studies described above, two studies examined the efficacy of
Internet-delivered AMP. Carlbring et al. (2012) examined the effect of attentional bias
modification delivered via the Internet with no physical contact with the participants.
These researchers suggested that a large number of trials have found that CBT
delivered over the Internet can be as effective as face-to-face CBT, even in direct
comparison. Therefore, it would be useful to examine whether attention training,
an intervention with much fewer needs for therapist contact than CBT, could also
be delivered via the Internet. After a diagnostic interview, 79 participants were
randomized to one of two attention training programs. In the active condition the
participant was trained to direct attention away from threat, whereas in the placebo
condition the probe appeared with equal frequency in the position of the threatening
and neutral stimuli. Participants in both conditions received training via the Internet
utilizing a PDT with pictures of threatening and neutral faces. Results were analyzed
on an intention-to-treat basis, including all randomized participants. Immediate and
4-month follow-up results revealed a significant decrease in anxiety over time on
all measured dimensions (social anxiety scales, general anxiety and depression levels,
quality of life); however, the active and control group did not differ on these
measures at posttreatment. Similarly, Boettcher, Berger, and Renneberg (2011) did
not find pre- to posttreatment group differences between active and control Cognitive
Bias Modification (CBM) conditions when delivered via the Internet. However, at
4-month follow-up there was some suggestion of an advantage of the active CBM
condition for depressive symptoms and a marginally significant effect on social anxiety
symptoms. These studies suggest that computerized attentional bias modification may
need to be altered before dissemination for the Internet.
The average controlled posttreatment between-group effect size on the primary
outcome measure across studies was large (Cohen’s d = 0.91), which is within the
range of those obtained for existing empirically supported cognitive behavioral and
pharmacological treatments for anxiety (Barlow, 2007). Moreover, a significantly
larger proportion of participants in the AMP group compared to the ACC group
no longer met diagnostic criteria for the principal anxiety disorder diagnosis at
postassessment (loss of diagnosis: AMP, range 50% to 72%; ACC, range 11% to
14%). Finally, two of the trials conducted a formal mediation analysis (Mackinnon
et al., 2002), which demonstrated that change in attentional bias for threat mediated
the reduction in interviewer-rated anxiety from pre- to postassessment (Amir, Beard,
Burns, et al., 2009; Amir, Beard, Taylor, et al., 2009). Thus, the central treatment
target of the AMP (attentional bias for threat) was shown to be a key mechanism of
action responsible for symptom reduction.
Recent meta-analyses provide further support for the clinical utility of AMP.
Hakamata et al. (2010) reviewed studies that compared AMP to a control condition
and found a medium effect size for AMP on anxiety overall (d = 0.61; CI =
0.42–0.81) with a larger effect specifically in clinical patients (d = 0.78; CI =
0.38–1.20). Many of the studies used a double-blind, placebo-controlled design,
allowing researchers to rule out the possibility of group differences that are due to
demand effects, expectancy, or credibility of the intervention. Finally, as Hakamata
et al. (2010) suggested, existing effect size estimates may potentially be enhanced
given the lack of rationale provided to participants, lack of therapist contact, and
brevity of these initial protocols.
Beard, Sawyer, and Hofmann (2012) identified 37 studies (41 experiments) with a
total of 2,135 participants who were randomized to training toward neutral, positive,
threat, or appetitive stimuli or to a control condition. Large effect size estimates were
obtained for neutral versus threat comparisons ( g =1 .06), neutral versus appetitive
( g = 1.41), and neutral versus control comparisons ( g = 0.80). These authors also
conducted fail-safe N calculation, suggesting that the effect size estimates were robust
for the training effects on attentional biases, but not for the effect on subjective
experiences. Beard et al. concluded that AMP has a moderate and robust effect on
attentional bias when using threat stimuli.
Multisession Studies of Attention Training in Depression

Wells and Beevers (2010) examined whether attention training with dysphoric stimuli
would lead to reduction of depressive symptoms compared to a no training condition
over multiple sessions. These researchers used the probe detection task with images.
Results indicated that attention training led to a reduction in depressive symptoms
with a medium to large effect size while the effect size for the no training condition
was near zero. Additionally, the training condition reduced bias for dysphoric stimuli
while the no training condition did not.
Conclusions
Consistent with recent reviews, the above summary suggests that attention is a
multifaceted construct that can be measured using a number of basic experimental
psychology paradigms. There is now ample evidence for the causal link between
attention and anxiety; however, issues remain as to which particular component
of attention is responsible for this effect. For example, at least one study found
that attention training toward threat is as effective as attention training away from
threatening information (Klumpp & Amir, 2010).
Researchers have begun to use this methodology for treatment; however, not all
results are positive. For example, three randomized placebo-controlled trials from
three different laboratories have shown that AMP is a useful treatment for social
anxiety disorder (Amir, Beard, Taylor, et al., 2009; Heeren et al., 2012; Schmidt
et al., 2009). These AMP studies were all conducted in laboratory settings. However,
two studies (Boettcher et al., 2011; Carlbring et al., 2012) that used a very similar
methodology but delivered the intervention via the Internet did not find group
differences in symptoms compared to an ACC. As these researchers speculated,
AMP conducted in a laboratory setting may have produced positive results due to
unintentional exposure effects produced by putting oneself in an unfamiliar setting
that involves contact with authorities (e.g., clinicians), assessment, and supervision
by research assistants. However, this explanation is not likely to account fully for the
obtained results of the studies conducted in the laboratory, as participants in the ACC
receive similar levels of unintentional exposure, but do not show the same level of
symptom reduction as do participants in the AMP group.
On the other hand, an interactive hypothesis suggests that the effective ingredient
in AMP is a change in vulnerability to experience anxiety, but only when participants
are in an anxiety-provoking situation (MacLeod et al., 2002). Indeed, single session
studies (Amir et al., 2008, MacLeod et al., 2002; Najmi & Amir, 2010) show
that AMP does not result in any change in anxiety after training. However, when
participants are faced with an anxiety-provoking situation (e.g., solving unsolvable
anagrams, or giving a speech in the case of socially anxious individuals) then those
receiving AMP are less likely to show an increase in anxiety when compared to the
ACC group.
Accordingly, it is not surprising that the two studies that delivered interventions
over the Internet (presumably in the participants’ homes), thereby minimizing the
number of interpersonal interactions that contribute to anxiety in socially anxious
participants (Boettcher et al., 2011; Carlbring et al., 2012), produced the weakest
effect of AMP when compared to ACC. Indeed, a recent study conducted by the
Carlbring group (Kuckertz et al., in press) examined this hypothesis by providing
AMP on the Internet while also instructing participants to self-activate their social
anxiety fears prior to completing the attention training sessions. Participants in that
study complied with the instructions approximately half the time. Their results suggest
that this instructional difference may partially explain positive findings resulting from
AMP. While the researchers did not find a positive correlation between the number of
times participants self-induced anxiety and reduction in social anxiety symptoms, they
did find that participants who completed at least one self-induced anxiety exercise
prior to completing AMP training experienced a significantly greater reduction in
social anxiety symptoms than those who did not engage in any exposure exercises.
Moreover, the effect size for this Internet-delivered version of AMP was similar to the
laboratory-delivered versions described and also matches an Internet-delivered CBT
program used as a comparison condition.
In summary, although AMP has been shown to be effective in treating anxiety,
questions remain regarding third-party variables (e.g., severity of the disorder, level
of bias before training, interaction with unintended exposure) that may interact
with the efficacy of attention training and should be examined in future research.
Only one study (Amir, Taylor, & Donohue, 2011) has systematically examined
predictors of response to AMP. Consistent with their hypothesis, these researchers
found that individuals who presented at pretreatment with an attentional bias toward
threat benefited more from attention training than participants who did not present
with an initial attentional bias. Moreover, Boettcher and colleagues (2011) did not
find differences in social anxiety reductions between active attention training and a
control condition; however, their participants did not present with attentional bias at
pretreatment. This lack of initial attentional bias may, in part, account for their null
results.
Although the primary aim of the studies reviewed above was to compare AMP
to a control condition (i.e., the ACC), it is not at all clear that the ACC would
be an inert intervention. Indeed, in early studies of attention training (MacLeod
et al., 2002) researchers compared the efficacy of a manipulation designed to direct
attention away from threat, to a condition designed to train attention toward

threat-relevant information. However, as these two interventions were both active in
training attention, it was not possible for these authors to disentangle the effect of
each condition in isolation. That is, group difference may have been the result of
either condition alone or their combination. In later studies (e.g., Amir et al., 2008)
researchers reasoned that a clearer picture could emerge if one were to compare
attention training away from threat to a control condition where no contingency
existed between the location of the threat items and the location of the probe. The
so-called ACC may be more useful in examining the effect of attention training away
from threat, but it is unlikely that it is truly a control condition. That is, research
suggests that the ACC also results in reduction of anxiety symptoms. For example,
although the Internet-based trials (Boettcher et al., 2011; Carlbring et al., 2012)
described above did not demonstrate differential effects of AMP versus ACC, they
both demonstrated a main effect of time for all participants, indicating that both
AMP and ACC were effective in reducing symptoms. Similar results were obtained
when comparing within-group effect sizes for ACC conditions (d = 0.50) with the
effect sizes obtained from placebo conditions in other studies (d = 0.32). The ACC
used in these studies may result in reductions in anxiety to the extent that it changes
attentional bias. That is, if the participants enter the study without an attentional bias
toward threat, then the 50/50 contingency present in the ACC would serve as a
control condition. However, if participants enter the study with an extant attentional
bias toward threat (e.g., 80/20 bias toward threat), then the ACC would act as a low
dose AMP for these individuals. Indeed the results of the comparison of effect sizes
for ACC and other control conditions support this hypothesis, as a dose response
hypothesis would be consistent with the rank ordering of effect sizes for AMP, ACC,
and control conditions (Bair-Haim, 2010; Eysenck et al., 2007).
Future Directions
The application of findings from basic experimental psychology to developing treat-

ments for a clinical condition is of interest for both theoretical and practical reasons.
Indeed, AMPs have been one of the success stories regarding this venture. However,
questions remain regarding the application and enhancement of these methodologies
in mainstream clinical practice. For example, it is not clear that the paradigms used
to train attention have adequate psychometric properties (e.g., reliability) required
of most clinical instruments. Indeed, the measurement and interpretation of reaction
time data have a rich and extensive literature often ignored by clinical psychologists
and experimental psychopathologists interested in using reaction time data (Ratcliff &
Van Dongen, 2011; Ratcliff, Van Zandt, & McKoon, 1999). For example, diffusion
modeling allows researchers to hypothesize models that can create simulated data that
can then be compared to experimental data obtained from participants. Few studies
(for an exception, see White, Ratcliff, Vasey, & McKoon, 2010) have used these
methodologies when examining reaction time data.
Finally, it is necessary to triangulate on the constructs of interest (i.e., change
in attentional bias) using different measure of attention (e.g., Posner cueing task,
antisaccade task) as well as other methodologies including neuroimaging (e.g., func-

tional magnetic resonance imaging) functions and neuro-modulation technique (i.e.,
transcranial magnetic stimulation). For example, to examine the neural mechanisms
underlying AMP, Taylor et al. (in press) combined AMP with functional neuroimag-
ing to test whether AMP exerts its effect via modification of neural substrates that are
centrally involved in emotion processing. To this end, 14 individuals with elevated
social anxiety symptoms completed an emotional face-processing task before and
after AMP, and were subsequently asked to give an impromptu speech. AMP induced
attenuated activation from pre- to post-AMP in the bilateral amygdala, bilateral insula,
and subgenual anterior cingulate cortex but increased activation in several regions of
the prefrontal cortex. Moreover, individuals with greater enhancement of ventrome-
dial prefrontal cortex activation after AMP showed diminished attentional bias for
threat and attenuated anxiety reactivity to the speech. These researchers concluded
that computerized attention modification may not only attenuate bottom-up anxiety-
related processes but also foster deployment of top-down brain processes aimed to
regulate anxiety.
Before these methods can be used by cognitive behavioral therapists, some clinical
issues should be addressed. For example, patient satisfaction is critical in most
interventions, but is often overlooked in AMP. The probe detection paradigm was
developed over 25 years ago and is based on paradigms from cognitive psychology,
originally conceptualized as a onetime measure of attention allocation (Mathews &
MacLeod, 1985). However, this task may not be the most efficient method of training
attention. For example, the task is not sensitive to participants’ increased familiarity
with it, which results in faster and more accurate responses. As AMP techniques
are, by definition, based on learning principles, it is important to take into account
participants’ performance in presenting the stimuli. One outcome of this static
parameter space is that participants report that the task is tedious (Beard, Weisberg, &
Amir, 2011). We are currently developing a second generation AMP (S-AMP) that is
designed to be more effective by using the participants’ reaction times and accuracy to
modify the parameters of the program such that participants are always presented with
the optimal level of difficulty when completing the task. Moreover, points, levels, and
informative colored probes have been incorporated into the program to make it more
interactive. Finally, participants can track their progress throughout the tasks. These
modifications allow the paradigm to be more interactive, game-like, and engaging,
thereby increasing participants’ satisfaction and compliance. A preliminary result from
a pilot study comparing S-AMP with the original probe detection paradigm (AMP)
indicates an increase in patients’ satisfaction when using S-AMP as compared to AMP.
Additionally, after completion of S-AMP, participants showed more compliance with
self-conducted exposure exercises they were asked to complete.
Clinical Application
Recent reviews have called for utilizing AMP as an adjunctive intervention to CBT as
well as other therapeutic interventions (i.e., pharmacology; see Beard, 2011; Hakamata
et al., 2010; Hallion & Ruscio, 2011). Beard (2011) suggested that bias modification
programs could increase response rates for participants completing CBT, help patients
better engage in exposure therapy, and assist cognitive restructuring by bypassing auto-
matic mental habits. Recent studies by Amir and Taylor (2012) and Riemann, Kuck-
ertz, Rozenman, Weersing, and Amir (2013) have addressed these calls for research.
Amir and Taylor (2012) utilized an integrated computer-delivered treatment
program combining both AMP and computerized CBT (CCBT) that could be
self-administered in the home (or other settings) for patients suffering from GAD.
Results indicated that patients experienced significant symptom reductions from
pre- to postassessment with medium to large treatment effects and 79% no longer
met diagnostic criteria for GAD. Moreover, findings suggest that AMP plus CCBT
may be an effective and easily accessible treatment option for individuals with
anxiety. Furthermore, Riemann et al. (2013) examined the effect of AMP compared
to a control (ACC) as an adjunctive intervention to CBT and pharmacological
interventions in children diagnosed with a primary anxiety disorder. Results indicated
that AMP augmented CBT and pharmacological treatments when compared to ACC.
Clinically significant change was determined by the criteria defined by Jacobson and
Truax (1991) and was assessed using the Screen for Child Anxiety Related Emotional
Disorders (SCARED; Birmaher et al., 1997, 1999). Scores indicated that 52.4% of
youth in the AMP group demonstrated clinically significant change in symptoms
compared to 4.8% in the ACC group.
In summary, augmenting current therapeutic interventions (CBT, pharmacology)
has only been studied recently, yet appears to be beneficial. More research examining
AMP as an adjunctive intervention is necessary; however, clinicians versed in CBT
should consider integrating AMP into current treatment protocols in order to enhance
treatment response.
Concluding Remarks
In summary, researchers have established a link between basic attention processes and
anxiety symptoms. More recently, these links have been translated into theory-driven
treatment for anxiety disorders. Although encouraging and promising, questions
remain regarding the basic mechanisms involved in attention training as well as the
best method for incorporating attention training into clinical practice.
References
Amir, N., Beard, C., Burns, M., & Bomyea, J. (2009). Attention modification program
in individuals with generalized anxiety disorder. Journal of Abnormal Psychology, 118,
28–33.
Amir, N., Beard, C., Taylor, C. T., Klumpp, H., Elias, J., Burns, M., & Chen, X. (2009).
Attention training in individuals with generalized social phobia: A randomized controlled
trial. Journal of Consulting and Clinical Psychology, 77 , 961–973.
Amir, N., Elias, J., Klumpp, H., & Przeworski, A. (2003). Attentional bias to threat in social
phobia: Facilitated processing of threat or difficulty disengaging attention from threat?
Behaviour Research & Therapy, 41, 1325–1335.
Amir, N., & Taylor, C. (2012). Combining computerized home-based treatment for gen-
eralized anxiety disorder: An attention modification and cognitive behavioral therapy.
Amir, N., Taylor, C. T., & Donohue, M. C. (2011). Predictors of response to an attention
modification program in generalized social phobia. Journal of Consulting and Clinical
Amir, N., Weber, G., Beard, C., Bomyea, J., & Taylor, C. T. (2008).The effect of a single-
session attention modification program on response to a public-speaking challenge in
socially anxious individuals. Journal of Abnormal Psychology, 117 , 860–868.
Bair-Haim, Y. (2010). Research review: Attention bias modification (ABM): A novel treatment
for anxiety disorders. Journal of Child Psychology and Psychiatry, 51, 859–870.
Bar-Haim, Y., Dominique, L., Pergamin, L., Bakermans-Kranenburg, M. J., & van Ijzendoorn,
M. H. (2007). Threat related attentional bias in anxious and nonanxious individuals: A
meta-analytic study. Psychological Bulletin, 133, 1–24.
Bargh, J. A. (2011). Unconscious thought theory and its discontents: A critique of the critiques.
Social Cognition, 29, 629–647.
Barlow, D. H. (Ed.). (2007). Clinical handbook of psychological disorders: A step-by-step treatment
manual (4th ed.). New York, NY: Guilford Press.
Beard, C. (2011). Cognitive bias modification for anxiety: Current evidence and future
directions. Expert Review of Neurotherapeutics, 11, 299–311.
Beard, C., Sawyer, A. T., & Hofmann, S. (2012). Efficacy of attention bias modification using
threat and appetitive stimuli: A meta-analytic review. Behavior Therapy, 43, 724–740.
doi:10.1016/j.beth.2012.01.002
Beard, C., Weisberg, R. B., & Amir, N. (2011). Combined cognitive bias modification
treatment for social anxiety disorder: A pilot trial. Depression and Anxiety, 28,
981–988.
Beck, A. T., & Clark, D. A. (1997). An information processing model of anxiety: Automatic
and strategic processes. Behaviour Research and Therapy, 35, 49–58.
Beck, A. T., Steer, R. A., & Brown, G. K. (1996). Manual for Beck Depression Inventory-II .
San Antonio, TX: Psychological Corporation.
Birmaher, B., Brent, D. A., Chiappetta, L., Bridge, J., Monga, S., & Baugher, M. (1999).
Psychometric properties of the Screen for Child Anxiety Related Emotional Disorders
(SCARED): A replication study. Journal of the American Academy of Child & Adolescent
Psychiatry, 38, 1230–1236.
Birmaher, B., Khetarpal, S., Brent, D., Cully, M., Balach, L., Kaufman, J., & Neer, S. M.
(1997). The Screen for Child Anxiety Related Emotional Disorders (SCARED): Scale
construction and psychometric characteristics. Journal of the American Academy of Child
& Adolescent Psychiatry, 36, 545–553.
Bishop, S. J. (2009). Trait anxiety and impoverished prefrontal control of attention. Nature
Neuroscience, 12, 92–98.
Boettcher, J., Berger, T., & Renneberg, B. (2011). Internet-based attention training for social
anxiety: A randomized controlled trial. Cognitive Therapy and Research, 36, 522–536.
doi:10.1007/s10608-011-9374-y
Bradley, B. P., Mogg, K., & Lee, S. C. (1997) Attentional biases for negative informa-
tion in induced and naturally occurring dysphoria. Behavior and Research Therapy, 35,
911–927.
Bradley, B. P., Mogg, K., Millar, N., & White, J. (1995). Selective processing of negative
information: Effects of clinical anxiety, concurrent depression, and awareness. Journal of
Abnormal Psychology, 104, 532–536.
Carlbring, P., Apelstrand, M., Sehlin, H., Amir, N., Rousseau, A., Hofmann, S. G., &
Andersson, G. (2012). Internet-delivered attentional bias modification training in indi-
viduals with social phobia: A double blind randomized controlled trial. BMC Psychiatry,
12, 66.
Clasen, P. C., Wells, T. T., Ellis, A. J., & Beevers, C. G. (2012). Attentional biases and the
persistence of sad mood in major depressive disorder. Journal of Abnormal Psychology.
Advance online publication. doi: 10.1037/a0029211
Cougle, J. R., Wolitzky-Taylor, K. B., Lee, H., & Telch, M. J. (2007). Mechanisms of change
in ERP treatment of compulsive hand washing: Does primary threat make a difference?
Derakshan, N., & Eysenck, M. W. (2009). Anxiety, processing efficiency, and cognitive
performance. New developments from attentional control theory. European Psychologist,
14, 168–176.
Derryberry, D., & Reed, M. A. (2002). Anxiety-related attentional biases and their regulation
by attentional control. Journal of Abnormal Psychology, 111, 225–236.
Driver, J. (2001). A selective review of selective attention from the past century. British Journal
of Psychology, 92, 53–87.
Eizenman, M., Yu, L. H., Grupp, L., Eizenman, E., Ellenbogen, M., Gemar, M., & Levitan,
R. D. (2003). A naturalistic visual scanning approach to assess selective attention in major
depressive disorder. Psychiatry Research, 118, 117–128.
Eriksen, B. A., & Eriksen, C. W. (1974). Effects of noise letters upon identification of a target
letter in a nonsearch task. Perception and Psychophysics, 16, 143–149.
Eysenck, M. W. (1992). Anxiety: The cognitive perspective. Hove, England: Psychology Press.
Eysenck, M. W. (1997). Anxiety and cognition: A unified theory. Hove, England: Psychology
Press.
Eysenck, M. W., Derakshan, N., Santos, R., & Calvo, M. G. (2007). Anxiety and cognitive
performance: Attentional control theory. Emotion, 7 , 336–353.
Fan, J., McCandliss, B. D., Sommer, T., Raz, M., & Posner, M. I. (2002). Testing the
efficiency and independence of attentional networks. Journal of Cognitive Neuroscience,
14, 340–347.
First, M. B., Spitzer, R. L., Gibbon, M., & Williams, J. B.W. (1994). Structured Clinical
Interview for Axis I DSM-IV Disorders: Patient edition. New York, NY: Biometrics
Research Department.
Forster, S., & Lavie, N. (2009). Harnessing the wandering mind: The role of perceptual
load. Cognition, 111, 345–355.
Fox, E. (1994). Attentional bias in anxiety: A defective inhibition hypothesis. Cognition &
Emotion, 8, 165–195.
Gotlib, I. H., & Joormann, J. (2010). Cognition and depression: Current status and future
directions. Annual Review of Clinical Psychology, 6, 285–312.
Hakamata, Y., Lissek, S., Bar-Haim, Y., Britton, J. C., Fox, N. A., Leibenluft, E., & Pine, D. S.
(2010). Attention bias modification treatment: A meta-analysis toward the establishment
of novel treatment for anxiety. Biological Psychiatry, 68, 982–990.
Hallion, L. S., & Ruscio, A. M. (2011). A meta-analysis of the effect of cognitive bias
modification on anxiety and depression. Psychological Bulletin, 137 , 940–958.
Hamilton, M. (1959). The assessment of anxiety states by rating. British Journal of Medical
Heeren, A., Lievens, L., & Philippot, P. (2011). How does attention training work in social
phobia: Disengagement from threat or re-engagement to nonthreat? Journal of Anxiety
Disorders, 25, 1108–1115.
Heeren, A., Reese, H. E., McNally, R. J., & Philippot, P. (2012). Attention training toward
and away from threat in social phobia: Effects on subjective, behavioral, and physiological
measures of anxiety. Behavior Research and Therapy, 50, 30–39.
Hofmann, S. G. (2000). Self-focused attention before and after treatment of social phobia.
Holmes, A. J., & Pizzagalli, D. A. (2008). Spatio-temporal dynamics of error processing
dysfunctions in major depressive disorder. Archives of General Psychiatry, 65,
179–188.
Ingram, R. E., Bernet, C., & McLaughlin, S. (1994). Attentional allocation processes in
individuals at risk for depression. Cognitive Therapy and Research, 18, 317–332.
Jacobson, N. S., & Truax, P. (1991). Clinical significance: A statistical approach to defin-
ing meaningful change in psychotherapy research. Journal of Consulting and Clinical
Klumpp, H., & Amir, H. (2010). Preliminary study of attention training to threat and neutral
faces on anxious reactivity to a social stressor in social anxiety. Cognitive Therapy and
Research, 34, 263–271.
Kosslyn, S. M., Brown H. D., & Dror, I. E. (1999). Aging and the scope of visual attention.
Gerontology, 45, 102–109.
Koster, E. H. W., Crombez, G., Verschuere, B., & De Houwer, J. (2006). Attention to threat
in anxiety-prone individuals: Mechanisms underlying attentional bias. Cognitive Therapy
and Research, 30, 635–643.
Kuckertz, J. M., Gildebrant, E., Liliequist, B., Karlström, P., Väppling, C., Bodlund, O.,
& Carlbring, P. (in press). Internet-delivered treatment for social anxiety disorder: A
randomized trial of cognitive behavior therapy vs. cognitive bias modification.
Lavie, N. (2005). Distracted and confused?: Selective attention under load. Trends in Cognitive
Sciences, 9, 75–82.
Lavie, N. (2010). Attention, distraction, and cognitive control under load. Current Directions
in Psychological Science, 19, 143–148.
Li, S. W., Tan, J. Q., Qian, M. Y., & Liu, X. H. (2008). Continual training of attentional bias
in social anxiety. Behaviour Research & Therapy, 46, 905–912.
Liebowitz, M. R. (1987). Social phobia. Modern Problems of Pharmacopsychiatry, 22, 141–173.
Lundh, L. G., & Ost, L. G. (2001). Attentional bias, self-consciousness and perfectionism
in social phobia before and after cognitive behavioral therapy. Scandinavian Journal of
Mackinnon, D. P., Lockwood, C. M., Hoffman, J. M., West, S. G., & Sheets, V. (2002).
A comparison of methods to test mediation and other intervening variable effects.
Psychological Methods, 7 , 83–104.
MacLeod, C., Mathews, A., & Tata, P. (1986). Attentional bias in emotional disorders. Journal
of Abnormal Psychology, 1, 15–20.
MacLeod, C., Rutherford, E. M., Campbell, L., Ebsworthy, G., & Holker, L. (2002). Selective
attention and emotional vulnerability: Assessing the causal basis of their association
through the experimental manipulation of attentional bias. Journal of Abnormal Psychology,
111, 107–123.
Mathews, A., & MacLeod, C. (1985). Selective processing of threat cues in anxiety states.
Mathews, A., & MacLeod, C. (2002). Induced processing biases have causal effects on
anxiety. Cognition and Emotion, 16, 331–354.
Mathews, A., & MacLeod, C. (2005). Cognitive vulnerability to emotional disorders. Annual
Review of Clinical Psychology, 1, 167–195.
Mathews, A., Ridgeway, V., & Williamson, D. A. (1996) Evidence of attention to threatening
stimuli in depression. Behavior and Research Therapy, 34, 695–705.
Mattia, J. I., Heimberg, R. G., & Hope, D. A. (1993). The revised Stroop color-naming task
in social phobics. Behavior and Research Therapy, 31, 305–313.
McCabe, S., & Gotlib, I. H. (1993). Attentional processing in clinically depressed subjects: A
longitudinal investigation. Cognitive Therapy Research, 17 , 359–377.
McNally, R. J. (1995). Automaticity and the anxiety disorders. Behaviour Research and Therapy,
33, 747–754.
Meyer, T. J., Miller, M. L., Metzger, R. L., & Borkovec, T. D. (1990). Development and
validation of the Penn State worry questionnaire. Behaviour Research and Therapy, 28,
487–495.
Mogg, K., & Bradley, B. P. (1998). A cognitive-motivational analysis of anxiety. Behaviour
Mogg, K., & Bradley, B. P. (2005). Attentional bias in generalized anxiety disorder versus
depressive disorder. Cognitive Therapy and Research, 29, 29–45.
Mogg, K., Bradley, B. P., & Williams, R. (1995) Attentional bias in anxiety and depression:
The role of awareness. British Journal of Clinical Psychology, 34, 17–36.
Mogg, K., Bradley, B. P., Williams, R., & Mathews, A. (1993) Subliminal processing of
emotional information in anxiety and depression. Journal of Abnormal Psychology, 102,
304–311.
Moray, N. (1959). Attention in dichotic listening: Affective cues and the influence instructions.
Quarterly Journal of Experimental Psychology, 11, 56–60.
Najmi, S., & Amir, N. (2010). The effect of attention training on a behavioral test of contam-
ination fears in individuals with subclinical obsessive–compulsive symptoms. Journal of
Ouimet, A. J., Gawronski, B., & Dozois, D. J. A. (2009). Cognitive vulnerability to anxiety: A
review and an integrative model. Clinical Psychology Review, 29, 459–470.
Pashler, H., Johnson, J., & Ruthruff, E. (2001). Attention and performance. Annual Review
of Psychology, 52, 629–651.
Pessoa, L. (2009). How do emotion and motivation direct executive control? Trends in
Cognitive Sciences, 13, 160–166.
Pessoa, L., McKenna, M., Gutierrez, E., & Ungerleider, L. G. (2002). Neural processing of
emotional faces requires attention. Proceedings of the National Academy of Sciences of the
United States of America, 99, 11458–11463.
Pishyar, R., Harris, L. M., & Menzies, R. G. (2008). Responsiveness of measures of attentional
bias to clinical change in social phobia. Cognition and Emotion, 22, 1209–1227.
Posner, M. I. (1980). Orienting of attention. Quarterly Journal of Experimental Psychology, 32,
3–25.
Posner, M. I., & Peterson, S. E. (1990). The attention system of the human brain. Annual
Review of Neuroscience, 13, 25–42.
Posner, M. I., Rothbart, M. K., Sheese, B. E., & Tang, Y. (2007). The anterior cingulate gyrus
and the mechanism of self-regulation. Cognitive, Affective & Behavioral Neuroscience, 7 ,
391–395.
Ratcliff, R., & Van Dongen, H. P. A. (2011). A diffusion model for one-choice reaction time
tasks and the cognitive effects of sleep deprivation. Proceedings of the National Academy of
Sciences, 108, 11285–11290.
Ratcliff, R., Van Zandt, T., & McKoon, G. (1999). Connectionist and diffusion models of
reaction time. Psychological Review, 106, 261–300.
Reese, H. E., McNally, R. J., Najmi, S., & Amir, N. (2010). Attention training for reducing
spider fear in spider-fearful individuals. Journal of Anxiety Disorders, 24, 657–652.
Riemann, B. C., Kuckertz, J. M., Rosenman, M., Weersing, V. R., & Amir, N. (2013).
Augmentation of youth cognitive behavioral and pharmacological interventions with
attention modification: A preliminary investigation. Depression and Anxiety, advance
online publication. PMID: 23658147.
Schmidt, N. B., Richey, J. A., Buckner, J. D., & Timpano, K. R. (2009). Attention training
for generalized social anxiety disorder. Journal of Abnormal Psychology, 118, 5–14.
Sheehan, D. V. (1983). The anxiety disease. New York, NY: Scribner.
Shiffrin, R. M., & Schneider, W. (1977). Controlled and automatic human information
processing: II. Perceptual learning, automatic attending, and a general theory. Psychological
Review, 84, 127–190.
Simons, D. J., & Chabris, C. F. (1999). Gorillas in our midst: Sustained inattentional blindness
for dynamic events. Perception, 28, 1059–1074.
Spielberger, C. D., Gorsuch, R. L., Lushene, R., Vagg, P. R., & Jacobs, G. A. (1983). Manual
for the State-Trait Anxiety Inventory. Palo Alto, CA: Consulting Psychologist Press.
Tallis, F., Eysenck, M., & Mathews, A. (1992). A questionnaire for the measurement of
nonpathological worry. Personality and Individual Differences, 13, 161–168.
Taylor, C. T., Aupperle, R. L., Flagan, T., Simmons, A. N., Amir, N., Stein, M. B., & Paulus,
M. P. (in press). Neural Correlates of a Computerized Attention Modification Program
in Anxious Subjects. Social Cognitive and Affective Neuroscience.
Turner, S. M., Beidel, D. C., & Dancu, C. V. (1996). Social phobia and anxiety inventory:
Manual. Toronto, Canada: Multi-Health Systems.
Turner, S. M., Beidel, D. C., Dancu, C. V., & Stanley, M. A. (1989). An empirically derived
inventory to measure social fears and anxiety: The social phobia and anxiety inventory.
Psychological Assessment: Journal of Consulting and Clinical Psychology, 1, 35–40.
Van Bockstaele, B., Koster, E. H. W., Verschuere, B., Crombez, G., & De Houwer, J. (2012).
Limited transfer of threat bias following attentional retraining. Journal of Behavior Therapy
and Experimental Psychiatry, 43, 794–800.
Van Bockstaele, B., Verschuere, B., De Houwer, J., & Crombez, G. (2010). On the costs
and benefits of directing attention toward or away from threat-related stimuli: A classical
conditioning experiment. Behaviour Research and Therapy, 48, 692–697.
Van Bockstaele, B., Verschuere, B., Koster, E. H. W., Tibboel, H., De Houwer, J., &
Crombez, G. (2011). Effects of attention training on self-reported, implicit, physiological
and behavioural measures of spider fear. Journal of Behavior Therapy and Experimental
Wells, A., White, J., & Carter, K. (1997). Attention training: Effects on anxiety and beliefs in
panic and social phobia. Clinical Psychology and Psychotherapy, 4, 226–232.
Wells, T. T., & Beevers, C. G. (2010). Biased attention and dysphoria: Manipulating selective
attention reduces subsequent depressive symptoms. Cognition & Emotion, 24, 719–728.
doi:10.1080/02699930802652388
White, C. N., Ratcliff, R., Vasey, M. W., & McKoon, G. (2010). Anxiety enhances threat
processing without competition among multiple inputs: A diffusion model analy-
sis. Emotion, 10, 662–677.
Williams, J. M. G., Mathews, A., & MacLeod, C. (1996).The emotional Stroop task and
psychopathology. Psychological Bulletin, 120, 3–24.
Williams, J. M. G., Watts, F. N., MacLeod, C., & Mathews, A. (1997). Cognitive psychology
and emotional disorders (2nd ed.). Chichester, England: John Wiley & Sons, Ltd.
Wisco, B. E. (2009). Depressive cognition: Self-reference and depth of processing. Clinical
Psychology Review, 29, 382–392.
10
Habit Reversal
Michael P. Twohig, Ellen J. Bluett,
Kate L. Morrison, and Michelle R. Woidneck
Utah State University, United States
Introduction
Habit reversal is a multicomponent behavioral procedure originally developed by

Azrin and Nunn in 1973 and presented in their book Habit control in a day (Azrin &
Nunn, 1973a). This treatment package was tested for a large variety of clinical issues
including tic disorders, trichotillomania, skin picking, thumb sucking, and other oral
habits. Modified versions of the treatment have been used with temporomandibular
joint disorders and stuttering. Since habit reversal’s inception, research has shown
that the treatment can be simplified into three main treatment components and still
remain effective. This simplified procedure has also been shown to be an effective
treatment for a wide range of other behaviors and for individuals of varying ages.
Currently, habit reversal is often incorporated with cognitive procedures, but it is still
the cornerstone of a variety of treatment packages for repetitive behavior problems
and obsessive-compulsive spectrum disorders. This chapter will cover the model on
which habit reversal is based, its empirical support, and a basic clinical overview of
its use.
Traditional Habit Reversal
The original habit reversal procedure developed by Azrin and Nunn (1973b) concep-
tualized nervous habits and tics as initially normal responses to stressful psychological
or physical events that, over time, become habitual. These researchers theorized that
the continued action strengthens the muscle groups used to engage in the habit-
ual behavior and that the opposing, unused muscle groups subsequently weaken.
This results in less ability to consciously refrain from engaging in the response and

DOI: 10.1002/9781118528563.wbcbt10
further inattention to the occurrence of the nervous habit. Azrin and Nunn (1973b)
suggested that social reinforcement, such as sympathy, aids in strengthening the
habitual response.
In order to decrease the occurrence of “nervous” habits, Azrin and Nunn (1973b)
recommended introducing a response that competes with the ability to engage in
the behavior. Before introducing an incompatible response, however, awareness of
the action must first be developed. Only then can a person engage in a competing
response to strengthen the unused muscles and disrupt the habitual chain of responses.
Reversing or eliminating social reinforcement that may be occurring for the target
behavior was also suggested by Azrin and Nunn (1973b). The initial protocol
included four phases: awareness training, competing response practice, habit control
motivation, and generalization training. Awareness training consists of response
description (describing and acting out target behaviors to the therapist), response
detection (labeling when the target occurs), early warning (detecting early signs of
the target behavior), and situation awareness training (discussion and description of
situations where the behavior is most likely to occur).
The treatment then moves into the competing response practice stage. Within
this stage, a response is trained that is incompatible with the target behavior. The
competing response procedure was adapted from previous overcorrection procedures
used to treat self-stimulation in children with autism and developmental delays (Foxx
& Azrin, 1972, 1973a, 1973b). For example, a child with a thumb sucking behavior
will use a competing response of clenching her fists instead of engaging in thumb
sucking, or a person with an elbow tic will press his elbow into his side. According to
Azrin and Nunn (1973b) the competing response must (a) be opposite of the habit,
(b) be done for a few minutes, (c) produce increased awareness by an equivalent level
of tense muscles as those involved in the habit, (d) be unnoticeable by others and easy
to engage in, and (e) strengthen the opposing muscles to the habit. The competing
response is held for approximately three minutes either with the presence of an urge
to engage in a habit or immediately after engaging in the habit.
The next phase of the protocol is to increase motivation to control the habit. Azrin
and Nunn (1973b) recognized that clients need to be engaged and motivated to
participate in the habit reversal techniques for it to be effective. In order to address
this issue they suggest implementing the Habit Inconvenience Review which involves
the therapist and client discussing the embarrassment, inconveniences, and distress
experienced because of the habitual behavior. Social support is addressed next and
involves having loved ones encourage the engagement in competing responses by
reinforcing good effort, by commenting on appearance after a habit-free period, and
by reminding the client to engage in the competing response when he or she misses a
cue or was unaware of a habit. The therapist will also make phone calls to collect data
and reinforce competing responses during that same contact. Because adults choose
to present to treatment, their motivation is usually more accessible than children who
were brought by their parents and do not choose to get rid of their habit. In this
situation, parents are asked to guide children through the competing response when
the child forgets or does not engage in it.
The next stage is generalization training. This includes practicing the competing
response with the therapist until it is correctly used, followed by symbolic rehearsal.
Habit Reversal 205
During symbolic rehearsal, the client imagines situations in which habits are more
likely to occur and visualizes him- or herself engaging in the competing response
contingent on that urge. To further generalization, the client and the therapist have
a conversation in nonhabit reversal talk during which the client is to note when he or
she is engaging in habits. If the client does not notice this behavior, then the therapist
gently reminds him or her by staring at the body part that is part of the competing
response, raising eyebrows, or saying “hmmm” (Azrin & Nunn, 1973b).
Modifications to the Original Procedure:

Simplified Habit Reversal Treatment
Studies have been conducted to determine which aspects of the original Azrin
and Nunn (1973b) protocol are essential. Research has shown that not all of
the components initially listed are necessary and that other conceptualizations of the
occurrence of tics and habits, as well as the mechanism of change in habit reversal, may
be more accurate. One of the initial changes to the original package was a reduction
in total intervention length when Miltenberger, Fuqua, and McKinley (1985) found
that awareness training and engaging in a competing response alone showed no
difference in treatment effects than the full Azrin and Nunn (1973b) protocol. The
authors noted that the competing response aspect of the protocol cannot be done
without first doing awareness training, as it is impossible to know when to engage in
the competing response if one is unaware of the habit. Various studies have found
that self-monitoring and awareness training alone or in combination can be sufficient
(Ladouceur, 1979; Ollendick, 1981; Wright & Miltenberger, 1987).
Woods, Miltenberger, and Lumley (1996) sequentially introduced aspects of habit
reversal in order of least to most effortful to determine which aspects of the treatment
were necessary. The four phases of treatment were (a) awareness training, (b)
awareness training and self-monitoring, (c) awareness training, self-monitoring, and
social support, and (d) awareness training, social support, and use of a competing
response. Two of the four participants required the full simplified treatment (awareness
training, competing response, and social support), one required awareness training
and self-monitoring, and one only needed awareness training to reduce or eliminate
tics. In a larger study Twohig, Woods, Marcks, and Teng (2003) compared three 50-
minute sessions of simplified habit reversal training consisting of awareness training,
competing response training, and social support to an attentional control condition in
adult nail biting. Results supported simplified habit reversal and further highlighted
the possible simplicity of the intervention. An investigation of an even more simplified
version of this treatment showed no differences among 40 adult nail biters who were
treated with either the three aforementioned aspects of simplified habit reversal or
awareness training plus competing response training alone (Flessner et al., 2005).
Additional research is needed to determine whether this two-component treatment
remains effective for children and adolescents, as social support may be an essential
treatment component for this population.
In addition to not needing all the components of the original treatment package to
produce clinically significant results, findings have shed light on the possible process
of change underlying habit reversal. While the function of awareness training is largely
to help the individual know when to use the competing response, the function of the
competing response is still somewhat unclear; however, there is some evidence as to
why it is useful. Not surprisingly, the competing response must be contingent on the
habitual behavior rather than at prescribed times throughout the day (Miltenberger
& Fuqua, 1985), calling into question the idea that competing responses are building
muscles opposite to the habit or tic. Surprisingly, multiple researchers showed that the
competing response need not be related to the habitual behavior (Sharenow, Fuqua,
& Miltenberger, 1989; Woods et al., 1999). Sharenow et al. (1989), for example,
found that fist clenching can be an effective competing response for an eye-blinking
tic. Woods et al. (1999) showed that fist clenching and clenching knees are both
effective with oral digital habits. Nevertheless, most therapists and researchers who
use habit reversal use a competing response that is related to the habitual behavior
such as making fists for skin picking or hair pulling or actions that are opposite to the
tic (Miltenberger et al., 1998).
The final relevant finding that sheds light on the possible process of change has to
do with the proper duration of the competing response. A study comparing 5-second,
1-minute, and 3-minute competing responses found that all three conditions were
equally useful in reducing the rate of the habit from pretreatment to posttreatment;
however, notable relapse was seen in the 5-second condition at 3-month follow-up
compared to the other two conditions (Twohig & Woods, 2001a). At the clinical end,
these results suggest that a competing response of at least 1 minute is preferred. These
results also suggest that some amount of meaningful learning is occurring during the
competing response and that a longer duration is better than a very brief one.
Summary
This brief review suggests that habit reversal has been in development and use since
the early 1970s. Habit reversal was originally developed as a multicomponent package
and has since been shortened into a brief treatment focusing on competing response
training aided by the awareness training component. Research indicates that the
competing response needs to be done contingent on the warning signs (urges to
engage in the behavior or preliminary steps to the behavior) or the target behavior
itself. The competing response may be of any form, but should be at least a minute in
duration or longer.
Data on the Effectiveness of Habit Reversal
In the following section we continue with a review of the major disorders for which
habit reversal has been shown to be effective (see Table 10.1 for a list of controlled
trials). A recent meta-analysis consisting of 18 studies and 575 participants found that
habit reversal was an efficacious treatment for a wide range of maladaptive behaviors in
varied samples (Bate, Malouff, Thorsteinsson, & Bhullar, 2011). Furthermore, Bate
et al. (2011) found that habit reversal was equivalently effective across disorders in
which it is commonly used, including tics, stuttering, nail biting, thumb sucking, and
Table 10.1 Controlled Studies of Habit Reversal and Its Variants
Study Age and (N) Dependent variable Outcome
Oral-digital
Azrin et al. (1980d) Children (30) Frequency of finger HRT > bitter
sucking substance
Azrin et al. (1982) Children (10) Frequency of oral HRT > NP
habit
Christensen & Children (30) Frequency of thumb HRT = DR > WL
Sanders (1987) sucking
Woods et al. (1999) Children (26) Frequency of finger HRT (using similar
sucking CR) = HRT (using
dissimilar CR) > WL
Nail biting
Azrin et al. (1980c) Adults (97) Frequency of nail HRT > NP
biting
Horne & Wilkinson Adults (40) Nail length and SR HRT + NC = HRT +
(1980) frequency of nail NC + TG = NC +
biting TG > WL
Twohig et al. (2003) Adults (25) Nail length HRT > supportive
psychotherapy
Flessner et al. (2005) Adults (40) Nail length and SR SHRT = AT + CR
frequency of nail
biting
Temporomandibular
disorders
Gramling et al. Adults (16) Pain level HRT > control
(1996)
Townsend et al. Adults (20) Pain level HRT (with minimal
(2001) therapist contact) >
WL
Glaros et al. (2007) Adults (8) Pain level HRT = splint
Tic disorders
Azrin et al. (1980a) Adolescents/ Frequency of tics HRT > NP
adults (22)
Miltenberger et al. Mixed (9) Frequency of MT HRT = CR + AT
(1985)
Azrin & Peterson Mixed (10) Frequency of MT HRT > WL
(1990) and VT
O’Connor et al. Adults (13) Frequency of MT HRT = cognitive
(1997) behavioral
O’Connor et al. Adults (47) Frequency of tics HRT > WL
(2001)
Wilhelm et al. (2003) Adults (29) YGTSS HRT > supportive
psychotherapy
Verdellen et al. Mixed (43) YGTSS HRT = exposure +
(2004) response prevention
(Continued Overleaf )
Table 10.1 (Continued)
Study Age and (N) Dependent variable Outcome
Deckersbach et al. Adults (28) YGTSS HRT > supportive

(2006) psychotherapy
Piacentini et al. Children/ YGTSS HRT > control group
(2010) adolescents
(126)
Franklin et al. (2011) Adolescents Tic severity HRT = HRT + ACT
(13)
Trichotillomania
Azrin et al. (1980b) Adolescents/ Instance or duration HRT > NP
adults (34) of hair pulling
Ninan et al. (2000) Adults (16) Multiple self-report HRT > clomipramine
measures > placebo
van Minnen et al. Adults (40) MGHHS HRT > WL >
(2003) fluoxetine
Skin picking
Teng et al. (2006) Adults (19) Frequency of picking HRT > WL
Stuttering
Azrin et al. (1979) Adults (38) Stuttering episodes RB > SD
Ladouceur et al. Mixed (16) Syllables stuttered RB = RB
(1981)
Ladouceur et al. Adults (12) Syllables stuttered RB = RB + SM = RB
(1982) + SM + BF of
respiration = RB +
SM + BF of
respiration + BF of
muscle tension
Ladouceur & Adolescents/ Syllables stuttered RB with parental
Martineau (1982) adults (21) assistance = RB
without parental
assistance >WL
Saint-Laurent & Adults (40) Syllables stuttered Intensive RB =
Ladouceur (1987) intensive RB +
maintenance phase =
spaced RB = spaced
RB + maintenance
phase > placebo
Waterloo & Adults (32) Syllables stuttered RB > WL
Gotestam (1988)
Notes. AT = awareness training; BF = biofeedback; CR = competing response; DR = differential

reinforcement; FU = follow-up; HRT = habit reversal training; MGHHS = Massachusetts General
Hospital Hairpulling Scale; NC = nail care; NP = negative practice; Post = posttreatment; Pre =
pretreatment; Red = reduction; SD = systematic desensitization; SHRT = simplified habit reversal
training; SM = self-monitoring; SR = self-report; TG = target goals; YGTSS = Yale Global Tic Severity
Scale; RB = regulated breathing; WL = wait-list.
Habit Reversal 209
lip biting. This meta-analysis revealed that, compared to other control conditions,
habit reversal was more effective from pretreatment to posttreatment.
Oral Habits
Azrin, Nunn, and Frantz-Renshaw (1982) initially found that habit reversal was
an effective treatment for a variety of self-destructive oral habits including biting,
chewing, licking, or sucking of the tongue, cheeks, lips, and roof of the mouth.
In this study 10 adults and children were treated with a single 2-hour session of
either habit reversal or negative practice (intentionally engaging in a behavior until it
becomes aversive). In a 22-month follow-up these researchers found that individuals
treated with habit reversal reduced their oral habits by 99%, whereas those treated
with negative practice reduced their oral habits by only 60% (Azrin et al., 1982).
A comparison trial examined habit reversal versus the use of a bitter substance for
treating 30 children with problematic thumb sucking. Habit reversal was shown to
reduce thumb sucking behavior by 95% in comparison to a bitter substance treatment
which only reduced thumb sucking behavior by 35% (Azrin, Nunn, & Frantz-
Renshaw, 1980d). In a study comparing habit reversal to differential reinforcement
for thumb sucking, both conditions reduced thumb sucking with no significant
difference between groups (Christensen & Sanders, 1987). Woods and colleagues
(1999) compared the efficacy of similar versus dissimilar competing responses in
children with chronic oral habits, a majority of whom had thumb sucking as their
primary complaint. Both groups showed a significant decrease in oral habit behavior
compared to the control group, although no differences were found in treatment
gains between groups. As is evidenced in this review, there are more data on the
utility of habit reversal for children with oral-digital habits than for adults; this is likely
because this problem area is more common in that age group.
Nail Biting
Several earlier studies examined the efficacy of habit reversal in treating nail biting, a
problematic behavior found in both adults and children. Azrin and Nunn (1973b)
hypothesized that nail biting occurred for a number of reasons including response
chaining, limited awareness, excessive practice, and tolerance. In a preliminary study
of habit reversal for nail biting, habit reversal training was found to be effective
immediately after a single 2-hour session in both adults and children (Nunn & Azrin,
1976). A larger study compared habit reversal to negative practice with 97 adults
who bit their nails (Azrin, Nunn, & Frantz, 1980c). Concurrent with earlier studies,
habit reversal reduced nail biting by 99% through 5-month follow-up compared to
a reduction of only 60% in those treated with negative practice. Yet another study
compared three conditions: habit reversal where part of the competing response was
functional nail care (clipping, filing), habit reversal plus nail care and target goals,
and nail care plus target goals to a control group. Both conditions that included
habit reversal were more successful at decreasing nail biting behavior, whereas the
condition that excluded habit reversal was found to be only semi-successful (Horne &
Wilkinson, 1980).
More recent studies have examined the effects of simplified habit reversal on nail
biting, which consists of awareness training, competing response training, and social
support. In a study that compared simplified habit reversal to a social support control
condition, adults in the simplified habit reversal condition had significantly greater
nail length than did those in the control condition (Twohig et al., 2003). One study
evaluated the necessity of a social support component in simplified habit reversal
for treating nail biting by comparing two versions of simplified habit reversal, one
with social support and one without. Although both treatment conditions produced
significant effects on reducing nail biting behavior, no significant difference was found
between treatment conditions (Flessner et al., 2005). Also of note, a study conducted
by Twohig and Woods (2001a) compared the efficacy of habit reversal across 1-
minute, 3-minute, and 5-second competing response durations. Results showed an
increase in nail length across all groups; however, long-term results only occurred in
the 1- and 3-minute groups.
Temporomandibular Disorder
Temporomandibular disorder is also called “TMD” or “TMJ” by many health profes-
sionals. Temporomandibular disorder includes a number of disorders of the jaw joints,
the muscles involved, dental occlusion, or the involved nerves. Habit reversal has been
shown effective in treating temporomandibular disorder. Several smaller studies have
found that habit reversal is effective at reducing facial pain associated with temporo-
mandibular disorder (Gramling, Neblett, Grayson, & Townsend, 1996; Peterson,
Dixon, Talcott, & Kelleher, 1993). Furthermore, two studies with women found that
only habit reversal was efficacious for reducing pain due to temporomandibular disor-
der when compared to a wait-list or an oral splint (Glaros, Kim-Weroha, Lausten, &
Franklin, 2007; Townsend, Nicholson, Buenaver, Bush, & Gramling, 2001). Within
the same family, habit reversal has been shown to reduce pain associated with bruxism,
a severe and common dental problem that is described as grinding or gnashing of the
teeth or clenching and clicking of the teeth (Glaros & Rao, 1977; Olkinuora, 1969;
Rosenbaum & Ayllon, 1981a).
Tic Disorders
The larger category of tic disorders includes Tourette’s disorder (both motor and
vocal tics) and chronic tic disorders (either motor or vocal tics). The effects of habit
reversal on transient tic disorder (presence of tics for brief periods of time) have not
been tested for obvious reasons. Although pharmacotherapy is the most widely used
treatment for treating Tourette’s disorder, habit reversal is effective in treating this
condition (Carr & Chong, 2005; Cook & Blacher, 2007; Himle, Woods, Piacentini,
& Walkup, 2006). One review implemented the criteria for evidence-based treat-
ment created by the Task Force on Promotion and Dissemination of Psychological
Procedures by Division 12 of the American Psychological Association to examine
29 studies using habit reversal as a psychosocial treatment for tic disorders. Only
12 studies were used in their final analysis, concluding that due to methodological
shortcomings habit reversal was considered a probably efficacious treatment for tic
Habit Reversal 211
disorders (Carr & Chong, 2005). Following this review, Cook and Blacher reviewed
several treatments used to treat tics including habit reversal training, massed negative
practice, self-monitoring, contingency management, exposure and response preven-
tion, and cognitive behavioral treatment. After specifically reviewing the 20 studies,
including those in the Carr and Chong (2005) review, they found that habit reversal
was a well-established treatment for tic disorders (Cook & Blacher, 2007).
Given that habit reversal has been most researched with tic disorders, only the
larger studies are reviewed in detail in this chapter. See Table 10.1 for controlled
studies of habit reversal for tic disorders. An earlier controlled trial, examining
unspecified tic disorders, compared habit reversal to massed negative practice and
found that habit reversal reduced tics by 92% versus a reduction of 33% in massed
negative practice (Azrin, Nunn, & Frantz, 1980a). Yet another study found that habit
reversal, compared to habit reversal plus cognitive therapy, reduced self-reported tics
posttreatment with no difference between groups (O’Connor, Gareau, & Borgeat,
1997). In more recent studies, habit reversal was compared to supportive therapy for
treating adults with Tourette’s disorder, which resulted in a significant improvement
in the habit reversal group compared to the supportive therapy group (Deckersbach,
Rauch, Buhlmann, & Wilhelm, 2006; Wilhelm et al., 2003). Finally, only one
study to date has compared habit reversal to exposure plus response prevention in
treating Tourette’s disorder. Results showed a significant reduction in tic severity for
both groups, with no significant difference between groups on outcome measures
(Verdellen, Keijsers, Cath, & Hoogduin, 2004).
In the largest study to date on the psychosocial treatment of Tourette’s disorder,
126 children and adolescents, across three sites, were treated with Comprehensive
Behavioral Intervention for Tics (CBIT) which has habit reversal as its primary com-
ponent (Piacentini et al., 2010). CBIT outperformed the supportive psychotherapy
and education condition in reducing tic severity. Notably, 52% in the CBIT condi-
tion versus 14% in the control condition were rated as much or very improved as a
result of the intervention. Despite the empirical evidence for behavioral treatment for
Tourette’s disorder, including habit reversal, a recent study with two national surveys
found that most clients do not receive this efficacious behavioral treatment (Woods,
Conelea, & Himle, 2010).
Trichotillomania
Trichotillomania is characterized by excessive hair loss due to chronic hair pulling.
A recent systematic review examined randomized control trials that investigated the
efficacy of habit reversal training, pharmacotherapy with selective serotonin reuptake
inhibitors, and pharmacotherapy with clomipramine to one another or a placebo
control condition (Bloch et al., 2007). While the paper only reviewed seven studies
with a total of 157 completers, habit reversal training was found to be the most
effective treatment (Bloch et al., 2007).
As in the case of many of the disorders previously discussed, Azrin, Nunn, and
Frantz (1980b) were among the first to compare habit reversal training to negative
practice in 34 individuals diagnosed with trichotillomania. In this study, habit reversal
training was more effective than negative practice. Hair pulling was reduced by 99%
on the first day of habit reversal. In contrast, hair pulling was reduced by only 69%
during the third week of negative practice. Supporting these initial results, a multiple
baseline design examining the frequency of hair pulling found that habit reversal
reduced hair pulling after one session and eliminated the behavior within 3 weeks
(Rosenbaum & Ayllon, 1981b). Yet another study employed habit reversal training
in a group setting for five individuals, in which three of the five maintained treatment
gains at 1-month follow-up and two continued to exhibit treatment improvements
at 6-month follow-up. In addition, several studies have compared the efficacy of
habit reversal training to pharmacotherapy. One randomized control trial compared
clomipramine to habit reversal and a control condition. Habit reversal was significantly
more efficacious than the control and clomipramine conditions (Ninan, Rothbaum,
Marsteller, Knight, & Eccard, 2000). Another randomized trial compared 12 weeks of
fluoxetine to biweekly sessions of habit reversal and a 12-week wait-list control. Habit
reversal was more efficacious than fluoxetine although the between-group difference
was only significant at a trend level (van Minnen, Hoogduin, Keijsers, Hellenbrand, &
Hendriks, 2003).
Skin Picking
Despite the prevalence of skin picking, there has been minimal research conducted
on effective treatments (Teng, Woods, & Twohig, 2006). Two case studies found
that habit reversal was an efficacious treatment for those with skin picking disorder
measured by both the frequency of picking and intensity or severity levels (Deckers-
bach, Wilhelm, Keuthen, Baer, & Jenike, 2002; Twohig & Woods, 2001b). A larger
pilot study examined 19 participants who were assigned to either a wait-list control
or simplified habit reversal. Determined by both self-reported frequency of picking
and photos examined for severity of damage, participants in the habit reversal group
indicated a 77% reduction in skin picking frequency compared to a 16% reduction in
the control group. Photograph ratings also indicated a significant reduction in skin
damage in the habit reversal group compared to the wait-list control group (Teng
et al., 2006).
Stuttering
An adapted version of habit reversal, known as regulated breathing, was created
specifically for stuttering (Azrin & Nunn, 1974). Regulated breathing treatment
contains very similar components to habit reversal training including awareness
training, relaxation, competing response training (usually diaphragmatic breathing
prior to word utterance), motivation training, and generalization training. A review
of studies that implemented regulated breathing was conducted by Woods, Twohig,
Fuqua, and Hanley (2000). The authors concluded that regulated breathing produced
a 70.5% decrease in stuttering and a 22.4% increase in speech rate, with rates
maintaining at 4 to 10 months posttreatment. An initial efficacy study conducted
by Azrin and Nunn (1974) found that regulated breathing decreased stuttering
for all but one of 14 participants. Many studies followed confirming that regulated
Habit Reversal 213
breathing is an effective treatment for stuttering (e.g., Williamson, Epstein, & Coburn,
1981).
Various modifications to the original regulated breathing protocol have been tested.
A series of smaller studies found that the usage of a simplified regulated breathing
protocol was effective for treating males with a stuttering disorder (Gagnon &
Ladouceur, 1992; Wagaman, Miltenberger, & Arndorfer, 1993). Similar results were
found in two case studies with adults (Miltenberger, Wagaman, & Arndorfer, 1996).
Furthermore, two studies in particular examined the effects of implementing awareness
training in addition to the regulated breathing procedure. Both studies showed
that these procedures resulted in a reduction of stuttering; however, the addition
of awareness training did not result in better outcomes than regulated breathing
alone (Ladouceur, Boudreau, & Théberge, 1981; Ladouceur, Côté, Leblond, &
Bouchard, 1982). Yet another study examined the addition of parental assistance
to regulated breathing versus regulated breathing alone versus a wait-list condition.
Results showed that the addition of parental assistance did not increase treatment
outcome over the standard regulated breathing treatment (Ladouceur & Martineau,
1982). One additional study utilized a wait-list control to evaluate the efficacy of
regulated breathing. Although the groups did not differ at baseline, the regulated
breathing group improved significantly more than did the control group at 8-month
follow-up (Waterloo & Gotestam, 1988).
Enhanced Habit Reversal Variations
The original habit reversal procedure contained components, such as relaxation, aimed
at addressing the internal states that are associated with habit behaviors and tics. Since
that time, technology has increased and more empirically supported techniques have
been developed to address issues such as anxiety and poor motivation to engage in
treatment. Initially, cognitive behavioral components were added to simplified habit
reversal (Keuthen, Stein, & Christenson, 2001), but since that time techniques from
newer forms of cognitive behavioral therapy, such as acceptance and commitment
therapy (ACT; Twohig & Woods, 2004) and dialectical behavior therapy (DBT;
Keuthen et al., 2010), have been used to support habit reversal. It is hypothesized
that the habit reversal procedure is not as effective with those who already attend
to and are aware of their habits but are engaging in them to reduce, alter, or avoid
physical or emotional experiences, and that treatment components from cognitive
behavioral therapy might aid treatment (Keuthen et al., 2010; Twohig & Woods,
2004).
Thus far, ACT enhanced habit reversal has been tested with individuals with
trichotillomania (Twohig & Woods, 2004; Woods, Wetterneck, & Flessner, 2006),
Tourette’s disorder (Franklin, Best, Wilson, Loew, & Compton, 2011), and chronic
skin picking (Flessner, Busch, Heideman, & Woods, 2008). The database for its
use with trichotillomania is substantial and available as a published treatment manual
(Woods & Twohig, 2008), whereas its application to Tourette’s disorder is preliminary
and not yet supported empirically.
Although ACT and DBT have overlap in concept, one of the main differences is
that within DBT there is a focus of change strategies for internal experiences as well as
the use of acceptance procedures (Keuthen et al., 2010). In ACT, instead, acceptance
is taught as an alternative to attempts to avoid or alter internal experiences. DBT and
habit reversal has been tested in an open trial (N = 10) in the treatment of trichotil-
lomania with reductions in trichotillomania from pretreatment to posttreatment, and
modest improvements at 3- and 6-month follow-up (Keuthen et al., 2010, 2011).
Clinical Overview: Brief Simplified Habit Reversal Manual
As presented previously in this chapter, simplified habit reversal is a relatively straight-

forward intervention. This intervention can be fully implemented in one session, but
in most trials it is implemented in the first session, and reviewed and practiced in
two subsequent sessions. Simplified habit reversal contains two main components
(awareness and competing response training) and one additional component (social
support) used to increase compliance. This section provides a general review of the
procedure for its clinical use.
Awareness Training
The function of the awareness training phase of habit reversal is to help the client
be aware of the times he or she will need to engage in the competing response. This
is necessary because, in most situations, there are some instances of the repetitive
behavior that occur outside of consciousness. By the end of the awareness training
module, the client should be aware of the behaviors that precede the repetitive behav-
ior (often called “warning signs”), the actions involved in the repetitive behavior, and
the inner experiences that precede or go along with the action (often called “urges”).
Awareness training begins by having the client describe the target behavior and all
aspects of it. One useful strategy is to have the client practice the movements involved
in the repetitive behavior. The same thing is done with the actions that precede the
repetitive behavior. Using an example of trichotillomania, the client would practice
and think about the movements that are involved in hair pulling as well as the actions
that usually precede pulling such as rubbing one’s hair or resting one’s elbow on the
arm of a chair. After awareness is enhanced, the client’s ability to detect these actions
can be strengthened by asking him or her to detect the therapist’s mimicked instances
of the warning sign or the repetitive action. This is usually practiced for a few minutes
or until the client is reliably detecting the occurrences. If a client does not detect an
instance, he or she should simply be informed that one had occurred. An example of
how this phase can be described to the client is as follows:
THERAPIST: OK, now that we are pretty clear on what your warning signs are and what
the pulling looks like, I would like to practice helping you get better at catching when
they occur. A good way to begin to do this is to have me do some of these things and
have you catch me. So, if you are willing, I will either engage in one of your warning
signs or put my hand to my hair like I am about to pull, and when you see that, I just
Habit Reversal 215
want you to raise a finger or say “There’s one.” I am not aiming to make you feel
self-conscious or embarrassed, we are only doing this so that you can catch these things
outside of these sessions. We will do this for about five minutes. In the meantime we
can talk about whatever we like.
After the client is reliably detecting the occurrences of therapist-portrayed warning

signs and repetitive behaviors, the therapist should have the client practice detecting
his or her own warning signs and repetitive behaviors. This occurs more naturally
for certain repetitive behaviors such as tics, whereas those with trichotillomania are
unlikely to pull hair during a treatment session. If the behavior is unlikely to occur,
the client should be instructed to mimic his or her own warning signs and repetitive
behaviors in session. Additionally, the client should note if an urge to engage in one
of the repetitive behaviors occurs. Urges are quite difficult for the therapist to detect
so the client will have to report on their occurrence. This is structured just like the
therapist-portrayed behaviors in that it continues until the warning signs and the
repetitive behaviors are reliably detected, and the client is informed if he or she fails to
detect one. Engaging in a conversation that is not about therapy can be useful while
working on detecting the client’s warning signs, repetitive behaviors, and urges. The
following text provides an illustration:
THERAPIST: Now it is your turn to practice catching your warning signs, actual
behaviors, and urges. When any one of these three things occurs I want you to raise a
finger or say “There’s one.” This just lets me know that you knew it occurred.
Sometimes these things occur less often because of being in a therapy session. If that is
the situation for you, then I would like you to mimic what happens outside of therapy.
The point of this work is to help you become more familiar with what is involved with
your repetitive behavior. We can talk about things other than your repetitive behavior
while you practice this. We will do this for around five minutes. If I see a warning sign
or the behavior and you do not give me an indication you knew it occurred, I will point
it out to you.
Once the client is aware of the behaviors that precede the repetitive behavior, the
behavior itself, and the urges that are involved in it, the session can move on to
competing response training.
Competing Response Training

Competing response training teaches the client to engage in another action whenever
a warning sign, the repetitive behavior, or an urge occurs. The client is asked to
engage in this behavior for at least a minute or until the urge to engage in the action
is no longer present. Generally, competing responses that are related to the repetitive
behavior are trained because they appear more externally valid, but unrelated actions
can also be successful. Common examples of competing responses are making fists or
putting one’s hands in one’s lap for hair pulling and skin picking or other oral-digital
habits. Competing responses for tics are usually opposite to the behavior such as
pressing the arms to the side for an arm tic. Diaphragmatic breathing is used in
response for a vocal tic.
The competing response is trained in a similar way that awareness training occurred.
First, the therapist describes the way a competing response should be used and then
it is demonstrated for both the warning signs and the actual repetitive behavior. This
could occur as follows:
THERAPIST: Now we are going to practice not engaging in the repetitive behavior by
replacing it with another behavior. This new action is called a competing response. I
would like you to engage in the competing response for at least a minute whenever a
warning sign occurs, if the behavior occurs, or if you experience an urge to engage in
the behavior. If the urge is around for longer than a minute, continue with the
competing response until the urge significantly lessens. I will teach you a good
competing response for each repetitive behavior you do. If you are ever in a situation
where the competing response is hard to do, that is not an issue, just engage in some
activity that will make the behavior difficult. For example, if you are driving and cannot
make fists with your hands, just keep both hands firmly on the steering wheel.
After demonstrating its use, the client is asked to spend five minutes practicing the
competing response after the warning signs and five minutes after the actual behavior.
The warning signs and actual behaviors may have to be mimicked as they may not
occur in session. If any instances occur without a subsequent competing response,
they should be pointed out to the client. After sufficient practice has occurred and
the client understands the use of the competing response, he or she is instructed to
engage in the competing response after each warning sign, occurrence of the repetitive
behavior, or urge. This can be described as follows:
THERAPIST: You are doing a really nice job with these competing responses. I would
like you to continue to use this competing response each time the warning sign,
behavior, or urge occurs. I would like you to do this for a minute or until the urge has
lessened. For many people this is hundreds of times a day. I know that is a lot, but it
will certainly lessen with time. Each time you do the competing response and not the
repetitive behavior, your body is learning it does not need to do the repetitive behavior.
It is learning other ways to handle these urges. So while you may have to do the
competing response 300 times per day this week, it might be 100 times a day next
week, and so on. Eventually, these warning signs and these repetitive behaviors will
lessen and you will not have to do the competing response very often. You will miss
some chances to do the competing response; that is fine. Still, the more you work at it
the less this repetitive behavior will occur.
Finally, once the client is aware of the pertinent aspects of the repetitive behavior
and is competent in the use of the competing response, social support training can be
implemented.
Social Support Training

The goal of social support is to increase awareness of the target behavior and reinforce
the use of the competing response. This aspect of the treatment is pretty simplistic
when used with adults, but can be a little more involved when used with younger
clients. In either case, the person or people who are around the client most often are
Habit Reversal 217
asked to reinforce the correct use of the competing response and remind the client
to use it if he or she is seen engaging in the target behavior. Adults are usually just
asked to tell a person they live with to help remind them when they are engaging
in the repetitive behavior and praise them if they are doing the competing response
correctly. The caregivers of younger clients often come into session and this process is
explained by the therapist. Specifically, the caregiver is asked to simply point out the
target behavior if seen occurring without a subsequent competing response. Only a
brief reminder is necessary. For many younger clients, and sometimes adult ones too,
a token system, where successful use of the competing response can earn tokens or
points for a larger reward, can really help with the implementation of the program.
As the use increases, the program can be faded out.
Session Two Onward

This whole procedure can easily be trained in one session. Subsequent sessions are
seen as opportunities to check in on progress and assist the client with any troubles
that he or she might be having with the treatment. Commonly, clients will experience
gains but still be engaging in the target behavior at a lesser level after the initial
session. This progress should be praised and the client should be reminded that gains
are gradual and that continued engagement in the intervention will increase the odds
of meeting his or her treatment goals. All remaining time should be spent reviewing
the awareness and competing response training modules of the treatment.
Summary
Habit reversal and its variants have existed since the 1970s and have been shown to
be helpful in treating a variety of repetitive behaviors. The original treatment has been
shortened into a more simplified version while appearing to maintain effectiveness.
Lately, habit reversal is being used as an empirically supported technique, rather than
a stand-alone treatment, and being incorporated with other aspects of treatment.
No matter how it is incorporated into treatment, data suggest that habit reversal is
a useful treatment technique for addressing repetitive behavior problems across age
groups.
References
Azrin, N. H., & Nunn, R. G. (1973a). Habit control in a day. New York, NY: Simon &
Schuster.
Azrin, N. H., & Nunn, R. G. (1973b). Habit reversal: A method of eliminating nervous habits
and tics. Behaviour Research and Therapy, 11, 619–628.
Azrin, N. H., & Nunn, R. G. (1974). A rapid method of eliminating stuttering by a regulated
breathing approach. Behaviour Research and Therapy, 12, 279–286.
Azrin, N. H., Nunn, R. G., & Frantz, S. E. (1979). Comparison of regulated-breathing versus
abbreviated desensitization on reported stuttering episodes. Journal of Speech & Hearing
Disorders, 44, 331–339.
Azrin, N. H., Nunn, R. G., & Frantz, S. E. (1980a). Habit reversal vs negative practice
treatment of nervous tics. Behavior Therapy, 11, 169–178.
Azrin, N. H., Nunn, R., & Frantz, S. E. (1980b). Treatment of hairpulling (trichotillomania):
A comparative study of habit reversal and negative practice training. Journal of Behavior
Azrin, N. H., Nunn, R. G., & Frantz, S. E. (1980c). Habit reversal vs. negative practice
treatment of nailbiting. Behaviour Research and Therapy, 18, 281–285.
Azrin, N. H., Nunn, R. G., & Frantz-Renshaw, S. E. (1980d). Habit reversal treatment of
thumbsucking. Behaviour Research and Therapy, 18, 395–399.
Azrin, N. H., Nunn, R. G., & Frantz-Renshaw, S. E. (1982). Habit reversal vs negative practice
treatment of self-destructive oral habits (biting, chewing or licking of the lips, cheeks,
tongue or palate). Journal of Behavior Therapy and Experimental Psychiatry, 13, 49–54.
Azrin, N. H., & Peterson, A. L. (1990). Treatment of Tourette Syndrome by habit reversal: A
waiting-list control group comparison. Behavior Therapy, 21, 305–318.
Bate, K. S., Malouff, J. M., Thorsteinsson, E. T., & Bhullar, N. (2011). The efficacy of habit
reversal therapy for tics, habit disorders, and stuttering: A meta-analytic review. Clinical
Bloch, M. H., Landeros-Weisenberger, A., Dombrowski, P., Kelmendi, B., Wegner, R., Nudel,
J., … Coric, V. (2007). Systematic review: Pharmacological and behavioral treatment for
trichotillomania. Biological Psychiatry, 62, 839–846.
Carr, J. E., & Chong, I. M. (2005). Habit reversal treatment of tic disorders: A methodological
critique of the literature. Behavior Modification, 29, 858–875.
Christensen, A. P., & Sanders, M. R. (1987). Habit reversal and differential reinforcement
of other behaviour in the treatment of thumb-sucking: An analysis of generalization and
side-effects. Journal of Child Psychology and Psychiatry, 28, 281–295.
Cook, C. R., & Blacher, J. (2007). Evidence-based psychosocial treatments for tic disorders.
Deckersbach, T., Rauch, S., Buhlmann, U., & Wilhelm, S. (2006). Habit reversal versus
supportive psychotherapy in Tourette’s disorder: A randomized controlled trial and
predictors of treatment response. Behaviour Research and Therapy, 44, 1079–1090.
Deckersbach, T., Wilhelm, S., Keuthen, N. J., Baer, L., & Jenike, M. A. (2002). Cognitive-
behavior therapy for self-injurious skin picking: A case series. Behavior Modification, 26,
361–377.
Flessner, C. A., Busch, A. M., Heideman, P. W., & Woods, D. W. (2008). Acceptance-enhanced
behavior therapy (AEBT) for trichotillomania and chronic skin picking: Exploring the
effects of component sequencing. Behavior Modification, 32, 579–594.
Flessner, C. A., Miltenberger, R. G., Egemo, K., Kelso, P., Jostad, C., Johnson, B., …
Neighbors, C. (2005). An evaluation of the social support component of simplified habit
reversal. Behavior Therapy, 36, 35–42.
Foxx, R. M., & Azrin, N. H. (1972). Restitution: A method of eliminating aggressive-disruptive
behavior of retarded and brain damaged patients. Behaviour Research and Therapy, 10,
15–27.
Foxx, R. M., & Azrin, N. H. (1973a). The elimination of autistic self-stimulatory behavior by
overcorrection. Journal of Applied Behavior Analysis, 6, 1–14.
Foxx, R. M., & Azrin, N. H. (1973b). Toilet training the retarded: A rapid program for day
and nighttime independent toileting. Champaign, IL: Research Press.
Franklin, M. E., Best, S. H., Wilson, M. A., Loew, B., & Compton, S. N. (2011). Habit
reversal training and acceptance and commitment therapy for Tourette syndrome: A pilot
project. Journal of Developmental and Physical Disabilities, 23, 49–60.
Habit Reversal 219
Gagnon, M., & Ladouceur, R. (1992). Behavioral treatment of child stutterers: Replication
and extension. Behavior Therapy, 23, 113–129.
Glaros, A. G., Kim-Weroha, N., Lausten, L., & Franklin, K. (2007). Comparison of habit
reversal and a behaviorally-modified dental treatment for temporomandibular disorders:
A pilot investigation. Applied Psychophysiology and Biofeedback, 32, 149–154.
Glaros, A. G., & Rao, S. M. (1977). Bruxism: A critical review. Psychological Bulletin, 84,
767–781.
Gramling, S. E., Neblett, J., Grayson, R., & Townsend, D. (1996). Temporomandibular
disorder: Efficacy of an oral habit reversal treatment program. Journal of Behavior Therapy
and Experimental Psychiatry, 27 , 245–255.
Himle, M. B., Woods, D. W., Piacentini, J. C., & Walkup, J. T. (2006). Brief review of habit
reversal training for Tourette syndrome. Journal of Child Neurology, 21, 719–725.
Horne, D. J., & Wilkinson, J. (1980). Habit reversal treatment for fingernail biting. Behaviour
Keuthen, N. J., Rothbaum, B. O., Falkenstein, M. J., Meunier, S., Timpano, K. R., Jenike,
M. A., & Welch, S. (2011). DBT-enhanced habit reversal treatment for trichotillomania:
3- and 6-month follow-up results. Depression and Anxiety, 28, 310–313.
Keuthen, N. J., Rothbaum, B. O., Welch, S., Taylor, C., Falkenstein, M., Heekin, M., …
Jenike, M. A. (2010). Pilot trial of dialectical behavior therapy-enhanced habit reversal
for trichtotillomania. Depression and Anxiety, 27 , 953–959.
Keuthen, N. J., Stein, D. J., & Christenson, G. A. (2001). Help for hairpullers: Understanding
and coping with trichotillomania. Oakland, CA: New Harbinger.
Ladouceur, R. (1979). Habit reversal treatment: Learning an incompatible response or increas-
ing the subject’s awareness? Behaviour Research and Therapy, 17 , 313–316.
Ladouceur, R., Boudreau, L., & Théberge, S. (1981). Awareness training and regulated-
breathing method in modification of stuttering. Perceptual and Motor Skills, 53, 187–194.
Ladouceur, R., Côté, C., Leblond, G., & Bouchard, L. (1982). Evaluation of regulated-
breathing method and awareness training in the treatment of stuttering. Journal of Speech
& Hearing Disorders, 47 , 422–426.
Ladouceur, R., & Martineau, G. (1982). Evaluation of regulated-breathing method with and
without parental assistance in the treatment of child stutterers. Journal of Behavior Therapy
Miltenberger, R. G., & Fuqua, R. W. (1985). A comparison of contingent vs non-contingent
competing response practice in the treatment of nervous habits. Journal of Behavior
Miltenberger, R. G., Fuqua, R. W., & McKinley, T. (1985). Habit reversal with muscle tics:
Replication and component analysis. Behavior Therapy, 16, 39–50.
Miltenberger, R. G., Fuqua, R. W., & Woods, D. W. (1998). Applying behavior analysis
to clinical problems: Review and analysis of habit reversal. Journal of Applied Behavior
Analysis, 31, 447–469.
Miltenberger, R. G., Wagaman, J. R., & Arndorfer, R. E. (1996). Simplified treatment and
long term follow-up for stuttering in adults: A study of two cases. Journal of Behavior
Therapy and Experimental Psychiatry, 27 , 181–188.
Ninan, P. T., Rothbaum, B. O., Marsteller, F. A., Knight, B. T., & Eccard, M. B. (2000). A
placebo-controlled trial of cognitive-behavioral therapy and clomipramine in trichotillo-
mania. Journal of Clinical Psychiatry, 61, 47–50.
Nunn, R. G., & Azrin, N. H. (1976). Eliminating nail-biting by the habit reversal procedure.
O’Connor, K. P., Brault, M. M., Robillard, S. S., Loiselle, J. J., Borgeat, F. F., & Stip, E. E.
(2001). Evaluation of a cognitive-behavioural program for the management of chronic tic
and habit disorders. Behaviour Research and Therapy, 39, 667–681.
O’Connor, K., Gareau, D., & Borgeat, F. (1997). A comparison of a behavioural and a
cognitive-behavioural approach to the management of chronic tic disorders. Clinical
Psychology & Psychotherapy, 4, 105–117.
Olkinuora, M. (1969). A review of the literature on, and a discussion of studies of bruxism and
its psychogenesis and some new psychological hypotheses. Suomen Hammaslääkäriseuran
Toimituksia Finska Tandläkarsällskapets Förhandlingar, 65, 312–324.
Ollendick, T. H. (1981). Self-monitoring and self-administered overcorrection: The modifica-
tion of nervous tics in children. Behavior Modification, 5, 75–84.
Peterson, A. L., Dixon, D. C., Talcott, G., & Kelleher, W. J. (1993). Habit reversal treatment
of temporomandibular disorders: A pilot investigation. Journal of Behavior Therapy and
Experimental Psychiatry, 24, 49–55.
Piacentini, J., Woods, D. W., Scahill, L., Wilhelm, S., Peterson, A. L., Chang, S., … Walkup, J.
T. (2010). Behavior therapy for children with Tourette disorder: A randomized controlled
trial. JAMA: Journal of the American Medical Association, 303, 1929–1937.
Rosenbaum, M. S., & Ayllon, T. (1981a). Treating bruxism with the habit-reversal technique.
Rosenbaum, M. S., & Ayllon, T. (1981b). The habit-reversal technique in treating trichotillo-
mania. Behavior Therapy, 12, 473–481.
Saint-Laurent, L., & Ladouceur, R. (1987). Massed versus distributed application of the
regulated-breathing method for stutterers and its long-term effect. Behavior Therapy, 18,
38–50.
Sharenow, E. L., Fuqua, R. W., & Miltenberger, R. G. (1989). The treatment of muscle tics
with dissimilar competing response practice. Journal of Applied Behavior Analysis, 22,
35–42.
Teng, E. J., Woods, D. W., & Twohig, M. P. (2006). Habit reversal as a treatment for chronic
skin picking: A pilot investigation. Behavior Modification, 30, 411–422.
Townsend, D., Nicholson, R. A., Buenaver, L., Bush, F., & Gramling, S. (2001). Use of
a habit reversal treatment for temporomandibular pain in a minimal therapist contact
format. Journal of Behavior Therapy and Experimental Psychiatry, 32, 221–239.
Twohig, M. P., & Woods, D. W. (2001a). Evaluating the duration of the competing response
in habit reversal: A parametric analysis. Journal of Applied Behavior Analysis, 34, 517–
520.
Twohig, M. P., & Woods, D. W. (2001b). Habit reversal as a treatment for chronic skin
picking in typically developing adult male siblings. Journal of Applied Behavior Analysis,
34, 217–220.
Twohig, M. P., & Woods, D. W. (2004). A preliminary investigation of acceptance and
commitment therapy and habit reversal as a treatment for trichotillomania. Behavior
Therapy, 35, 803–820.
Twohig, M. P., Woods, D. W., Marcks, B. A., & Teng, E. J. (2003). Evaluating the efficacy
of habit reversal: Comparison with a placebo control. Journal of Clinical Psychiatry, 64,
40–48.
van Minnen, A., Hoogduin, K. A., Keijsers, G. P., Hellenbrand, I., & Hendriks, G. J. (2003).
Treatment of trichotillomania with behavioral therapy or fluoxetine: A randomized,
waiting-list controlled study. Archives of General Psychiatry, 60, 517–522.
Verdellen, C. J., Keijsers, G. J., Cath, D. C., & Hoogduin, C. L. (2004). Exposure with
response prevention versus habit reversal in Tourette’s syndrome: A controlled study.
Habit Reversal 221
Wagaman, J. R., Miltenberger, R. G., & Arndorfer, R. E. (1993). Analysis of a simplified

treatment for stuttering in children. Journal of Applied Behavior Analysis, 26, 53–51.
Waterloo, K. K., & Gotestam, K. G. (1988). The regulated-breathing method for stuttering:
An experimental evaluation. Journal of Behavior Therapy and Experimental Psychiatry, 19,
11–19.
Wilhelm, S., Deckersbach, T., Coffey, B. J., Bohne, A., Peterson, A. L., & Baer, L. (2003).
Habit reversal versus supportive psychotherapy for Tourette’s disorder: A randomized
controlled trial. American Journal of Psychiatry, 160, 1175–1177.
Williamson, D. A., Epstein, L. H., & Coburn, C. (1981). Multiple baseline analysis of the
regulated breathing procedure for the treatment of stuttering. Journal of Fluency Disorders,
6, 327–339.
Woods, D. W., Conelea, C. A., & Himle, M. B. (2010). Behavior therapy for Tourette’s
disorder: Utilization in a community sample and an emerging area of practice for
psychologists. Professional Psychology: Research and Practice, 41, 518–525.
Woods, D. W., Miltenberger, R. G., & Lumley, V. A. (1996). Sequential application of major
habit-reversal components to treat motor tics in children. Journal of Applied Behavior
Analysis, 29, 483–493.
Woods, D. W., Murray, L. K., Fuqua, R., Seif, T. A., Boyer, L. J., & Siah, A. (1999).
Comparing the effectiveness of similar and dissimilar competing responses in evaluating
the habit reversal treatment for oral–digital habits in children. Journal of Behavior Therapy
Woods. D. W., & Twohig, M. P. (2008). Trichotillomania: An ACT-enhanced behavior therapy
approach therapist guide. New York, NY: Oxford University Press.
Woods, D. W., Twohig, M. P., Fuqua, R., & Hanley, J. M. (2000). Treatment of stuttering
with regulated breathing: Strengths, limitations, and future directions. Behavior Therapy,
31, 547–568.
Woods, D. W., Wetterneck, C. T., & Flessner, C. A. (2006). A controlled evaluation of
acceptance and commitment therapy plus habit reversal for trichotillomania. Behaviour
Wright, K. M., & Miltenberger, R. G. (1987). Awareness training in the treatment of head
and facial tics. Journal of Behavior Therapy and Experimental Psychiatry, 18, 269–274.
11
Contingency Management
Treatments
Shannon A. Byrne and Nancy M. Petry
University of Connecticut Health Center, United States
Contingency management (CM) is a behavioral treatment that relies on operant

conditioning, or the premise that behaviors resulting in positive outcomes are more
likely to be repeated. CM has been widely applied in the treatment of substance use
disorders and involves three basic tenets (Higgins, Budney, & Bickel, 1994; Petry,
2000). First, the clinician identifies a readily detectable target behavior, such as drug
abstinence verified by a negative urine toxicology test. Second, patients earn tangible
reinforcers when they demonstrate the target behavior. Finally, the reinforcers are
not awarded when the target behavior does not occur. The clinician uses a behavioral
contract to define the specific behavior to be monitored, the schedule of monitoring,
and the contingencies to be imposed. CM is not typically used as a stand-alone
intervention, but rather is integrated into other treatments.
This chapter presents the fundamentals of CM. The first section describes research
evidence of the efficacy of CM, especially as it relates to the treatment of substance
use disorders. The second section further explains the basic tenets of CM, discussing
important elements of a CM intervention. The next sections identify types of rein-
forcers that can be used and issues that may arise with implementation of CM.
The final section presents data on the combined effects of CM with other forms of
cognitive behavioral therapy (CBT).
Research Evidence
CM procedures have been most widely studied in the context of substance abuse
treatment. Multiple clinical trials have demonstrated that CM interventions, involving
the provision of tangible reinforcers contingent on objective measures of drug
abstinence, have been effective in reducing illicit drug use (e.g., Higgins, Stitzer,

DOI: 10.1002/9781118528563.wbcbt11
Bigelow, & Liebson, 1986; Kidorf & Stitzer, 1996; Peirce et al., 2006; Preston
et al., 1998). In the largest study of CM to date, over 400 stimulant-abusing patients
beginning outpatient substance abuse treatment at one of six community-based
treatment centers across the United States were randomly assigned to usual care or
usual care plus abstinence-based reinforcers (Petry, Alessi, Marx, Austin, & Tardif,
2005). All patients submitted urine samples twice a week for 12 weeks, and patients
in the CM group earned draws from a prize bowl when samples were negative for
stimulants. The prize bowl contained 500 slips of paper, half of which earned prizes
worth $1 to $100 in value and the other half stated “good job” but did not result in
a tangible reinforcer. Draws were provided on an escalating schedule, such that the
number of draws increased by one for each week in which both samples were negative.
The number of draws was reset to one after submission of a positive sample, or after an
unexcused absence. On average, patients who were abstinent throughout the entire
study could earn about $400 in prizes. Patients in the CM condition achieved longer
durations of abstinence than did those in the usual care condition (4.4 vs. 2.6 weeks,
respectively). The CM group was also more likely than the usual care group to achieve
4, 8, and 12 weeks of consecutive abstinence, with odds ratios of 2.5, 2.7, and 4.5,
respectively. In addition, participants receiving CM stayed in treatment longer than
those in usual care (19.2 vs. 15.7 sessions, respectively). Average earnings in the CM
group were about $203 per participant.
In a parallel trial with methadone-maintained, stimulant-abusing patients, Peirce
et al. (2006) randomly assigned 388 patients to usual care or the same plus incentives
for abstinence from stimulants. As described above, patients randomized to the CM
condition earned draws from a prize bowl for providing drug-free urine samples,
with the number of draws increasing with continuous abstinence. Patients in the CM
condition were twice as likely as those in the usual care condition to submit stimulant-
and alcohol-negative samples. Individuals who received CM were approximately 3, 9,
and 11 times more likely than those who received usual care to achieve 4, 8, and 12
weeks of continuous abstinence, respectively.
Meta-analyses have also provided support for the efficacy of CM in the treatment
of substance use disorders. Dutra et al. (2008) examined 34 studies of psychosocial
substance use treatments, including CM, relapse prevention, and CBT. The strongest
effect sizes were for CM interventions. In meta-analyses of CM interventions specif-
ically, Prendergast, Podus, Finney, Greenwell, and Roll (2006) and Lussier, Heil,
Mongeon, and Badger (2006) compared CM to control conditions and found pos-
itive effects of CM for decreasing drug use. These meta-analyses also revealed that
CM is efficacious in reducing the use of many substances. Although the bulk of
the studies have focused on decreasing cocaine and/or opioid use, beneficial effects
of CM have also been noted in reducing use of nicotine (Hunt, Rash, Burke, &
Parker, 2010; Roll, Higgins, & Badger, 1996), alcohol (Petry, Martin, Cooney, &
Kranzler, 2000), marijuana (Budney, Moore, Rocha, & Higgins; 2006; Kadden, Litt,
Kabela-Cormier, & Petry, 2007), and benzodiazepines (Stitzer, Iguchi, & Felch,
1992).
CM interventions are clearly efficacious in terms of abstinence outcomes. Another
important benefit of CM is its impact on treatment attendance. Attrition from
drug-free substance abuse treatment programs is a significant problem, with 30%
Contingency Management Treatments 225
of patients leaving treatment within the first month, and over half dropping out
within the first 3 months (Hubbard et al., 1989; Kang et al., 1991; Simpson, 1981).
Further, several studies have reported that the most stable predictor of positive
outcomes in drug treatment is length of time in treatment (Hubbard, Craddock,
Flynn, Anderson, & Etheridge, 1997; Hubbard et al., 1989; Simpson & Sells, 1982).
In general, when CM is added to standard drug abuse treatment, patients stay in
treatment longer (e.g., Higgins, Budney, Bickel, Foerg, et al., 1994; Petry et al.,
2000).
CM interventions have been applied to reinforce both attendance and abstinence,
alone and in combination. Petry, Martin, and Simcic (2005) randomly assigned
cocaine-abusing methadone patients to standard treatment (including group coun-
seling) or the same plus CM. In the CM condition, patients earned draws from a
prize bowl for attending group therapy and for submitting cocaine-negative urine
samples. Patients in the CM condition submitted a greater proportion of cocaine-
negative samples (34.6% vs. 16.8%) and attended more group therapy sessions (6.6
weeks vs. 3.0 weeks) than did patients in standard treatment. In another study,
Petry, Weinstock, and Alessi (2011) randomly assigned 239 substance-abusing out-
patients to standard care with frequent urine screenings, and the same care plus
a CM intervention, delivered in the group context. Patients in the CM condition
earned chances to put their names in a hat by submitting drug-negative urine samples
and by attending group. During the group session, therapists drew names from a
hat and awarded those patients chances to win prizes ranging from $1 to $100.
Patients in the CM condition attended more days of treatment (17 vs. 14.7), stayed
in treatment for more continuous weeks (5.7 vs. 4.1), and had longer durations
of continuous abstinence (5.3 vs. 4.1) than did individuals in the standard care
condition.
The above studies demonstrate the efficacy of CM when both attendance and
abstinence are reinforced. In other studies, CM has been successfully applied to
attendance only. For example, Ledgerwood, Alessi, Hanson, Godley, and Petry
(2008) awarded patients, chances to put their name in a hat, with the patients earning
bonus chances when they attended groups on consecutive weeks (up to 16 slips for
16 consecutive weeks). Each week, a name was drawn from the hat, and the chosen
patient got to draw a slip from a prize bowl. This CM procedure was successful
in improving attendance; patients who were enrolled during the CM intervention
attended 80.4% of sessions, whereas patients enrolled during the non-CM phase
attended only 68.9% of the sessions. Petry, Martin, and Finocche (2001) used this
same attendance-based prize CM and increased group attendance from fewer than
two patients per week to an average of over 12 per week in an HIV drop-in center.
Similarly, Sigmon and Stitzer (2005) found that a prize-based CM intervention
increased attendance rates from 52% to 76% in methadone-maintained patients.
It is clear that CM procedures are efficacious for improving retention and drug
use outcomes in substance use treatments. It is important to note that results are
improved when CM is applied appropriately, with careful attention to behavioral
principles. The next section provides recommendations for CM interventions using
these principles, thereby increasing the likelihood that they will result in the desired
behavioral change.
Important Elements of Contingency Management

Interventions
In general, CM interventions for substance abuse disorders involve provision of a rein-

forcer for attendance or a drug-negative urine specimen or other objective measures
of substance use (e.g., carbon monoxide levels for cigarette smokers). Reinforcers may
include vouchers exchangeable for retail goods or services, or draws from a prize bowl
with the chance of winning prizes. If a patient attends treatment or submits a negative
sample, he or she will receive the reinforcer, and the amount of reinforcement earned
increases with successive negative samples. If a patient fails to attend treatment or
submits a positive sample, he or she would not receive a reinforcer that day and
would perhaps receive a slight punisher, such as a reset in amounts of vouchers or
prize draws to a low value on the next day of attendance or submission of a negative
sample.
This section further dissects the fundamentals of CM which, when used properly,
can promote substantial behavior change. Each step is important because it is associ-
ated with improved outcomes in CM treatments. Further details about each element
and step-by-step instructions for designing and implementing CM interventions can
be found in Petry (2012).
Objectively Quantified Behaviors

When designing CM interventions, it is imperative that the behavior to be reinforced
is objectively quantifiable. If abstinence is to be reinforced, objective and observed
drug screens should be used, and the monitoring schedule should be set up according
to the test’s ability to detect drug use (e.g., three times a week for cocaine or opioid
testing). On-site urine toxicology kits (e.g., OnTrak TesTstik, Varian, Inc., Palo Alto,
CA; Intoximeter Breathalyzer, Intoximeters, St Louis, MO) are useful for obtaining
results within 3 to 5 minutes of sample submission, and can detect any use of those
substances over a 2- to 3-day period.
Frequency
The frequency of occurrence of the target behavior, and the monitoring and rein-
forcement schedules, are other important variables to consider. The behavior to be
reinforced must be monitored regularly, and reinforced frequently. When designing
a CM intervention to reduce drug use, the objective is to detect every instance
of use of the target drug. In order to do so, CM interventions should objectively
monitor drug use at least twice a week, and ideally three times per week in the
initial stages of treatment (e.g., Cone & Dickerson, 1992; Saxon, Calsyn, Wells, &
Stanton, 1998). Frequent monitoring provides an opportunity not only to reinforce
each instance of the target behavior, but also to increase the chances that the patient
understands the expectations, as well as the connection between the behavior and the
reinforcer.
Immediacy
As stated above, it is important to ensure that the patient understands the connection
between the target behavior and the reinforcer. Learning is more likely to occur
when behavior is immediately followed by the consequence (Zeiler, 1977), and it is
therefore important to reinforce drug abstinence (or other target behaviors) as soon
as possible. If there is a delay between the desired behavior and the presentation
of the reinforcer, the behavior is less likely to be altered. For example, Roll, Reilly,
and Johanson (2000) repeatedly presented a group of cigarette smokers with choices
between cigarette puffs or points that could be exchanged for different amounts of
money (10¢, $1, or $2), exchangeable either immediately after the session, or 1 or
3 weeks later. These researchers found that longer exchange delays increased the
number of choices for cigarettes. Similarly, Rowan-Szal, Joe, Chatham, and Simpson
(1994) found that drug-abusing patients achieved less abstinence when they had to
wait longer to exchange vouchers, compared to those who received a more immediate
exchange.
When clinics send urine samples to outside laboratories for screening, results are
not received until days later. This practice increases the time between the behavior
and the reinforcer, consequently decreasing the impact of the procedure. By using
on-site testing, urine toxicology results can be determined within minutes, and
reinforcers can be provided as soon as the negative result is determined. In their
study examining the impact of the delay of outcomes and reinforcement, Schwartz,
Lauderdale, Montgomery, Burch, and Gallant (1987) reported that on-site urine
testing systems are more likely than off-site systems to improve outcomes.
Magnitude
Another important factor to consider when designing a CM intervention is the mag-
nitude of the reinforcers. Several studies have demonstrated relationships between
the magnitude of the reinforcer and behavioral change (e.g., Businelle, Rash, Burke,
& Parker, 2009; Silverman, Chutuape, Bigelow, & Stitzer, 1999). For example,
Dallery, Silverman, Chutuape, Bigelow, and Stitzer (2001) found that tripling
voucher amounts (to a maximum of $3,369) for “treatment-resistant” drug-abusing
methadone patients increased the percentage of opioid- and cocaine-free samples
from 9% to 28%. These studies support the idea that larger magnitude reinforcers are
more likely to improve performance, and in most voucher-based CM studies at least
$1,000 over 12 weeks is needed to reduce drug using behavior.
Escalating Reinforcers and Bonuses

In substance use treatment, it is important to facilitate longer consecutive durations of
abstinence, which are associated with better long-term outcomes (Higgins, Badger, &
Budney, 2000). One way to promote longer periods of abstinence is to use escalating
reinforcers and bonuses for sustained behavior change. For example, voucher amounts
or prize draws can increase as patients achieve longer periods of abstinence. Patients
might earn one dollar or one draw for their first negative urine sample, two dollars
or draws for their second consecutive negative sample, three dollars or draws for their
third consecutive negative sample, and so on. In addition, voucher amounts and prize
draws are reset back to the lowest value when the patient provides a sample that is
not negative for the target substance, or fails to submit a scheduled sample.
This escalating system may be more expensive than providing a constant rate of
reinforcement. However, Roll et al. (1996) compared a constant schedule of rein-
forcement for negative urine samples to one with an escalating schedule. Although
the authors set both schedules to have the same maximal amount of reinforcement,
they found that the escalating voucher system resulted in longer durations of absti-
nence than did the constant reinforcement schedule. Longer durations of abstinence,
in turn, are associated with increased probability of long-term abstinence, after the
reinforcers are removed (Higgins, Badger, & Budney, 2000; Petry, Alessi, et al.,
2005; Petry, Alessi et al., 2006; Petry, Alessi, Hanson, & Sierra, 2007).
Consistency
One of the most crucial elements of a CM intervention is consistency. Urine samples
(or other behavioral targets) must be monitored throughout treatment. If the
consistency or frequency with which contingencies are applied decreases over time,
the patient may lapse to substance use without detection. In order to achieve and
maintain consistency, clinic staff themselves may need to be monitored and reinforced
for appropriate implementation of the CM procedures. Andrzejewski, Kirby, Morral,
and Iguchi (2000) found that counselors rarely implemented CM as intended (42%
of the time) when minimal feedback was provided. These researchers described two
procedures to ensure consistent application of CM treatments: In one counselors were
given regular graphical feedback on whether or not they met performance criteria, and
in the other they also earned drawings for a cash prize if they met those performance
criteria. Compliance with the intended CM protocol improved to 71% in the verbal
feedback procedure and 81% in the drawing procedure.
Petry, Alessi, Ledgerwood, and Sierra (2010) developed the 12-item Contingency
Management Competence Scale (CMCS), which measures therapists’ adherence to
the CM protocol and assesses elements such as using objective measures of target
behaviors, providing the correct number of draws, awarding draws with enthusiasm,
and informing patients of the number of draws they can earn in their next visit.
The authors trained therapists to administer abstinence-based CM to cocaine-abusing
patients in community-based clinics (Petry et al., 2010; Petry, Alessi, & Ledgerwood,
2012), and no therapist in these studies had prior experience with CM. Training
included didactics, role plays, and supervision by staff through ratings of audio
recordings of the sessions. Following the training, therapists’ scores on the CMCS
improved significantly. Importantly, scores on the competence scale were significantly
correlated with durations of abstinence achieved by patients, demonstrating that
accurate implementation of the CM intervention is essential for improving treatment
outcomes.
These data suggest that, with appropriate training, community-based clinicians can
effectively administer CM. Further, consistency-targeting methods can be integrated
into current clinic procedures, and will improve the effectiveness of CM interventions.
Social encouragement, along with reminders, examples, and even reinforcement, can
also be implemented to help clinicians execute CM treatments appropriately.
This next section gives readers an idea of what type of reinforcers might be best
suited to their program and patients. Specifically, this section describes the types of
reinforcers that may be used in CM interventions, including vouchers, prizes, cash, on-
site retail, and clinic privileges. The pros and cons of each reinforcer are also discussed.
Types of Reinforcers
Vouchers
The use of vouchers has been widely studied among the CM interventions for
decreasing drug use (e.g., Higgins, Budney, Bickel, Foerg et al., 1994; Higgins,
Wong, Badger, Ogden, & Dantona, 2000; Higgins et al., 2003; Silverman et al.,
1996). In this system, patients earn vouchers for each negative urine sample, and the
vouchers accumulate in a bank account of sorts. These vouchers are then exchanged
for desired goods, such as restaurant gift certificates, clothing, bus tokens, electronic
equipment, or movie tickets. To facilitate longer durations of abstinence, the voucher
amounts escalate as the number of consecutive negative urine samples increases, as
outlined earlier.
One advantage of the voucher system is its accommodation of individual prefer-
ences, as patients can spend them on just about any item. In addition, the likelihood
of patients exchanging vouchers for drugs is reduced, because cash is not provided.
Further, programs can veto requests for items that may facilitate drug use or other
problems (e.g., gift certificates to stores that sell alcohol, cigarettes, or weapons).
However, the voucher system has been criticized for its expense. Many research
studies using voucher reinforcers have applied systems in which clients can earn up
to $1,200 worth of goods during treatment (e.g., Bickel, Amass, Higgins, Badger,
& Esch, 1997; Higgins et al., 2000; Higgins, Budney, Bickel, Foerg, et al., 1994;
Higgins et al., 2003; Silverman et al., 1996), and average earnings are about $600
(e.g., Higgins, Budney, Bickel, Foerg, et al., 1994; Silverman et al., 1996). Additional
costs include staff time to purchase the requested items, which is estimated to be
more costly than the vouchers themselves (Olmstead & Petry, 2009). Lowering the
voucher reinforcement provided reduces efficacy, as described earlier. Therefore, it
may not be feasible to implement voucher-based CM in many clinical settings.
Cash
An alternative to the voucher system is to use cash as the reinforcer. Cash can be
used in the same way as vouchers, with increased amounts for consecutive periods
of abstinence, and reset of cash values when positive samples are submitted. Using
cash may be less expensive than vouchers, because staff time is not necessary to
purchase items. Also, patients often have a preference for cash over a voucher of the
same value, so changes in the target behavior may be achieved at a lower cost. In a
study by Shaner et al. (1997), cocaine-abusing patients with schizophrenia reduced
their substance use when $25 cash was provided. Elk et al. (1993, 1995) found
that patients who received $12–$15 per negative sample achieved abstinence from
cocaine. However, there have been some objections to the use of cash reinforcers.
Pragmatically, clinics may not have the necessary funds to institute a cash-based CM
intervention. Moreover, a common concern is that the cash may be used to purchase
drugs. However, the frequent monitoring of drug use in a CM intervention, and the
removal of reinforcers when drug use is identified, can alleviate this concern. Festinger
et al. (2005) examined the impact of cash reinforcement on drug use by randomizing
drug-abusing outpatients to receive various amounts of reinforcement ($10, $40,
or $70) for completing a 6-month follow-up assessment. The reinforcement was
provided in either cash or vouchers. After receiving the reinforcement, patients
were scheduled for another appointment 3 days later to provide specimens for drug
detection. Neither the amount nor the type of reinforcer had a significant effect
on rates of new drug use, suggesting that cash reinforcement is not associated with
increased drug use.
On-site Retail
An on-site retail program is similar to the voucher system described earlier, in that
patients can earn vouchers but they can then exchange them for tangible items directly
in the clinical setting. This system can be easier to implement than the voucher system,
because clinic staff are not required to shop for specific items at patients’ requests.
Further, clinics can solicit donated items from the community and local retailers,
reducing the cost (e.g., Amass & Kamien, 2004).
When an on-site retail system is in place, it is important to stock the “store”
with items that will motivate patients to complete the target behaviors. Several
studies have evaluated substance users’ preferred reinforcers (e.g., Amass, Bickel,
Crean, Higgins, & Badger, 1995; Chutaupe, Silverman, & Stitzer, 1998; Schmitz,
Rhoades, & Grabowski, 1994). Although cash was the most preferred item, patients
also expressed a desire for movie theater tickets, tickets to sports events, restaurant
gift certificates, bus passes, and bookstore gift certificates. Many of these items could
be solicited via donation. This type of intervention can reduce staff time required for
purchasing items and reduce cost for items, although it still requires significant staff
time for solicitation of donations.
Prizes
The prize-based CM system, in which patients can earn chances to draw slips of
paper from a bowl by submitting drug-negative samples, can also be used. The slips
are labeled with prizes of various magnitudes (e.g., small prizes worth $1, large
prizes worth $20, and jumbo prizes worth $100). As with the voucher system, the
escalating reinforcement schedule is used in this procedure: The number of draws
increases as patients earn consecutive time periods of abstinence. This procedure can
be implemented for a relatively lower cost than voucher-based CM, because patients
do not earn prizes for every instance of the target behavior, and the costs of the most
frequently won prizes are low ($1).
Prize-based CM has produced comparable results to voucher-based CM (e.g.,

Petry, Alessi, et al., 2005). Petry et al. (2007) randomized cocaine-abusing methadone
patients to 12 weeks of standard treatment, standard treatment plus voucher-based
CM (average maximum value of prizes of $585), or standard treatment plus prizes
with an expected maximum of $300. Patients in both CM groups achieved longer
durations of abstinence than those in standard treatment, and the CM conditions were
similar in terms of outcomes or amount of reinforcement earned. An economic analysis
further found that prize-based CM was more cost-effective than voucher-based CM
in engendering abstinence (Olmstead & Petry, 2009).
Research has demonstrated the benefits of this prize approach in a variety of
patient populations, including cocaine-dependent outpatients (Petry, Alessi, et al.,
2005; Petry, Peirce, et al., 2005), methadone patients (Petry & Martin, 2002;
Petry, Martin, & Simcic, 2005; Preston, Ghitza, Schmittner, Schroeder, & Epstein,
2008), HIV-positive substance abusers (Petry, Martin, & Finocche, 2001), alcohol-
dependent patients (Petry et al., 2000), and cigarette smokers (Alessi, Petry, & Urso,
2008). However, just like voucher CM, it is imperative that adequate magnitudes of
reinforcers be provided, or the intervention will be less likely to improve drug use
outcomes (Petry et al., 2004).
Clinic Privileges
With opioid substitution treatments, medication itself can be used as a reinforcer.
Methadone is highly reinforcing, and some studies have utilized these reinforcing
elements to induce behavioral change. For example, studies have applied take-
home privileges (Magura, Casriel, Goldsmith, Strug, & Lipton, 1988; Stitzer et al.,
1992), methadone dose changes (Higgins et al., 1986; Stitzer, Bickel, Bigelow, &
Liebson, 1986), and continued treatment (Calsyn & Saxon, 1987; Dolan, Black,
Penk, Robinowitz, & DeFord, 1985; McCarthy & Borders, 1985) as reinforcers in
methadone programs. While these types of reinforcers are not expensive, they are only
applicable within opioid agonist treatments, and clinic privileges alone are rarely of
sufficient magnitudes in other settings to modify drug use behaviors.
Issues in Contingency Management
This section presents some of the challenges and concerns related to CM, including
the cost of CM interventions, the utilization of urine specimens, and schedules for
detecting substance use and reinforcing abstinence. Ways to deal with these challenges
and minimize potential problems of CM treatments are also discussed.
Assessment of Substance Use

Reinforcement of drug-negative urine specimens can present some practical difficul-
ties, including costs for testing and ensuring validity of samples. On-site urine testing
systems, which provide immediate results, may not be reimbursable. Second, because
delivery of reinforcers is contingent on a negative urine sample, patients may attempt
to leave phony samples. Clinics can ensure validity by observing urine submission
and checking temperature, dilution, and pH of the sample (for issues related to urine
testing, see Coleman & Baselt, 1997; Crouch, Frank, Farrell, Karsch, & Klaunig,
1998; Preston, Silverman, Schuster, & Cone, 1997).
There are also some practical problems in terms of analyzing urine samples in
some CM interventions. First, it may be challenging to differentiate illicit drug use
from licit drug use in some cases. For example, methadone, some other opioids, and
benzodiazepines can be taken illicitly or by prescription; therefore, it may not be
possible to design CM interventions that address use of these substances in persons
who have valid prescriptions for these medications. Also, several different types of
benzodiazepines exist, making it challenging to detect all forms of sedative use.
It is important to reinforce drug abstinence frequently, and to do so soon after
abstinence is determined. However, several factors can interfere with these principles
in practice. For example, liver disease (which can occur among intravenous drug
users and heavy alcohol drinkers) can slow down the metabolism of drugs, resulting
in a longer delay between a period of abstinence and the samples reading negative.
Similarly, clients with chronic marijuana use must achieve up to 4 weeks of abstinence
before their urine samples will read negative. Some marijuana dependent patients,
therefore, will not gain access to the reinforcers until a significant period of marijuana
abstinence has been achieved.
If the CM procedure targets alcohol or nicotine abstinence, the opposite problem
occurs. Alcohol use is identifiable by breath detectors for only a relatively short
period of time (e.g., 1–12 hours; Intoximeters, St Louis, MO). Therefore, an ideal
CM intervention would obtain breathalyzer readings several times a day in order to
detect any alcohol use. However, this practice would be impractical in nonresidential
treatment settings. One could assess alcohol use with urine or blood tests, although
these tests do not measure much further back than breath tests. Likewise, carbon
monoxide levels that are used to detect smoking must be taken several times daily
to detect all occasions of smoking. These technical constraints may prevent optimal
implementation of CM procedures for reinforcing abstinence from particular drugs.
Therefore, it is important to balance technological issues related to sensitivity of the
tests with behavioral principles in designing CM interventions.
Lack of Reinforcement During Treatment

Unfortunately, some patients in CM interventions do not achieve abstinence long
enough to provide a negative sample and therefore never receive reinforcement. For
example, in a sample of polydrug-using methadone patients, about half of the patients
did not leave a single negative sample or earn any reinforcement throughout the
12-week study (Iguchi et al., 1996; Stitzer et al., 1992). It is appropriate clinically
to target a single drug so that patients have a greater chance of achieving abstinence,
and consequently reinforcers, which may provide further motivation to maintain
abstinence. CM studies have found that interventions reinforcing abstinence from a
single substance not only have benefits for reducing use of that drug, but they may
also decrease nontargeted drug use (Petry et al., 2000). There is no evidence of drug
substitution in CM trials, and reinforcing abstinence from one substance has not been
shown to increase use of other drugs significantly (Kadden, Litt, Kabela-Cormier, &
Petry, 2009).
Another method to improve the chances of earning reinforcers is to give rein-
forcement for successive approximations toward abstinence. For example, one might
provide reinforcers contingent upon quantitative reductions in drug metabolites.
This procedure has been effective in reducing smoking by providing reinforcement
for reductions in smoking, rather than complete abstinence. Lamb, Kirby, Morral,
Galbicka, and Iguchi (2010) examined hard-to-treat smokers (e.g., those who did
not achieve any abstinence in a 10-day period) and easy-to-treat smokers (those
who had achieved abstinence at least once during the 10-day baseline period). They
randomized each of these types of smokers to 60 days of standard CM or CM
with shaping. In the standard CM condition, patients received reinforcers for breath
carbon monoxide (CO) levels less than 4 ppm. In the CM shaping condition, patients
received reinforcers for CO levels lower than the 7th-lowest of their last 9 samples,
or less than 4 ppm. Among the group of hard-to-treat smokers, patients assigned to
the CM shaping group were more likely than those assigned to the standard CM
procedure to achieve positive outcomes. Therefore, shaping can improve the efficacy
of CM for hard-to-treat smokers, and similar procedures may be helpful among
other groups of substance abusers who fail to earn reinforcement during usual CM
procedures.
Although shaping is likely useful for improving outcomes of difficult-to-treat
patients, most on-site testing systems, with the exception of those for alcohol and
nicotine, do not provide quantitative assessments of substance use or abstinence. As
technology advances, it may be possible to apply these procedures to other substance
use disorders. Other possibilities to enhance outcomes of difficult-to-treat substance
abusers include reinforcing attendance directly prior to the initiation of abstinence
(Stranger, Budney, Kamon, & Thostensen, 2009).
Potential Adverse Effects of Contingency Management

To date, few if any adverse effects of CM have been reported. In an analysis of
over 800 patients randomized to CM or standard care treatments, CM evidenced no
increases in adverse events (Petry et al., 2008).
Some researchers have expressed concerns about the similarities between the prize-
based CM procedure and gambling. There are high rates of comorbidity between
substance use disorders and pathological gambling (Petry, Stinson, & Grant, 2005),
and substance-abusing patients in recovery from pathological gambling are generally
excluded from prize-based CM studies. However, no studies have shown increases
in gambling behaviors among patients participating in the prize-based studies (e.g.,
Petry & Alessi, 2010; Petry & Martin, 2002: Petry, Kolodner, et al., 2006). Further,
the prize reinforcement system is not gambling because in the prize-based CM system
patients do not risk anything of value. Thus, the evidence to date indicates no adverse
effects of CM interventions.
Other researchers have expressed concern that removal of reinforcers after the
intervention period may precipitate relapse. However, no long-term follow-ups of
patients have found significant increases in relapse rates in CM treated patients relative
to non-CM treated patients. Conversely, long-term follow-ups have yielded either no

change relative to standard care interventions (Higgins, Wong, et al., 2000, 2003;
Petry, Alessi, et al., 2005; Rawson et al., 2002, 2006) or in some cases reductions in
drug use among patients who earlier received CM (Iguchi, Belding, Morral, Lamb,
& Husband, 1997; Kosten, Poling, & Oliveto, 2003; Petry & Martin, 2002; Petry,
Martin, & Simcic, 2005). As described in the next section, some studies have tried to
combine other interventions such as CBT to extend the benefits of CM.
Combining Contingency Management and Cognitive

Behavioral Therapy
Recent studies have examined the efficacy of combining CM with CBT in an attempt
to enhance the benefits of CM. CM is clearly efficacious for the treatment of sub-
stance use disorders, and reductions in substance use occur quite quickly when
CM is implemented appropriately. However, as is the case among all substance
use treatment interventions, a percentage of patients receiving CM relapse after
the intervention is discontinued. In comparison to CM, CBT (e.g., relapse preven-
tion) may produce a less immediate, although perhaps more enduring, reduction
in substance use (e.g., Carroll et al., 1994). In order to maximize the likelihood
of achieving and maintaining abstinence, studies have assessed whether a combi-
nation of CM and CBT would produce greater abstinence than either treatment
alone.
Rawson et al. (2002) randomly assigned methadone-maintained patients with
cocaine dependence to one of four 16-week treatments: (a) standard methadone
treatment, or the same plus (b) voucher-based CM for abstinence, (c) CBT, or
(d) a combination of CM and CBT. CM patients received escalating vouchers for
abstinence, and CBT patients attended manualized group therapy three times per
week. During treatment, patients in both CM conditions achieved greater abstinence
than did patients in the non-CM conditions. However, at the two follow-ups (26 and
52 weeks posttreatment), patients in the CBT plus CM condition achieved similar
abstinence to the CM and CBT conditions (per self-reported use and urinalysis).
Thus, adding CBT and CM did not produce greater abstinence at posttreatment or
follow-ups. Rawson and colleagues (2006) also compared CM to CBT in a sample
of non-methadone-maintained stimulant-dependent patients. Again, patients were
randomized to 16 weeks of voucher-based CM, CBT group therapy, or both. Results
were similar to those described above. During treatment, CM produced significantly
greater abstinence and treatment retention than CBT alone, and adding CBT to CM
did not improve outcomes. At follow-ups, however, members of all three groups
were equally likely to be abstinent. Together, these studies suggest that CM is
more effective than CBT during treatment, although CBT is equally efficacious for
promoting longer-term abstinence.
Interestingly, Epstein, Hawkins, Covi, Umbricht, and Preston (2003) found that
adding CBT to CM seemed to reduce CM’s positive effects during treatment, but
the combined intervention showed trends toward improved outcomes at follow-
up. Methadone-maintained cocaine users were randomly assigned to one of four
groups: a combination of CBT or standard group therapy and vouchers that were
either noncontingent on urinalysis results or contingent on cocaine-negative urine
samples. During the 12-week treatment, patients in the CM conditions achieved
longer durations of cocaine abstinence (9.8 consecutive specimens) than did those
in the noncontingent groups (3.0 consecutive specimens). There was no main effect
for CBT, and patients in standard care achieved similar durations of continuous
abstinence (6.7 specimens) to those in CBT (6.0 specimens). Unexpectedly, patients
in the CM plus CBT groups achieved shorter durations of continuous abstinence
(8.3 specimens) than the CM only group (11.3 consecutive specimens). However,
it should be noted that even when CBT was added, CM continued to produce
significantly greater abstinence than either of the noncontingent conditions. At the
12-month follow-up, there was a trend for the combination of CM and CBT to
produce greater abstinence than either treatment alone, although results were not
statistically significant.
CM and CBT are two of the most effective treatments for substance use disorders,
and it seems plausible that combining these two interventions may produce greater
abstinence than either treatment alone. However, as presented above, research does
not necessarily support this pattern. During treatment, CM is more efficacious
than CBT alone, although combining these treatments does not further improve
outcomes. In terms of longer-term abstinence, CM and CBT are equally efficacious,
although the Epstein et al. (2003) study suggested a trend for greater abstinence with
combined treatment. Overall, CM is certainly more efficacious during treatment than
other treatments alone, and produces long-term outcomes that are at least equally
favorable.
Summary
This chapter reviewed the efficacy of CM for the treatment of substance use disorders.
It described important behavioral principles of CM interventions that, when in place,
can produce substantial improvements in behavior. In addition, this chapter presented
a number of types of reinforcement that may be used in a CM intervention, and
addressed potential concerns about CM. Finally, studies that implemented CM with
and without CBT were described. CM has consistent and profound impacts on
improving behavior during the period when it is in place but, as is the case with
almost all treatments, more research is needed to examine methods for sustaining
improvements in the long term.
Acknowledgements
This study and preparation of this report were supported by NIH grants P30-
DA023918, R01-DA027615, R01-DA022739, RO1-DA13444, R01-DA018883,
R01-DA016855, RO1-DA14618, P50-DA09241, P60-AA03510, R01-DA024667,
T32-AA07290, and M01-RR06192.
References
Alessi, S. M., Petry, N. M., & Urso, J. (2008). Contingency management promotes smoking
reductions in residential substance abuse patients. Journal of Applied Behavior Analysis,
41, 617–622.
Amass, L., Bickel, W. K., Crean, J. P., Higgins, S. T., & Badger, G. J. (1995). Preferences for
clinic privileges, retail items, and social activities in an outpatient buprenorphine treatment
program. Journal of Substance Abuse Treatment, 13, 43–49.
Amass, L., & Kamien, J. (2004). A tale of two cities: Financing two voucher programs for
substance abusers through community donations. Experimental and Clinical Psychophar-
macology, 12, 147–155.
Andrzejewski, M. E., Kirby, K. C., Morral, A. R., & Iguchi, M. Y. (2000). Technology
transfer through performance management: The effects of graphical feedback and positive
reinforcement on drug treatment counselors’ behavior. Drug and Alcohol Dependence, 63,
179–186.
Bickel, W. K., Amass, L., Higgins, S. T., Badger, G. J., & Esch, R. A. (1997). Effects of adding
behavioral treatment to opioid detoxification with buprenorphine. Journal of Consulting
and Clinical Psychology, 65, 803–810.
Budney, A. J., Moore, B. A., Rocha, H. L., & Higgins, S. T. (2006). Clinical trial of
abstinence-based vouchers and cognitive-behavioral therapy for cannabis dependence.
Businelle, M. S., Rash, C. J., Burke, R. S., & Parker, J. D. (2009). Using vouchers to increase
continuing care participation in veterans: Does magnitude matter? American Journal on
Addictions, 18, 122–129.
Calsyn, D. A., & Saxon, A. J. (1987). A system for uniform application of contingencies for
illicit drug use. Journal of Substance Abuse Treatment, 4, 41–47.
Carroll, K. M., Rounsaville, B. J., Nich, C., Gordon, L. T., Wirtz, P. W., & Gawin, F.
H. (1994). One year follow-up of psychotherapy and pharmacotherapy for cocaine
dependence: Delayed emergence of psychotherapy effects. Archives of General Psychiatry,
51, 989–997.
Chutuape, M. A., Silverman, K., & Stitzer, M. L. (1998). Survey assessment of methadone
treatment services as reinforcers. American Journal of Drug and Alcohol Abuse, 24,
1–16.
Coleman, D. E., & Baselt, R. C. (1997). Efficacy of two commercial products for altering urine
drug test results. Journal of Toxicology-Clinical Toxicology, 35, 637–642.
Cone, E. J., & Dickerson, S. L. (1992). Efficacy of urinalysis in monitoring heroin and cocaine
abuse patterns: Implications in clinical trials for treatment of drug dependence. In R.
B. Jain (Ed.), Statistical issues in clinical trials for treatment of opioid dependence (pp.
46–58). Washington, DC: US Government Printing Office.
Crouch, D. J., Frank, J. F., Farrell, L. J., Karsch, H. M., & Klaunig, J. E. (1998). A multiple-site
laboratory evaluation of three on-site urinalysis drug-testing devices. Journal of Analytical
Toxicology, 22, 493–502.
Dallery, J., Silverman, K., Chutuape, M. A., Bigelow, G. E., & Stitzer, M. L. (2001). Voucher-
based reinforcement of opiate plus cocaine abstinence in treatment-resistant methadone
patients: Effects of reinforcer magnitude. Experimental and Clinical Psychopharmacology,
9, 317–325.
Dolan, M. P., Black, J. L., Penk, W. E., Robinowitz, R., & DeFord, H. A. (1985). Contracting
for treatment termination to reduce illicit drug use among methadone maintenance
failures. Journal of Consulting and Clinical Psychology, 53, 549–551.
Dutra, L., Stathopoulou, G., Basden, S. L., Leyro, T. M., Powers, M. B., & Otto, M. W.
(2008). A meta-analytic review of psychosocial interventions for substance use disorders.
Elk, R., Grabowski, J., Rhoades, H., Spiga, R., Schmitz, J., & Jennings, W. (1993). Compliance
with tuberculosis treatment in methadone-maintained patients: Behavioral interventions.
Journal of Substance Abuse Treatment, 10, 371–382.
Elk, R., Schmitz, J., Spiga, R., Rhoades, H., Andres, R., & Grabowski, J. (1995). Behavioral
treatment of cocaine-dependent pregnant women and TB-exposed patients. Addictive
Behaviors, 20, 533–542.
Epstein, D. H., Hawkins, W. E., Covi, L., Umbricht, A., & Preston, K. L. (2003). Cognitive-
behavioral therapy plus contingency management for cocaine use: Findings during
treatment and across 12-month follow-up. Psychology of Addictive Behaviors, 17 , 73–82.
Festinger, D. S., Marlow, D. B., Croft, J. R., Dugosh, K. L., Mastro, N. K., Lee, P. A., …
Patapis, N. S. (2005). Do research payments precipitate drug use or coerce participation?
Drug and Alcohol Dependence, 78, 275–281.
Higgins, S. T., Badger, G. J., & Budney, A. J. (2000). Initial abstinence and success in
achieving longer term cocaine abstinence. Experimental and Clinical Psychopharmacology,
8, 377–386.
Higgins, S. T., Budney, A. J., & Bickel, W. K. (1994). Applying behavioral concepts and
principles to the treatment of cocaine dependence. Drug and Alcohol Dependence, 34,
87–97.
Higgins, S. T., Budney, A. J., Bickel, W. K., Foerg, F. E., Donham, R., & Badger, G. J. (1994).
Incentives improve outcome in outpatient behavioral treatment of cocaine dependence.
Archives of General Psychiatry, 51, 568–576.
Higgins, S. T., Sigmon, S. C., Wong, C. J., Heil, S. H., Badger, G. J., Donham, R., … Anthony,
S. (2003). Community reinforcement therapy for cocaine-dependent outpatients. Archives
of General Psychiatry, 60, 1043–1052.
Higgins, S. T., Stitzer, M. L., Bigelow, G. E., & Liebson, I. A. (1986). Contingent methadone
delivery: Effects on illicit-opiate use. Drug and Alcohol Dependence, 17 , 311–322.
Higgins, S. T., Wong, C. J., Badger, G. J., Ogden, D. E. H., & Dantona, R. L. (2000b).
Contingent reinforcement increases cocaine abstinence during outpatient treatment and
1 year of follow-up. Journal of Consulting and Clinical Psychology, 68, 64–72.
Hubbard, R. L., Craddock, S. G., Flynn, P. M., Anderson, J., & Etheridge, R. M. (1997).
Overview of 1-year follow-up outcomes in the Drug Abuse Treatment Outcome Study
(DATOS). Psychology of Addictive Behaviors, 11, 261–278.
Hubbard, R. L., Marsden, M. E., Rachal, J. V., Harwood, H. J., Cavanaugh, E. R., &
Ginzburg, H. M. (1989). Drug abuse treatment: A national study of effectiveness. Chapel
Hill, NC: University of North Carolina Press.
Hunt, Y. M., Rash, C. J., Burke, R. S., & Parker, J. D. (2010). Smoking cessation in recovery:
A comparison of two different cognitive behavioral treatments. Addictive Disorders and
Their Treatment, 9, 64–74.
Iguchi, M. Y., Belding, M. A., Morral, A. R., Lamb, R. J., & Husband, S. D. (1997).
Reinforcing operants other than abstinence in drug abuse treatment: An effective
alternative for reducing drug use. Journal of Consulting and Clinical Psychology, 65,
421–428.
Iguchi, M. Y., Lamb, R. J., Belding, M. A., Platt, J. J., Husband, S. D., & Morral, A.
R. (1996). Contingent reinforcement of group participation versus abstinence in a
methadone maintenance program. Experimental and Clinical Psychopharmacology, 4,
315–321.
Kadden, R. M., Litt, M. D., Kabela-Cormier, E., & Petry, N. M. (2007). Abstinence rates
following behavioral treatments for marijuana dependence. Addictive Behaviors, 32,
1220–1236.
Kadden, R. M., Litt, M. D., Kabela-Cormier, E., & Petry, N. M. (2009). Increased drinking in
a trial of treatments for marijuana dependence: Substance substitution? Drug and Alcohol
Dependence, 105, 168–171.
Kang, S. Y., Kleinman, P. H., Woody, G. E., Millman, R. B., Todd, T. C., Kemp, J., & Lipton,
D. S. (1991). Outcomes for cocaine abusers after once-a-week psychosocial therapy.
Kidorf, M., & Stitzer, M. L. (1996). Contingency use of take-homes and split dosing to reduce
illicit drug use of methadone patients. Behavior Therapy, 27 , 41–51.
Kosten, T., Poling, J., & Oliveto, A. (2003). Effects of reducing contingency management
values on heroin and cocaine use for buprenorphine- and desipramine-treated patients.
Addiction, 98, 665–671.
Lamb, R. J., Kirby, K. C., Morral, A. R., Galbicka, G., & Iguchi, M. Y. (2010). Shaping
smoking cessation in hard-to-treat smokers. Journal of Consulting and Clinical Psychology,
78, 62–71.
Ledgerwood, D. M., Alessi, S. M., Hanson, T., Godley, M. D., & Petry, N. M. (2008). Con-
tingency management for attendance to group substance abuse treatment administered
by clinicians in community clinics. Journal of Applied Behavior Analysis, 41, 517–526.
Lussier, J. P., Heil, S. H., Mongeon, J. A., & Badger, G. J. (2006). A meta-analysis
of voucher-based reinforcement therapy for substance use disorders. Addiction, 101,
192–203.
Magura, S., Casriel, C., Goldsmith, D. S., Strug, D., & Lipton, D. (1988). Contingency
contracting with polydrug-abusing methadone patients. Addictive Behavior, 13, 113–118.
McCarthy, J. J., & Borders, O. T. (1985). Limit setting on drug abuse in methadone
maintenance patients. American Journal of Psychiatry, 142, 1419–1423.
Olmstead, T. A., & Petry, N. M. (2009). The cost-effectiveness of prize-based and voucher-
based contingency management in a population of cocaine- or opioid-dependent patients.
Drug and Alcohol Dependence, 102, 108–115.
Peirce, J. M., Petry, N. M., Stitzer, M. L., Blaine, J., Kellogg, S., Satterfield, F., … Li, R. (2006).
Effects of lower-cost incentives on stimulant abstinence in methadone maintenance
treatment: A National Drug Abuse Treatment Clinical Trials Network study. Archives of
Petry, N. M. (2000). A comprehensive guide to the application of contingency management
procedures in clinical settings. Drug and Alcohol Dependence, 58, 9–25.
Petry, N. M. (2012). Contingency management for substance abuse treatment: A guide to
implementing this evidence-based practice. New York, NY: Routledge/Taylor & Francis
Group.
Petry, N. M., & Alessi, S. M. (2010). Prize-based contingency management is efficacious
in cocaine-abusing patients with and without recent gambling participation. Journal of
Substance Abuse Treatment, 39, 282–288.
Petry, N. M., Alessi, S. M., Carroll, K. M., Hanson, T., MacKinnon, S., Rounsaville, B., &
Sierra, S. (2006). Contingency management treatments: Reinforcing abstinence versus
adherence with goal-related activities. Journal of Consulting and Clinical Psychology, 74,
592–601.
Petry, N. M., Alessi, S. M., Hanson, T., & Sierra, S. (2007). Randomized trial of contingent
prizes versus vouchers in cocaine-using methadone patients. Journal of Consulting and
Petry, N. M., Alessi, S. M., & Ledgerwood, D. M. (2012). A randomized trial of contingency
management delivered by community therapists. Journal of Consulting and Clinical
Psychology. Advance online publication. doi:10.1037/a0026826
Petry, N. M., Alessi, S. M., Ledgerwood, D. M., & Sierra, S. (2010). Psychometric properties
of the Contingency Management Competence Scale. Drug and Alcohol Dependence, 109,
167–174.
Petry, N. M., Alessi, S. M., Marx, J., Austin, M., & Tardif, M. (2005). Vouchers versus prizes:
Contingency management treatment of substance abusers in community settings. Journal
Petry, N. M., Kolodner, K. B., Li, R., Peirce, J. M., Roll, J. M., Stitzer, M. L., & Hamilton, J.
A. (2006). Prize-based contingency management does not increase gambling. Drug and
Alcohol Dependence, 83, 269–273.
Petry, N. M., & Martin, B. (2002). Low-cost contingency management for treating cocaine-
and opioid-abusing methadone patients. Journal of Consulting and Clinical Psychology,
70, 398–405.
Petry, N. M., Martin, B., Cooney, J. L., & Kranzler, H. R. (2000). Give them prizes and they
will come: Contingency management for treatment of alcohol dependence. Journal of
Petry, N. M., Martin, B., & Finocche, C. (2001). Contingency management in group treatment:
A demonstration project in an HIV drop-in center. Journal of Substance Abuse Treatment,
21, 89–96.
Petry, N. M., Martin, B., & Simcic, F. (2005). Prize reinforcement contingency management
for cocaine dependence: Integration with group therapy in a methadone clinic. Journal of
Petry, N. M., Peirce, J. M., Stitzer, M. L., Blaine, J., Roll, J. M., Cohen, A., … Li, R.
(2005). Effect of prize-based incentives on outcomes in stimulant abusers in outpatient
psychosocial treatment programs: A National Drug Abuse Treatment Clinical Trials
Network study. Archives of General Psychiatry, 62, 1148–1156.
Petry, N. M., Roll, J. M., Rounsaville, B. J., Ball, S. A., Stitzer, M., Peirce, J. M., … Carroll, K.
M. (2008). Serious adverse events in randomized psychosocial treatment studies: Safety
or arbitrary edicts? Journal of Consulting and Clinical Psychology, 76, 1076–1082.
Petry, N. M., Stinson, F. S., & Grant, B. F. (2005). Comorbidity of DSM-IV pathological
gambling and other psychiatric disorders: Results from the national epidemiological survey
on alcohol and related conditions. Journal of Clinical Psychiatry, 66, 564–574.
Petry, N. M., Tedford, J., Austin, M., Nich, C., Carroll, K. M., & Rounsaville, B. J. (2004).
Prize reinforcement contingency management for treating cocaine users: How low can
we go, and with whom? Addiction, 99, 349–360.
Petry, N. M., Weinstock, J., & Alessi, S. M. (2011). A randomized trial of contingency
management delivered in the context of group counseling. Journal of Consulting and
Prendergast, M., Podus, D., Finney, J., Greenwell, L., & Roll, J. (2006). Contingency
management for treatment of substance use disorders: A meta-analysis. Addiction, 101,
1546–1560.
Preston, K. L., Ghitza, U. E., Schmittner, J. P., Schroeder, J. R., & Epstein, D. H. (2008).
Randomized trial comparing two treatment strategies using prize-based reinforcement of
abstinence in cocaine and opiate users. Journal of Applied Behavior Analysis, 41, 551–563.
Preston, K. L., Silverman, K., Higgins, S. T., Brooner, R. K., Montoya, I, Schuster, C. R.,
& Cone, E. J. (1998). Cocaine use early in treatment predicts outcome in a behavioral
treatment program. Journal of Consulting and Clinical Psychology, 66, 691–696.
Preston, K. L., Silverman, K., Schuster, C. R., & Cone, E. J. (1997). Assessment of cocaine
use with quantitative urinalysis and estimation of new uses. Addiction, 92, 717–727.
Rawson, R. A., Huber, A., McCann, M., Shoptaw, S., Farabee, D., Reiber, C., & Ling, W.
(2002). A comparison of contingency management and cognitive-behavioral approaches
during methadone maintenance treatment for cocaine dependence. Archives of General
Rawson, R. A., McCann, M. J., Flammino, F., Shoptaw, S., Miotto, K., Reiber, C., & Ling, W.
for stimulant-dependent individuals. Addiction, 101, 267–274.
Roll, J. M., Higgins, S. T., & Badger, G. J. (1996). An experimental comparison of three
different schedules of reinforcement of drug abstinence using cigarette smoking as an
exemplar. Journal of Applied Behavior Analysis, 29, 495–505.
Roll, J. M., Reilly, M. P., & Johanson, C. E. (2000). The influence of exchange delays
on cigarette versus money choice: A laboratory analog of voucher-based reinforcement
therapy. Experimental and Clinical Psychopharmacology, 8, 366–370.
Rowan-Szal, G., Joe, G. W., Chatham, L. R., & Simpson, D. D. (1994). A simple reinforcement
system for methadone clients in a community-based treatment program. Journal of
Substance Abuse Treatment, 11, 217–223.
Saxon, A. J., Calsyn, D. A., Wells, E. A., & Stanton, V. V. (1998). The use of urine toxicology
to enhance patient control of take-home doses in methadone maintenance: Effects on
reducing illicit drug use. Addiction Research, 6, 203–214.
Schmitz, J. M., Rhoades, H., & Grabowski, J. (1994). A menu of potential reinforcers
in a methadone maintenance program. Journal of Substance Abuse Treatment, 11,
425–431.
Schwartz, B., Lauderdale, R. M., Montgomery, M. L., Burch, E. A., & Gallant, D. M. (1987).
Immediate versus delayed feedback on urinalysis reports for methadone maintenance
patients. Addictive Behaviors, 12, 293–295.
Shaner, A., Roberts, L. J., Eckman, T. A., Tucker, D. E., Tsuang, J. W., Wilkins, J. N., &
Mintz, J. (1997). Monetary reinforcement of abstinence from cocaine among mentally ill
patients with cocaine dependence. Psychiatric Services, 48, 807–810.
Sigmon, S. C., & Stitzer, M. L. (2005). Use of low-cost incentive intervention to improve
counseling attendance among methadone maintained patients. Journal of Substance Abuse
Treatment, 29, 253–258.
Silverman, K., Chutuape, M. A., Bigelow, G. E., & Stitzer, M. L. (1999). Voucher-based
reinforcement of cocaine abstinence in treatment-resistant methadone patients: Effects of
reinforcement magnitude. Psychopharmacology, 146, 128–138.
Silverman, K., Wong, C. J., Higgins, S. T., Brooner, R. K., Montoya, I. D., Contoreggi, C., …
Preston, K. L. (1996). Increasing opiate abstinence through voucher-based reinforcement
therapy. Drug and Alcohol Dependence, 41, 157–165.
Simpson, D. D. (1981). Treatment for drug abuse: Follow-up outcomes and length of time
spent. Archives of General Psychiatry, 38, 875–880.
Simpson, D. D., & Sells, S. B. (1982). Effectiveness of treatment for drug abuse: An overview
of the DARP research program. Advances in Alcohol & Substance Abuse, 2, 7–29.
Stitzer, M. L., Bickel, W. K., Bigelow, G. E., & Liebson, I. A. (1986). Effects of methadone
dose contingencies on urinalysis test results of polydrug-abusing methadone-maintenance
patients. Drug and Alcohol Dependence, 18, 341–348.
Stitzer, M. L., Iguchi, M. Y., & Felch, L. J. (1992). Contingent take-home incentive: Effects
on drug use of methadone maintenance patients. Journal of Consulting and Clinical
Stranger, C., Budney, A. J., Kamon, J., & Thostensen, J. (2009). A randomized trial of
contingency management for adolescent marijuana abuse and dependence. Drug and
Alcohol Dependence, 105, 240–247.
Zeiler, M. D. (1977). Elimination of reinforced behavior: Intermittent schedules of not-
responding. Journal of the Experimental Analysis of Behavior, 25, 23–32.
12
Social Skills and Problem-Solving
Training
Kim T. Mueser and Jennifer D. Gottlieb
Boston University, United States
Susan Gingerich
Philadelphia, United States
Social skills training is a systematic approach to teaching interpersonal skills, such as

conversational skills and assertiveness, based on social learning theory. Complex social
skills are broken down into constituent elements, which are taught through a set
of programmatic learning activities, including modeling, behavioral rehearsal in role
plays, positive and corrective feedback following role plays to shape (approximations)
the targeted skills, and home assignments for the individual to practice the skill
outside of the session. Social skills training can be provided on a group or individual
basis, and is one of the most widely used cognitive behavioral techniques, with
applications to a broad range of clinical populations as well as more generally to
improving interpersonal effectiveness in nonclinical populations.
Problem-solving training is based on many of the same principles as social skills
training, but focuses on teaching a standard sequence of steps aimed at facilitating
the identification of effective solutions to problems, either by the individual him-
or herself, or with another person (such as a partner or spouse) or in a family.
Although some programs focus mainly on social skills and others on problem-solving
skills, many combine training in both skills. For this reason, we describe the critical
ingredients of both social skills and problem-solving training.
This chapter begins with a brief history of the development of social skills and
problem-solving training. Next, specific types of social skills are discussed, followed by
methods for assessing social skills. The logistics of providing social skills and problem-
solving training are described. Then, social skills training procedures are reviewed,
followed by problem-solving training. The use of skills training to address a wide
range of different needs in both clinical and nonclinical populations is highlighted,
with reference to the burgeoning research literature on skills training. As an enormous
clinical and research literature on skills training has emerged over the past several

DOI: 10.1002/9781118528563.wbcbt12
decades, this chapter will focus on explicating the basic methods of skills training and
will provide examples of the use of skills training to address a variety of problems and
goals, without attempting to provide a comprehensive survey of the many different
applications of the techniques.
A Brief History of Social Skills and Problem-Solving Training
The methods incorporated into social skills and problem-solving training developed
gradually, beginning over half a century ago. Salter (1949) was one of the first
to pioneer the use of role playing as a psychotherapeutic device in order to help
individuals express themselves, and help them overcome symptoms such as depression
and anxiety. Wolpe (1958), addressing the problem of social anxiety in his book
Psychotherapy by Reciprocal Inhibition, theorized that if people could be taught to
communicate with others in a strong, confident manner (e.g., good eye contact, firm
and loud voice tone), this assertive style would be incompatible with, and therefore
inhibit, anxious feelings. Wolpe used role plays to help clients practice more assertive
behavior in order to reduce their social anxiety. Lazarus (1966) demonstrated the
benefits of repeated behavioral rehearsal in role plays combined with instructions and
feedback to shape performance.
In the 1960s, Bandura (1969) initiated a series of seminal studies aimed at eval-
uating the role of social modeling in learning new social behaviors. This research
demonstrated that simply seeing another person model (engage in) a novel behavior,
including observing the positive consequences of the behavior, served as a powerful
learning experience that was often sufficient for the observer to be able to mimic
or perform the same behavior, in the hopes of obtaining similar reinforcement. As
modeling became recognized as a potent tool for teaching social behaviors, skills
training procedures began to incorporate it along with repeated role playing and feed-
back to hone individuals’ interpersonal skills over successive trials. Success with these
efforts led to the “packaging” of these strategies into the basic standardized format
known today as social skills training, including modeling (demonstrating) the skill,
behavioral rehearsal (practice) in role plays, positive and corrective feedback to shape
the behavioral performance, and home assignments to practice the skill on one’s own.
Early applications of these skills training procedures focused initially on teaching
people how to “stand up for themselves” verbally in social situations in which others
were infringing on their rights (e.g., someone butting in line in front of the person) by
clearly stating their opinion (i.e., negative assertion), such as by saying, “Excuse me,
but I was in line in front of you. Please go to the end of the line, where new people are
supposed to join it.” The teaching of negative assertion skills was soon also extended
to helping people communicate positive feelings and appreciation to each other (i.e.,
positive assertion), such as, “I really like how kind you are to animals. You are really a
very empathic person.” These approaches to skills training, often delivered in group
settings, soon became known as assertiveness training, which spawned a wide range of
programs and books for clinical and nonclinical populations alike (M. J. Smith, 1985).
It soon became apparent that positive and negative assertion skills were but two of a
wide range of social domains that could be targeted with these skills training methods
Social Skills and Problem-Solving Training 245
(Bellack & Hersen, 1979). For example, Hersen and Bellack (1976) and Liberman
(2007) began to evaluate the use of skills training methods to address the profound
impairments in social functioning common in people with schizophrenia, whereas
other applications focused on such diverse populations as individuals with intellectual
disability (Antonello, 1995), children (Matson, 2010), and couples with marital
distress (Jacobson & Margolin, 1979). Social skills and problem-solving training
became the broadly accepted term to describe this systematic approach to teaching
more effective interpersonal skills.
What are Social Skills?
Social skills can be broadly defined as the interpersonal skills necessary to achieve
instrumental goals, such as purchasing an item at a store, and affiliative goals, such
as striking up a friendly conversation with a stranger (Liberman, DeRisi, & Mueser,
1989). A more detailed description is provided by Bellack and Hersen (1979), who
define social skills as the
ability to express both positive and negative feelings in the interpersonal context without
suffering consequent loss of reinforcement. Such skill is demonstrated in a large variety
of interpersonal contexts and involves the coordinated delivery of appropriate verbal and
nonverbal responses. In addition, the socially skilled individual is attuned to the realities
of the situation and is aware when he is likely to be reinforced for his efforts (p. 512).
Components of Social Skill

In order to facilitate the teaching of social skills, specific types or components of inter-
personal behavior have been identified. Skills training typically focuses on four broad
categories of social skill, including paralinguistic features, nonverbal skills, interactive
balance, and verbal content. Within each broad category, training focuses on specific
components of social skill, as briefly described below and summarized in Box 12.1.
Paralinguistic features refer to the vocal characteristics of speech, such as voice
tone, loudness, affect, and fluency. Nonverbal skills include behaviors such as facial
expressiveness, use of gestures, body orientation, and interpersonal distance. Together,
paralinguistic features and nonverbal skills are critical to communicating the overall
meaning of an interaction, and at times they may be more important than the actual
verbal content of what is said. For example, someone who declines the offer of an
alcoholic drink at a party by saying, “No thank you” in a soft and meek voice tone
may be viewed by others as being unsure or ambivalent about drinking, leading to
further offers, cajoling, or pressure to accept a drink.
All social interactions involve some “give and take” between two (or more) people
balancing between their own needs and goals in the situation, and responding to
the other person. The interactive balance of an interaction refers to each individual’s
sensitivity to this interplay. Examples of key features of interactive balance include the
relevance of each person’s statements to the overall conversational topic, the relative
amount of time each person talks (i.e., if one person talks much more than the other
Box 12.1 Components of social skill

Paralinguistic elements
Voice tone, pitch, and inflection
Loudness
Affect
Fluency
Clarity
Nonverbal skills
Eye contact
Facial expression
Use of gestures
Body orientation
Interpersonal distance
Interactive balance
Latency of response to other person
Relative amount of time talked
Responsiveness
Verbal content
Relevance to conversational topic
Social appropriateness to situation
Specificity of communication (e.g., verbal feeling statement, clear
behavioral referents)
either that person may feel overly responsible for holding up the conversation, or the
other may feel not enough opportunity to express his or her perspective), and the
latency of response to the other person’s statements (i.e., too long a pause before a
response can make the conversation feel awkward and strained, whereas too short a
pause or frequent interruptions can create an impression of the conversation being
rushed or the other person not listening).
The verbal content refers to the words and phrases used in the communication,
regardless of the manner in which it was spoken. There are numerous possible
dimensions along which verbal content can vary, such as its appropriateness to the
situation, the degree of specificity, whether feeling statements are made, and the choice
of particular words. There are also many nuances of the verbal content of interactions
that can influence the effectiveness of someone communicating something to another
person. For example, when people are upset with someone else, they often “blame”
the other person for their upset feeling (e.g., “You made me mad when you were
late for dinner again”), which can put them on the defensive, and make them less
willing to acknowledge their behavior and talk about the situation. A more effective
alternative is to modify the verbal content slightly so that the person “owns” his or
her feeling (e.g., “I was really upset that you were late for dinner again last night”),
which is often more effective in leading to a discussion, and considering possible ways
of avoiding the conflict in the future.
Social Cognition
Social skills are necessary for fruitful interactions with other people, but alone they are
insufficient. It has long been recognized that effective communication also requires the
ability to perceive relevant social information accurately in different social situations,
and based on that information to identify appropriate and optimal responses (McFall,
1982; Trower, Bryant, & Argyle, 1978; Wallace et al., 1980). Social cognition is the
ability to perceive critical social information during social encounters, and to process
that information in order to determine the best response (Strack & Förster, 2009).
There is a wide range of social cognition skills, as summarized in Box 12.2. These
skills can be broadly divided into those related to the recognition of different social
situations that may constrain the range of appropriate behavior (e.g., school, work,
partner or spouse, family, friends, in a store, in a public place such as a park), the
understanding of social and cultural mores as they relate to these social situations
(e.g., disclosure of personal information to friends, family or spouses/partners vs.
coworkers or strangers), and the ability to understand the other person’s feelings,
thoughts, and intentions. Poor social cognition skills can lead to ineffective or
inappropriate behavior, and thus interfere with the person’s ability to achieve his or
her interpersonal or instrumental goals.
Box 12.2 Social cognition skills

Perception of others’ emotions
Facial expression recognition
Recognition of feelings from voice tone and affect
Recognition of situational/contextual cues, such as:
Relationships between different people (e.g., family members, friends,
spouse/partner, stranger, coworker, supervisor, professional, public
servant)
The nature of the social situation
Ability to infer others’ motives, intentions, or thoughts (theory of mind)
Knowledge of relevant social and cultural mores
The accurate perception of the other person’s thoughts and feelings during an
interaction can be especially important. Recognizing what the person is feeling during
the interaction, based on his or her facial expression, voice tone, and gestures, can
have implications for how to respond, especially considering that emotions are often
not verbally expressed, and must be decoded based on facial and paralinguistic cues.
For example, if the other person begins to sound bored during a conversation, it may
be desirable to change the topic, or to end the conversation gracefully. For another
example, if the other person appears angry or upset, it may be desirable to verify what
he or she is feeling, and attempt to understand the nature of the concern, and possibly
explore ways of addressing it.
In addition to recognizing the other person’s feelings, the ability to infer the other
person’s motives, intentions, and thoughts based on indirect information (called
theory of mind) is also critical. People often do not directly say what is on their mind,
but their true thoughts and motives may be apparent from what they do say, their
behavior, and the situation. For example, if two people were sitting in a warm room
with all the windows closed, one person might give a hint to the other person to
open the window by saying something like “It sure is warm in here!,” “Wouldn’t a
good breeze be nice?,” or “Wouldn’t it be nice if someone opened the window?”
The accurate detection of relevant interpersonal and situational cues that allow an
understanding of what the other person is thinking is critical to demonstrating
sensitivity to others, as well as to avoiding coercion or exploitation. The ability to
infer other people’s thoughts accurately is particularly impaired in some psychiatric
disorders, such as schizophrenia (Penn, Corrigan, Bentall, Racenstein, & Newman,
1997), and autism and Asperger’s syndrome (Sicile-Kira & Grandin, 2004).
Knowledge of situational cues, as well as social and cultural mores regarding social
behavior, is another critical dimension of social cognition. For example, different types
of behavior are appropriate in different types of social situations, such as at work, with
friends, with family, at a store, or at a public gathering (e.g., a concert). Thus, divulging
sensitive personal about one’s health or relationship problems would often be regarded
as inappropriate if it were to a stranger or in most work situations, but might be
appropriate to family members or friends. Similarly, there are many “unwritten rules”
in social situations that are important to be aware of (Myles, Trautman, & Schelvan,
2004), such as asking another person at a party how much money he or she makes.
In addition, the rules of appropriate social behavior vary across different cultures, and
thus a person needs to be aware of the pertinent rules in the culture in which he
or she is currently. For example, in most Western cultures it is considered socially
appropriate to look at the other person’s eyes (or close to the eyes) when talking to
them, but in many eastern cultures deference to an authority figure (e.g., an employer
or parent) is shown by avoiding direct eye contact during social interactions.
Problem-Solving Skills
The ability to solve problems, both interpersonal and non-interpersonal, is a critical
skill for personal success, since obstacles are invariably encountered on the way toward
achieving personal goals. Effective problem solving with other people requires good
social and social cognition skills, although these skills alone are often insufficient
to resolve many problems. Problem-solving skills are a specific set of behaviors or
steps designed to maximize the resolution of a particular problem (e.g., define the
problem, brainstorm possible solutions, evaluate possible solutions, etc.) (D’Zurilla

& Goldfried, 1971). Problem-solving skills can be taught to facilitate an individual’s
ability to solve problems on his or her own, or aimed at teaching people how to
solve problems together. The focus of social problem-solving training can be on
improving skills for reducing conflict, solving externally based problems people may
face together, or addressing a problem that one has that requires another’s help.
Problem-solving skills can also be used to help people determine the most effective
strategies for taking steps toward personal or shared goals.
Assessment of Social Skills
A wide range of strategies can be used to assess an individual’s social skills, including
self-reports, informant reports (e.g., from a family member, friend, or clinician),
naturalistic observations, and role plays. No single assessment strategy is perfect.
Therefore, a combination of assessment methods is usually most useful.
Individuals vary in their insight into their own social difficulties, needs, and skills.
Some individuals are very aware of social problems they may have (e.g., not doing well
at work or school, not having close friends), whereas others may not. Information
about the individual’s satisfaction with different areas of his or her life may provide
clues to possible problems in social skill in areas such as friendship, work or school, or
family relationships. Self-report measures of social skill are most effective when they
probe the individual’s satisfaction with, and confidence in, his or her ability to interact
with other people in different situations. Assessments need to be specific to different
social situations because people may be skillful in some circumstances (e.g., at work
or school), but not others (e.g., with acquaintances or friends).
While self-report information is often very useful in understanding social skills,
all self-evaluations are subject to bias. In addition, some people lack insight into
their social behavior and its effects on other people. Some people may overestimate
their skills for interacting with other people, whereas others may underestimate their
skills. For example, when people with bipolar disorder have episodes of mania or
hypomania, they are often overly confident in their abilities (including social ones),
even to the point of grandiosity, which can lead to a range of social problems and
negative consequences (Goodwin & Jamison, 2007). In contrast, people with social
phobia or depression are prone to underestimating their skills for interacting with
other people (Beck, Rush, Shaw, & Emery, 1979; Heimberg & Becker, 2002).
Significant others can provide valuable insights into a person’s strengths and
weaknesses in social situations. Informants such as family members, teachers, friends,
and clinicians are often privy to information about an individual’s social skills,
and specific areas that may be in need of improvement. While the reports of
informants can often be revealing and useful, like self-reports, they may be subject
to bias in that the informant may have beliefs or attitudes about the person that
could color his or her perceptions of their social skills. In addition, informants
often lack information about an individual’s social performance in a variety of
situations. Family members may know little about how a relative interacts with
friends or in social situations involving drugs or alcohol. Similarly, teachers may
have valuable observations about a student’s skills when interacting with peers in
the classroom and on school grounds, but may have little or no information about
how they respond to peer pressure around issues such as smoking, drinking, or
sex.
Naturalistic observations may be another useful assessment method for some
individuals. Naturalistic observations should be conducted with the permission of the
individuals, and can provide valuable insights into how they interact with others in
certain social situations, such as how a child interacts with peers at the playground,
how a couple experiencing marital distress interact with one another while attempting
to solve a problem, how someone handles social situations at the workplace, or how a
client who is hospitalized interacts with other clients on the unit. Clearly, naturalistic
observations are not feasible in many social situations (e.g., during interactions with
close friends, during intimate situations, or in many situations involving alcohol or
drugs).
A final technique for assessing social skills is the use of role play tests. Role
plays are simulated social interactions in which an individual interacts with another
person (a “confederate”) for a brief period of time to demonstrate how he or
she would handle a particular situation. Role play tests usually include practice
in a variety of different situations related to the overall area of social behavior
that is the focus of assessment (e.g., starting conversations, resolving conflicts,
interacting with family members, responding to one’s boss or customers), with
at least a few role play scenarios conducted for each social situation. Role plays
are usually brief, typically lasting between one and four minutes, with the general
nature of the confederate’s responses scripted in advance to ensure standardization.
The individual’s performance in the role play is usually videotaped or audio-
taped, with specific dimensions of social skill subsequently rated using standardized
scales.
Extensive research has demonstrated the reliability and validity of role play tests as
measures of social competence (Bellack, Brown, & Thomas-Lohrman, 2006; Bellack,
Hersen, & Lamparski, 1979; Bellack, Morrison, Mueser, Wade, & Sayers, 1990).
Performance on role plays is strongly related to naturalistic observations of social
skill, as well as objective evaluations based on both self-report and informant-based
assessments. While role play assessments provide useful and very specific information
about an individual’s social skills in different situations, they can be time consuming
and require additional resources to administer, and thus their use in clinical practice
is often limited.
Role play tests provide valuable information about a person’s specific social skills and
overall social competence when interacting in different social situations. Nevertheless,
just because someone demonstrates a skill in a role play test does not mean that
the person actually uses those skills in the appropriate social situations. However,
performance in role play tests does indicate that the social skill is in the person’s
behavioral repertoire, and that he or she is capable of using it. There are a variety
of reasons why someone who is capable of particular social skills may not use them
regularly (e.g., lack of confidence, fear of negative consequences, lack of opportunities,
anxiety). These reasons can be addressed in the context of skills training.
Nonskill Factors which Can Affect Social Competence

Although social skills can have an important influence on an individual’s social
competence and functioning, not all problems in social adjustment are the result of
impairments in social skill. The recognition of other factors that can also influence
social functioning is critical, since successful intervention may require attention to
these factors in addition to, or instead of, teaching social skills. These factors fall
under the general categories of mood disturbances, other psychiatric symptoms,
environmental factors, cultural norms, and medication side effects.
Mood disturbances. Problems with mood, such as depression, anxiety, or anger, may
result in a person not using social skills of which they are capable. For example, positive
mood can facilitate creative problem solving, and thus more effective social behavior.
Depressed mood, on the other hand, which is often associated with hopelessness and
poor self-esteem (American Psychiatric Association, 2000), can result in people not
using critical skills when interacting with other people, or even giving up entirely
on pursuing their personal goals. Anxiety can interfere with the ability of people to
use skills they are capable of when their attention is diverted by their physiological
overarousal (e.g., pounding heart, muscular tension, excessive perspiration) or their
worries about the situation at hand. Anxiety can also lead people to avoid social
situations relevant to achieving their goals. Intense feelings of anger or annoyance
can produce similarly distracting physiological reactions, lead to the unrestrained
expression of negative feelings that can worsen the situation, and interfere with the
person’s ability to listen and hear the other person’s perspective, preventing the
resolution of the problem.
Other psychiatric symptoms. A variety of other symptoms can also contribute to poor
social competence, independent of social skill. One category of symptoms that can
affect social functioning is the negative symptoms of schizophrenia, such as apathy,
anhedonia (lack of pleasure), asociality (avoidance of social contact), alogia (paucity
of speech), and blunted affect (e.g., diminished facial and vocal expressiveness)
(Andreasen, 1982). For example, people with negative symptoms may fail to initiate
interactions or use relevant skills because they lack the motivation to pursue personal
goals (Sayers, Curran, & Mueser, 1996), they expect to experience less pleasure from
interactions or other potentially enjoyable activities (Gard, Kring, Gard, Horan, &
Green, 2007), they inaccurately underestimate their likelihood of success in those
situations (Grant & Beck, 2009; Rector, Beck, & Stolar, 2005), or they perceive that
they possess limited energy resources which need to be conserved (Pratt, Mueser,
Smith, & Lu, 2005).
Another group of symptoms that can interfere with social functioning is psy-
chotic symptoms, such as hallucinations, delusions, and bizarre behavior. People with
persistent psychotic symptoms often experience difficulties in their interpersonal rela-
tionships because their lack of contact with reality interferes with the creation of a
common ground for establishing understanding between two people, an important
precondition for rewarding communication (or because a symptom, such as auditory
hallucinations, creates an internal distraction which makes communication difficult).
Psychotic symptoms can be stigmatizing when they frighten other people due to
themes such as paranoia, leading to social avoidance and potentially contributing to
the person’s social isolation.
Environmental factors. The environments in which people live and spend time can
have a profound influence on the likelihood that they will be able to use skills in their
behavioral repertoires. Similarly, such factors can also interfere with learning skills in
social skills training, or limiting the opportunity people have to use particular skills by
not providing sufficient reinforcement for those skills in appropriate situations. For
example, in some psychiatric hospitals, clients may be reinforced by staff members
for assuming the “sick role” (i.e., extremely passive behavior), and attempts to
break out of this mold by more goal-directive behavior may be actively discouraged
(Wing & Brown, 1970). For another example, when a depressed person lives with
a domineering partner, he or she may be actively discouraged from becoming more
assertive unless that partner is involved in, understands, and supports the individual’s
desire to become more assertive.
Cultural factors. Cultural norms influence both social skill and social confidence.
Cultures may vary in the established norms for behavior based on factors such as
gender, age, and relationships to others. Behaviors deemed “unassertive” in one
culture may be viewed as “normal” and desirable in another culture. Awareness of
the cultural norms of the group to which the individual belongs is critical in order
to understand cultural factors that may contribute to what appear to be problems in
social functioning, and adapting any interventions to address such problems (Samuels,
Schudrich, & Altschul, 2009).
Medication side effects. The side effects of medication can also interfere with social
functioning. One side effect of conventional antipsychotic medications is akinesia
(a reduction in facial expressiveness and use of gestures), which can make a person
appear less socially skilled. Some psychotropic medications can cause drowsiness,
making them less attentive to others’ communication, and less effective at conveying
their own thoughts, feelings, interests, and desires to others.
Logistics of Social Skills Training
When the primary focus of a program is on improving social skills, training is most
often provided in a group format. Provision of skills training in a group format
has several advantages over the individual format, including cost-effectiveness, more
opportunities for participants to observe other people using targeted skills, mutual
support among group members for learning and practicing skills, and a greater variety
of feedback for each participant’s skills. However, the provision of skills training in
an individual format is a viable alternative to group-based skills training, and has
the advantage of permitting more individualized training as well as training in the
person’s natural environment.
Social skills training is also often combined with other therapeutic techniques,
such as cognitive behavioral therapy (Wright, Basco, & Thase, 2005), motivational
interviewing (Miller & Rollnick, 2002), psychoeducation (Brown, 2011), family
interventions (Mueser & Glynn, 1999), or couples therapy (Jacobson & Christensen,
1998). Similarly, skills training is frequently incorporated into broad-based programs
for psychiatric and substance use disorders, as well as into health promotion and
prevention programs (e.g., healthy eating or sexual behavior, substance abuse pre-
vention), training programs for employees or professionals (e.g., customer relations,
communicating with patients), and relationship enhancement programs. Regardless
of the particular format in which social skills training is provided, the basic teaching
techniques are the same.
Social skills training groups usually include between four and eight people, and
preferably not more than 10, with sessions lasting between 45 and 90 minutes. This
group size permits enough time for all participants to practice and hone their skills
in role plays based on feedback from others, which is the sine qua non of the social
skills training approach. Skills training is most effective when several sessions can
be conducted per week (e.g., two sessions per week), although conducting weekly
sessions is a viable alternative.
Skills training groups usually have either one or two leaders. There are several
advantages to having two leaders. First, having two leaders can facilitate the modeling
of new skills to group participants because the leaders can demonstrate the skill in role
plays with each other, while also providing group members with a greater variety of
potential role models. Second, when groups are co-led, one leader can primarily attend
to presenting the skills training curriculum, orchestrating role plays and feedback, and
collaboratively developing home assignments with participants to practice the skills
on their own, leaving the second leader free to attend to group process issues and
ensuring that all participants are actively involved in the group. Third, with co-leaders
it is possible to split the group into two smaller groups within part of a session,
providing more opportunity for each participant to engage in role play practice and
receive feedback, and thereby hone his or her skills. However, skills training can be
also be conducted with a single leader, which is often more cost-effective.
Social skills training programs vary in their length, depending on the population
and the broadness of the targeted areas of social functioning. Skills training programs
can be a brief as just a few weeks, or extend over one or more years. Longer-term skills
training programs are often required when the focus is on improving social functioning
in individuals with substantial impairments, such as those with schizophrenia or other
serious mental illness, people with intellectual disabilities, or individuals with autism
or Asperger’s syndrome.
Skills training groups can be conducted using either an open- or closed-group
format. With a closed-group format, the same individuals begin and end the group
at the same time, and no new people can join the group once it has started. When
all the skills training curriculum has been taught, the group ends, and all participants
“graduate” together. With an open-group format, new participants can join the group
at any time, as long as they are committed to attending sessions on a regular basis.
The curriculum in an open group is taught on a continuous revolving basis, with the
teaching of the last curriculum topic in the sequence of topics followed by teaching
of the first topic. The group begins with some participants, and then others can join
the ongoing group, with each member remaining in the group until he or she has
received training in all the curriculum topics at least once.
Closed groups can facilitate the development of stronger group cohesion, but have
disadvantages because group members may move or get jobs or may leave the group
for other reasons. Closed-group formats may also require individuals to have to wait
longer periods of time before they can participate in a group. The open-group format
allows people to join the group without having to wait for a new group to start, and
facilitates the maintenance of a minimum group size by adding new participants to
replace members who have dropped out or left the group for other reasons. When
skills training groups are conducted in an open-group format, a leader of the group
usually meets individually with each person at least once or twice to understand his
or her personal goals, and to provide an orientation to the skills training approach.
Social skills training can be conducted at any location. When groups are conducted,
they are frequently held in a clinic, mental health center, school or business, or
community center. When social skills training is provided on an individual basis, the
training can be conducted in an even broader variety of locations, such as at the
individual’s home or locations in the community.
Skills training is usually conducted on the basis of a preplanned curriculum,
including specific skills broken down into component steps, a summary of the
rationale for learning each skill, and examples of common situations that can be used
to set up role plays of situations where the skill can be used. Curricula have been
established that cover a wide range of topic areas, depending on the specific needs of
the population, such as skills for having rewarding conversations and making friends,
assertiveness, resolving conflict, dealing with offers of or pressure to use alcohol or
drugs, parenting, intimacy and sexuality, interacting with doctors and other health
care providers, and work-related skills such as interacting with coworkers or customers.
Participants in skills training groups are sometimes given personal workbooks that
contain an outline of the skills taught and forms that can be completed to help each
individual personalize the skills training and keep track of opportunities or attempts
to use specific skills.
Social Skills Training Techniques
Group-based social skills training is conducted following a sequence of steps,

including:
1. establishing the rationale for the skill;

2. reviewing the steps of the skill;
3. modeling the skill in a role play and reviewing the role play with the group
members;
4. engaging a group member in a role play of the same situation, tailoring it to his
or her individual situation if possible;
5. providing (and eliciting) positive feedback for the role play;
6. providing (and eliciting) corrective feedback for the role play;
7. engaging the group member in another role play of the same situation;
8. providing (and eliciting) additional positive and corrective feedback;
9. engaging the other group members in role plays and providing feedback, as in
steps 4–8, and tailoring the role plays to each individual situation when possible;
and
10. developing home practice assignments that will be reviewed at the beginning of
the next session.
These steps are described briefly below, with an example provided in Box 12.3.
In order to teach a new skill, a rationale must first be established for the importance
of learning this skill. A combination of strategies can be used to develop the rationale,
including asking questions in the Socratic style (e.g., “Why might it be useful to
express a positive feeling to someone who has just done something for you?”), pro-
viding additional reasons for the importance of the skill, and exploring the relevance
of the skill to each participant’s personal goals and circumstances. The leader’s most
immediate goal is to harness participants’ motivation to learn the new skill.
After the importance of a skill has been established, the leader discusses the specific
components of the skill. For example, the skill of “expressing negative feelings” can be
broken down into the following five component behaviors: (a) looking at the person,
(b) speaking in a firm voice tone, (c) telling the person what he or she did to upset
you, (d) telling the person how it made you feel, and (e) suggesting how this can be
prevented from happening again in the future. The importance of each component
step is discussed (e.g., it is important to look at the person so that you can be sure
that you have their attention when you speak to him or her).
After discussing the different steps of the skill, the leader models the skill by
demonstrating it in a role play. To model the skill effectively, role plays are planned in
advance, are usually quite brief, and are based on situations that are both highly plau-
sible and likely to be encountered by the participants. Immediately after the role play,
the leader obtains feedback from the participants about what aspects of the skill were
performed well (including verbal content, nonverbal behaviors, paralinguistic features,
and interactive balance), and the overall effectiveness of the leader in the role play.
When group participants have had the opportunity to observe the leader model
the skill, one member is engaged in a role play of the same skill (generally initially
with the leader, rather than with another group member), usually based on the same
situation. The advantage of using the same role play situation at this point in the
training is that it minimizes the amount of effort the participant must make in order
to achieve a successful performance. Immediately following the role play, the leader
provides positive feedback about which specific steps of the skill were performed
well, and elicits additional positive feedback from other group participants. A critical
feature of social skills training is that a participant always receives immediate, positive,
and specific feedback following each role play. This feedback serves to encourage the
person’s efforts to perform the skill, as well as to reinforce specific behaviors that have
been done especially well.
After the positive feedback has been provided, the leader provides the participant
with corrective feedback, conveyed in a helpful, upbeat manner. Corrective feedback
can be provided directly by the leader, as well as elicited from other group participants.
Box 12.3 Example of the steps of social skills training in groups

on teaching the skill of “making a positive request”
Step 1. Establish the rationale for the skill.
The leader told the group that today’s session would be focusing on a new
skill, “Making a Positive Request,” and provided a brief introduction, saying,
“In everyone’s life, situations come up where we need to ask another person to
do something or even to change their behavior. A request is different from a
demand or from nagging, neither of which usually makes the other person want
to do what we are asking.”
She then asked the group, “How do you think making a request in a positive
way could be helpful to you in your life? What are some examples of recent
situations where you needed to ask people for things? How did it go?” The
group members gave examples of situations where they needed to make requests,
such as asking someone to help them with cooking, asking a friend to go out
to lunch, and requesting to use the family computer to look up directions
online.
Step 2. Review the steps of the skill.
Using a whiteboard, the leader wrote the steps of the skill:
Making a positive request:
1. Look at the person.

2. Say exactly what you would like the person to do. Use phrases like: “I would
appreciate it if you would _________” or “I would like you to ______” or “It
is important to me that you help me with_______.”
3. Tell the person how it would make you feel if they did what you are asking.
The leader then asked each group member to read a step of the skill aloud,
each time asking the whole group why that step was important. For example,
for Step 1, she asked, “Why is it important to look at the person when you are
making a request? How would this make your request more effective?” When
group members left out an important rationale for a step, she supplied it, by
saying something like, “For Step 2, one other reason for being specific in your
request is that it helps the other person know if they can do what you are
asking.”
Step 3. Model the skill in a role play and review the role play with the
group members.
The leader told the group, “I would like to show you an example of how I
might use this skill. I would like you to watch me to see if I follow the steps.
I am going to use the example of asking a friend to go out to lunch. I will do
a role play of this, and I am going to ask my co-leader to play the part of my
friend Katie.”
The leader then briefly modeled the three steps of the skill in a role play with
her co-leader. After the role play she asked the group participants for feedback
on her overall performance, and each step of the skill. For example, the leader
asked, “How did I do on Step 1? Was I looking at Katie?”
Step 4. Engage a group member in a role play of the same situation,

tailoring it to his or her individual situation if possible.
The leader said, “Now I would like to give each person a chance to practice the
skill. Jason, I would appreciate it if you would go first. The rest of the group will
watch and give you some feedback about how you used the steps. Remember
that we always start by giving each other positive feedback.”
She then set up a role play with Jason and her co-leader, Katie, saying, “To
make this as realistic as possible, I would like you to think of someone you
would like to ask out to lunch. How about your brother? Okay. Katie will play
the part of your brother. What is his name?” Then the leader asked for a few
more details, such as, “Where would you like to go for lunch? What day would
you like to suggest? The pizzeria in your neighborhood, on Saturday? Sounds
good. And just to think in advance, how would it make you feel if your brother
agreed to your idea of going out to lunch together?”
Step 5. Provide (and elicit) positive feedback for the role play.
The leader started by asking the participants a general question about Jason’s
role play: “What did you like about the way Jason practiced making a request?”
This was followed up by asking questions about Jason’s performance of each
step, such as, “What about Step 1? What did you like about the way Jason
looked at his brother when he asked him to go out for pizza together?” The
leader filled in gaps in feedback from the group, by saying, “Jason, I particularly
liked the way that you looked at your ‘brother’ the whole time. Your eye contact
was great.”
Step 6. Provide (and elicit) corrective feedback for the role play.
The leader asked the group members to come up with a few suggestions for
how Jason could improve his skills in another role play of the same situation,
rather than eliciting criticisms about his performance. She started with a general
question, “Was there anything that Jason could have done that would have made
his role play even better?” The leader also gave hints to the group participants
to consider some of the specific steps of the skill, such as asking, “Do you think
Jason was clear in expressing how he would feel if his brother accepted his
invitation?” The group agreed that the role play was good, but that it would be
even better if Jason had given a feeling statement, as suggested by Step 3.
Step 7. Engage the group member in another role play of the same
situation.
Keeping in mind the feedback from the group, the leader asked Jason to try
another role play of the same situation, and to include a feeling statement when
he asked his brother to join him for lunch. To help Jason identify an appropriate
feeling statement, she asked him how he would feel if his brother agreed to
go out to lunch together. Jason said, “It would make me feel good to have
something to look forward to on the weekend.” The leader encouraged Jason
to include that feeling statement in his next role play.
Step 8. Provide (and elicit) additional positive and corrective feedback.

When Jason had completed the role play, the leader elicited positive feedback
again from the group members about what Jason had done well, quickly going
through the steps that he had done well on the previous role play, and focusing
on the step that Jason was attempting to improve. She asked, “How was Jason’s
role play this time? For Step 3, did he include a feeling statement this time?
What was it? Did that make his request even more effective?”
Step 9. Engage the other group members in role plays and provide
feedback, as in steps 4–8. Tailor the role plays to each individual
situation when possible.
In role plays, Sarah practiced asking a friend to go for a walk in a local park, Toby
practiced asking his friend to play a video game, and Antonio practiced asking
his roommate to teach him how to cook one of his specialty dishes (omelets).
Some group members engaged in two role plays, while others benefited from
three role plays to improve their skill.
Step 10. Develop home practice assignments that will be reviewed at the
beginning of the next session.
The leader asked the group members to identify situations in which they
could use the skill of making positive requests outside the session. Some group
members said they would like to try the skill in the situations they had practiced
in their role plays (e.g., Jason planned to ask his brother to go out for pizza,
Antonio said he wanted to ask his roommate for a cooking lesson), whereas
others thought of different situations they were expecting to come up in the
following week. For example, Sarah said she wanted to practice asking her math
teacher for extra help on solving equations, in anticipation of a test coming
up soon. The group leader helped the members determine when and where
they would make their requests and encouraged them to either enter their own
assignment in their cell phone, or write it on a note card or sticky note before
leaving the session. The leader ended the session on a positive note, saying,
“You all did a great job on practicing making requests today, and I look forward
to hearing how it goes when you try it out in the coming week.”
Rather than providing negative feedback about skills that were performed poorly,
one or two suggestions are tactfully made to help the participant improve his or
her performance in another role play. In addition to giving suggestions for how to
improve the performance in the next role play, the leader can also demonstrate the
skill again, drawing attention to specific component behaviors that are targeted for
change.
After corrective feedback has been provided, one or two suggestions are made to the
participant to improve specific behaviors, and he or she then engages in another role
play. The same role play situation is used as in the first role play. This role play is then
followed by a similar sequence of specific, positive feedback, with the initial emphasis
on those skills targeted for change, followed by suggestions for improvement, and
potentially another one or two role plays, depending on the participant’s motivation
and improvement over the role plays. If verbal instructions and praise alone are
insufficient to produce significant behavior change in the role plays, the leader
may use a variety of other teaching techniques to facilitate improvement in social
performance, such as supplemental modeling by the leader, coaching (i.e., whispering
verbal prompts to the participants during the role play), or prompting (i.e., providing
the participant with nonverbal clues, such as hand signals, to modify his or her
behavior during a role play). The most critical issue when engaging a participant
in a series of role plays is that the person demonstrates some improvement in the
targeted skill from the first to the last behavioral rehearsal. This is the essence of
the shaping process, in which multiple role plays provide learning opportunities to
improve performance gradually over multiple trials.
After sufficient progress has been made over the role plays, and everyone has had
the opportunity to practice the skill, the leader collaboratively develops a homework
assignment with the participants to practice the skill on their own. The rationale
for practicing the skill outside of the session may need to be reviewed by the
participants (i.e., to use the skills in real-life situations and see how they work, and
what challenges are encountered). Home assignments to practice skills are most
effective when some specific situations to practice a skill can be identified by the
participants in advance. Possible obstacles to completing the assignment should be
anticipated.
The skills training sequence described above pertains to the introduction of a new
skill in a social skills training group. Usually one to three sessions are devoted to
teaching one skill before moving on to another. Following the introduction of a
new skill, the next session begins with a review of each group member’s assignment
to practice the skill on his or her own. Instead of having participants describe what
happened when they tried to use their skills, the leader engages each person in
setting up role plays of the situation in order to show what happened. Following
each role play, positive feedback and suggestions for change are provided by the
leader and participants, based on the methods previously described. Role plays can be
conducted based on either actual situations that occurred, or anticipated situations.
Practicing the skill across a variety of role play situations, as well as trying the skill
in real-life situations, facilitates the generalization of the skills to individuals’ daily
lives.
Maximizing Generalization of Social Skills
The primary aim of social skills training is to improve the social competence of
individuals by teaching or refining social skills. The training of skills in sessions
provides an opportunity to systematically harness the principles of social learning
theory, including modeling, behavioral rehearsal, positive and corrective feedback,
and shaping, to gradually improve the individual’s skills for interacting in specific
interpersonal situations. The assumption underlying skills training is that if individuals
can use their newly honed social skills in actual social situations they face in their daily
lives, these skills will be reinforced, which will strengthen them further, and increase
their ability to use them in a variety of similar situations.
Particular attention to ensuring that social skills are practiced in people’s actual
daily lives is critical when working with people who may have cognitive impairments.
Cognitive difficulties can interfere with the ability to remember to practice social
skills, or to identify appropriate situations in which to use social skills (Mueser,
Bellack, Douglas, & Wade, 1991; T. E. Smith, Hull, Romanelli, Fertuck, & Weiss,
1999). Examples of common disorders in which intellectual or cognitive abilities may
be compromised include schizophrenia, intellectual disability, autism, and traumatic
brain injury.
The most common approach to facilitating the generalization of social skills,
incorporated into all skills training groups, is to develop homework assignments
at the end of the session for the participants to practice the targeted skill. As
previously described, homework is routinely reviewed at the beginning of each
session, often using role plays, which can serve to identify real situations individuals
are facing in which they can use their skills, as well as to inform about the need
for additional training in the skill. People are most likely to follow through on
homework assignments when they are made collaboratively with the leader (rather
than unilaterally assigned by the leader); when specific times, places, and situations are
identified where the person can use the skill; when potential obstacles or challenges
are identified and briefly problem solved; and when a strategy is developed to
help the person remember to practice the skill. Although it is common for some
participants to forget to follow through on their home assignments, especially early in
a social skills training program, if concerted efforts are made by the leader to address
challenges to completing homework, most participants are capable of some degree of
follow-through.
In addition to assigning homework, in vivo community trips, either as a group or
individually, can facilitate the generalization of social skills to real world situations.
Trips to social settings where skills can be used provide people with valuable oppor-
tunities to practice their newly acquired social skills, and to hone them further with
the support of the trainer and others learning the skills (Glynn et al., 2002; Gottlieb,
Pryzgoda, Schuldberg, & Neal, 2005). Community trips are especially useful when
they involve common social situations, such as interacting with other people in stores,
restaurants, banks, or libraries, or using public transportation.
Another effective approach to improving the generalization of social skills is to use
the natural social supports people have in their daily lives to help them to use their skills
in appropriate situations. Indigenous supporters, such as family members, concerned

friends, or residential staff members, often have extensive contact with individuals
learning new social skills, and are in an ideal position to facilitate the use of skills in
naturally occurring social situations (Tauber, Wallace, & Lecomte, 2000). In order
to capitalize on naturally supportive people, it is important to have regular meetings
between the social skills trainers and supportive people in order to review with them
the skills that are being taught, and to obtain feedback about the individual’s use
of skills in naturally occurring situations (Bellack, Mueser, Gingerich, & Agresta,
2004).
Problem-Solving Training
The teaching of problem-solving skills involves a similar sequence of learning activities

to those described for social skills training. The steps of problem-solving training are
designed to encourage participants to consider as many solutions as possible to a
given problem or goal, and, based on evaluation of the possible solutions, to select
those which are most likely to be successful.
While social skills training focuses on teaching specific component behaviors
necessary for effective interactions, problem-solving training aims to teach a process
that optimizes the chances of solving a problem or achieving a goal (Popper, 1959).
The process of problem solving has been likened to the scientific method, in which the
essential task is to educate the person about how to think and approach psychological
or social problems in a more systematic, rational, and empirically based manner (Beck,
1963; Ellis, 1962). Thus, while social skills training tends to be content-oriented,
training in problem solving is aimed at teaching a set of processing skills designed to
facilitate goal attainment.
Problem-solving training is conducted by teaching a core set of steps, including:
1. defining the problem as specifically and simply as possible;

2. generating several possible solutions to the problem, without evaluating them
yet;
3. evaluating the solutions by identifying pros (advantages) and cons (disadvantages)
of each one;
4. choosing the best solution or combination of solutions, and considering what
solution has the best chance of succeeding (in a group or family format, this step
is done by the person who identified the problem, with input from others);
5. planning the steps for carrying out the solution; thinking about when and where
the solution will be implemented, and who/what will be involved (in a group
or family format, this step is primarily done by the person who identified the
problem, with help from others); and
6. setting a date to follow up the plan, and do additional problem solving if needed.
The basic steps of problem-solving training are briefly described here. As with the
techniques of social skills training described above, we focus on teaching problem-
solving skills in a group format.
Prior to initiating problem-solving training, the leader endeavors to develop in the

individual a problem-solving orientation in which problems are viewed as obstacles
which can be overcome or improved upon by systematically exploring and trying dif-
ferent possible solutions. Similarly, achieving short- and long-term goals is construed
as requiring the individuals to overcome a series of obstacles which are ordered in
logical sequence. The development of a problem-solving orientation can be facilitated
by providing examples of problems and their solutions, and reviewing the steps
of problem solving. However, in the long run, people learn to adopt a problem-
solving orientation through repeated prompting, practicing the steps of problem
solving on personally relevant problems, and experiencing the natural consequences
of implementing effective solutions to the problems.
Problem solving begins with identifying a problem that the person would like to
solve or a goal that the person wishes to achieve. Because the definition of a problem is
crucial to the solutions that will be generated and increases the possibility of successful
outcomes, the problem should be discussed in detail, and questions should be posed
such as, “Why is it a problem?,” “For whom is it a problem?,” and “Have you ever
tried to solve this problem in the past and what happened?” If the problem solving
is conducted with others who may be invested in the problem and its solution (such
as with families or couples), then multiple perspectives on the problem are sought
to ensure everyone’s involvement in the process, and, if the problem is shared by
more than one person, a mutually agreeable definition is reached so that each person
“owns” the problem.
When the nature of the problem or goal has been considered, the person must
arrive at a specific definition of it. In general, the more behaviorally specific the
definition, and the more circumscribed the problem, the greater the chance of solving
the problem. Large, complex problems and ambitious goals are best approached by
breaking them down into smaller, more manageable chunks, each of which is the
focus of problem solving. For couple- and family-based problem solving, all adults
present must agree on the definition of the problem in order for it to be solved
together.
When a problem or goal has been articulated, multiple solutions are then identified
for solving the problem or achieving the goal. People are urged to be as creative
as possible at this point of problem solving, and to avoid editing, censoring, or
evaluating any solutions that come to mind. Instead, all solutions are acknowledged,
with the expectation that suggesting even bad or inappropriate solutions may lead to
the identification of novel and innovative strategies. People who tend to be overly self-
critical and punitive may require extra practice at not immediately rejecting solutions
as soon as they are generated.
After a variety of possible solutions have been identified, each one is evaluated
in terms of its perceived effectiveness at solving the problem. This evaluation can
be standardized by routinely assessing the advantages and disadvantages of each
solution. Following the evaluation of solutions, the best solution or a combination
of solutions is selected. Often the best solution is quite evident after the advantages
and disadvantages of each solution have been considered. However, sometimes no
single solution is obviously best, or there is disagreement as to the best solution. In
such cases, the best solution is determined by combining different solutions, selecting
more than one solution to implement, or creating a new solution born from the
previously discussed ones.
Solutions to problems can only be effective if they are implemented. Furthermore, a
variety of obstacles can interfere with implementing the solutions. Therefore, planning
how to implement a solution is critical to successful resolution. Several factors are
important to consider when determining a plan for solving a problem. First, if more
than one person is involved in solving the problem, roles for implementing the
solution need to be agreed upon. Second, the resources needed to implement the
solution must be evaluated, such as money, expertise, information, or skills. Role
plays may be useful at this stage to help the individual practice the requisite skills
for implementing a solution. Third, possible obstacles to implementation should be
explored, and, if realistic ones are identified, tentative plans for dealing with them
should be determined. Finally, a time frame should be established for putting the
different steps of the solution into action. This time frame should include setting a
follow-up time when the success (or lack thereof) of the problem-solving plan can be
reviewed.
Although some problems are solved after a single attempt, many others are not,
and it is important for repeated efforts at problem solving to be conducted in order to
resolve the problem or achieve the goal. An important part of developing a problem-
solving orientation in individuals is conveying the idea that problem solving is often
an iterative process that requires multiple efforts in order to achieve success. Thus,
setting a follow-up time to review progress toward solving the problem maximizes
the chances that the problem will be solved, or at least substantial progress made,
over repeated efforts.
If the problem has been successfully resolved, then a new problem or goal can be
identified. On the other hand, if the problem remains, the leader teaches the participant
how to systematically identify where the problem-solving plan went wrong. This can
be accomplished by reviewing the steps of problem solving in the reverse order, until
the problematic step is identified, and a correction can be made, and a revised plan
then formulated. Thus, the first step in identifying where a problem-solving plan
went wrong is to determine if the solution was implemented as intended. If it was
not, then the implementation plan is modified in order to determine whether the
chosen solution will work. If the solution was implemented, but did not work and the
problem remains, then the next step is to evaluate whether other possible solutions
might be better, and then to use a different solution (or combination of solutions)
for solving the problem. This new solution (or combination of solutions) is then the
focus of a new implementation plan. As described before, the success of the plan is
followed up at a later time.
Training in problem solving is often taught using a record sheet to keep track of
the different steps of the skill. When the format of problem solving is with couples
or families, different people can take turns leading everyone together through the
problem-solving steps, with either the same or a different person keeping a record on
the worksheet. Over time and with practice, people can learn how to use the steps of
problem solving without maintaining a written record. Box 12.4 provides an example
of a record sheet for a problem-solving exercise, as applied to an individual working
on a problem.
Box 12.4 Example of steps of problem solving applied to an

individual’s problem
Step 1. Define the problem as specifically and simply as possible.
“I have not been able to find an apartment that I can afford on my present
income.”
Step 2. Generate several possible solutions to the problem. Do not
evaluate them yet.
1. Move in with roommates.

2. Look at apartments in neighborhoods that are less expensive.
3. Expand the search to include online listings.
4. Ask family and friends if they know of any apartments.
5. Get a job to increase my income.
Step 3. Evaluate the solutions by identifying pros (advantages) and cons

(disadvantages) of each one.
Pros Cons
1. Sharing an apartment is 1. I do not like living with room-
cheaper. mates.
2. Apartments are usually less 2. I need to be close to bus lines.
expensive when they are not in 3. There might be false listings.
the center of town. 4. They might not have contacts
3. Online listings are getting who rent.
popular. 5. Jobs are hard to find.
4. Friends and family might know
of apartments that are not
listed.
5. Income from a job would give
me more money for rent.
Step 4. Choose the best solution or combination of solutions. What

solution has the best chance of succeeding?
Expand my search for studio and one-bedroom apartments and start looking
for a part-time job.
Step 5. Plan the steps for carrying out the solution. Think about when
and where the solution will be implemented, and who/what will be
involved.
1. Get recommendations from friends about reputable apartment web sites.
Look for listings (start on Wednesday).
2. Call the restaurant where I used to be a waiter to see if they have any
openings (Thursday).
3. Look for “help wanted” signs in windows of restaurants in my neighborhood
(start on Friday).
4. Ask family about apartments, and about any part-time jobs they know about
(at family dinner on Saturday).
Step 6. Set a date to follow up the plan.

When following up, give yourself credit for what you have done so far. Decide
if your problem has been solved or whether you need to revise the plan or try
another one.
1. I will follow up in two weeks with the people who helped me come up with
my plan (group or family).
2. If I have a strong lead for an apartment and a job, we will figure out the
next steps to take.
3. If I do not have a strong lead for an apartment and a job, we will evaluate
the plan (what went well, what needs to be improved?).
Applications of Social Skills and Problem-Solving Training
Social skills and problem-solving training have been used to improve social func-
tioning and overall psychosocial adjustment in a wide range of both child and
adult clinical populations. One prominent application of skills training has been
in the treatment of individuals with developmental disorders. Skills training pro-
grams for these disorders have been developed that either directly focus on teaching
social skills to individuals, or teach parents how to foster more effective skills
in their children. For example, skills training programs have been developed for
children, adolescents, and adults with autism or Asperger’s syndrome (Baker,
2003; Laugeson, Frankel, Mogil, & Dillon, 2009; Myles et al., 2004; Reichow
& Volkmar, 2010; White, 2011), and intellectual or other developmental disabilities
(Coren, Hutchfield, Thomae, & Gustafsson, 2011; Drysdale, Casey, & Porter-
Armstrong, 2008; Matson, Mahan, & LoVullo, 2009; Valenti-Hein & Mueser,
1990).
Social skills and problem-solving training programs have been developed for a
wide range of psychiatric disorders in children, adolescents, and adults. For children
and adolescents, skills training programs have targeted disorders such as attention-
deficit/hyperactivity disorder (Rapoport, 2009), anxiety disorders (Matson, Sevin, &
Box, 1995), and conduct disorder (Webster-Stratton, Reid, & Hammond, 2001).
For adults, skills training interventions have been developed for common psy-
chiatric disorders such as schizophrenia (Bellack et al., 2004; Liberman, et al.,
1989), depression and suicidal behavior (Becker, 1987; Nezu, Nezu, & Perri,
1989; Salkovskis, Atha, & Storer, 1990), borderline personality disorder (Line-
han, 1993), social phobia (Heimberg & Becker, 2002), and substance abuse and
dependence (Monti, Abrams, Kadden, & Cooney, 2002). Skills training programs
have also been developed that target specific problems in clinical populations,
such as programs for people with serious mental illness focusing on improving
social and community functioning in older individuals (Pratt, Bartels, Mueser, &
Forester, 2008), vocational functioning (Tsang, Chan, & Wong, 2009; Wallace,
Tauber, & Wilde, 1999), and co-occurring substance abuse (Bellack, Bennett, &
Gearon, 2007; Mueser, Noordsy, Drake, & Fox, 2003; Roberts, Shaner, & Eckman,
1999). Similarly, skills training programs have been developed that address anger
and aggression problems in adolescents (Goldstein & McGinnis, 1997), offenders
(Deffenbacher, 1988; Novaco, 1997), people with developmental disabilities (Tay-
lor & Novaco, 2005), and people with a history of domestic violence (Maiuro,
1991).
In addition to the use of social skills and problem-solving training programs with
clinical populations, numerous programs have been developed to prevent or address
specific problems and improve social relationships. Skills training programs have been
developed for children and adolescents for the prevention of substance use and mental
health problems and to promote healthy interpersonal and lifestyle choices (e.g.,
assertiveness skills to resist sexual coercion) (Durlak, Weissberg, & Pachan, 2010;
Kimber, Sandell, & Bremberg, 2008). Similarly, skills-based prevention programs
have successfully targeted the prevention of health problems in adults, such as the
transmission or contraction of sexually transmitted diseases (Carey et al., 2004; Kelly
et al., 1994). Social skills and problem-solving training is a core component of many
programs aimed at addressing marital distress or improving relationship satisfaction
(Baucom & Epstein, 1990; Christensen & Jacobson, 2000; Gottman, 1999; Jacobson
& Christensen, 1998). Furthermore, multiple self-help books have been written,
based on the principles of social skills and problem-solving training, aimed at helping
people improve their social effectiveness, such as the ability to understand other
people in social situations (Flaxington, 2010; Pease & Pease, 2006), having rewarding
conversations (Barnes, 2012; Fine, 2005; Gabor, 2001; Garner, 1997; Poole, 2003),
standing up for oneself (Alberti & Emmons, 2008; Jakubowski & Lange, 1978),
developing close relationships (Heighway & Webster, 2008; Wygant, 2012), and
improving the quality of close relationships (Gottman, Notarius, Gonso, & Markman,
1986).
Finally, social skills and problem-solving training have been used in schools, busi-
nesses, and hospitals to teach interpersonal behaviors critical to effective performance.
For example, in the medical profession skills training programs have been developed
to teach effective communication skills in medical students (Clever et al., 2011),
pharmacy students (Mesquita et al., 2010), and oncology specialists (Barth & Lan-
nen, 2011). Similarly, skills training is often employed in training for a wide range
of other professions, especially those that require strong customer relations and
frequent interactions with the general public (e.g., staff in restaurants, hotels, and
stores).
Summary and Conclusions
Over the past several decades, social skills and problem-solving training have become
some of the most widely practiced interventions for the treatments of psychological
disorders in adults, as well as in the rehabilitation of people with developmental
disabilities. Furthermore, skills training has become incorporated into numerous
prevention programs, as well as in the training of employees. Therapies designed to
improve social and problem-solving skills are based on the assumption that people
are capable of learning more adaptive interpersonal and self-management skills, and
that these skills are most effectively taught in a systematic manner, employing the
principles of social learning theory. Training social and problem-solving skills can
be conducted in a variety of different formats, such as with individuals, groups,
couples, or families. Skills training approaches have enjoyed success across a broad
range of clinical problems, including social functioning in schizophrenia and other
serious mental illnesses, social anxiety, anger, marital distress, and substance abuse.
Expertise in teaching social and problem-solving skills is an important tool for clinical
psychologists, social workers, counselors, and other mental health professionals in
working with a broad range of clients.
References
Alberti, R. E., & Emmons, M. L. (2008). Your perfect right: Assertiveness and equality in your
life and relationships (9th ed.). Atascadero, CA: Impact.
Andreasen, N. C. (1982). Negative symptoms in schizophrenia. Archives of General Psychiatry,
39, 784–788.
Antonello, S. J. (1995). Social skills development: Practical strategies for adolescents and adults
with developmental disabilities. Boston, MA: Allyn & Bacon.
Baker, J. (2003). Social skills training for children and adolescents with Asperger syndrome and
social-communications problems. Shawnee Mission, KS: Autism Asperger Publishing Co.
Bandura, A. (1969). Principles of behavior modification. New York, NY: Holt, Rinehart and
Winston.
Barnes, A. (2012). How to start conversations & confidently talk with anyone. Seattle, WA:
CreateSpace.
Barth, J., & Lannen, P. (2011). Efficacy of communication skills training courses in oncology:
A systematic review and meta-analysis. Annals of Oncology, 22, 1030–1040.
Baucom, D. H., & Epstein, N. (1990). Cognitive-behavioral marital therapy. New York, NY:
Brunner/Mazel.
Beck, A. T. (1963). Thinking and depression: Idiosyncratic content and cognitive distortions.
Becker, R. (1987). Social skills training for depression. New York, NY: Elsevier Science.
Bellack, A. S., Bennett, M. E., & Gearon, J. S. (2007). Behavioral treatment for substance
abuse in people with serious and persistent mental illness: A handbook for mental health
professionals. New York, NY: Taylor and Francis.
Bellack, A. S., Brown, C. H., & Thomas-Lohrman, S. (2006). Psychometric characteristics of

role play assessments of social skill in schizophrenia. Behavior Therapy, 37 , 339–352.
Bellack, A. S., & Hersen, M. (1979). Research and practice in social skills training. New York,
NY: Plenum.
Bellack, A. S., Hersen, M., & Lamparski, D. (1979). Role play tests for assessing social skills: Are
they valid? Are they useful? Journal of Consulting and Clinical Psychology, 47 , 335–342.
Bellack, A. S., Morrison, R. L., Mueser, K. T., Wade, J. H., & Sayers, S. L. (1990). Role
play for assessing the social competence of psychiatric patients. Psychological Assessment,
2, 248–255.
Bellack, A. S., Mueser, K. T., Gingerich, S., & Agresta, J. (2004). Social skills training for
schizophrenia: A step-by-step guide (2nd ed.). New York, NY: Guilford Press.
Brown, N. W. (2011). Psychoeducational groups: Process and practice (3rd ed.). New York, NY:
Routledge.
Carey, M. P., Carey, K. B., Maisto, S. A., Gordon, C. M., Schroder, K. E. E., & Vanable,
P. A. (2004). Reducing HIV-risk behavior among adults receiving outpatient psychiatric
treatment: Results from a randomized controlled trial. Journal of Consulting and Clinical
Christensen, A., & Jacobson, N. S. (2000). Reconcilable differences. New York, NY: Guilford
Press.
Clever, S. L., Dudas, R. A., Solomon, B. S., Yeh, H. C., Levine, D., Bertram, A., … Cofrancesco,
J. J. (2011). Medical student and faculty perceptions of volunteer outpatients versus
simulated patients in communication skills training. Academic Medicine, 86, 1437–1442.
Coren, E., Hutchfield, J., Thomae, M., & Gustafsson, C. (2011). Parent training support for
intellectually disabled parents. Cochrane Database of Systematic Reviews, 6.
D’Zurilla, T. J., & Goldfried, M. R. (1971). Problem solving and behavior modification.
Deffenbacher, J. L. (1988). Cognitive-relaxation and social skills treatments of anger: A year
later. Journal of Counseling Psychology, 35, 414–418.
Drysdale, J., Casey, J., & Porter-Armstrong, A. (2008). Effectiveness of training on the commu-
nity skills of children with intellectual disabilities. Scandinavian Journal of Occupational
Therapy, 15, 247–255.
Durlak, J. A., Weissberg, R. P., & Pachan, M. (2010). A meta-analysis of after-school programs
that seek to promote personal and social skills in children and adolescents. American
Journal of Community Psychology, 45, 294–309.
Ellis, A. (1962). Reason and emotion in psychotherapy. New York, NY: Lyle Stuart.
Fine, D. (2005). The fine art of small talk: How to start a conversation, keep it going, build
networking skills—and leave a positive impression! New York, NY: Hyperion.
Flaxington, B. D. (2010). Understanding other people: The five secrets to human behavior
(2nd ed.). Henderson, NV: Motivational Press.
Gabor, D. (2001). How to start a conversation and make friends. New York, NY: Fireside.
Gard, D. E., Kring, A. M., Gard, M. G., Horan, W. P., & Green, M. F. (2007). Anhe-
donia in schizophrenia: Distinctions between anticipatory and consummatory pleasure.
Schizophrenia Research, 93, 253–260.
Garner, A. (1997). Conversationally speaking: Tested new ways to increase your personal and
social effectiveness. Los Angeles, CA: Lowell House.
Glynn, S. M., Marder, S. R., Liberman, R. P., Blair, K., Wirshing, W. C., Wirshing, D.
A., … Mintz, J. (2002). Supplementing clinic-based skills training with manual-based
community support sessions: Effects on social adjustment of patients with schizophrenia.
Goldstein, A. P., & McGinnis, E. (1997). Skillstreaming the adolescent: New strategies and
perspectives for teaching prosocial skills (2nd ed.). Champaign, IL: Research Press.
Goodwin, F. K., & Jamison, K. R. (2007). Manic depressive illness (2nd ed.). New York, NY:
Gottlieb, J. D., Pryzgoda, J., Schuldberg, D., & Neal, A. C. (2005). Generalization of skills
through the addition of individualized coaching: Development and evaluation of a social
skills training program in a rural setting. Cognitive and Behavioral Practice, 12, 324–338.
Gottman, J. M. (1999). The marriage clinic: A scientifically based marital therapy. New York,
NY: Norton.
Gottman, J. M., Notarius, C., Gonso, J., & Markman, H. (1986). A couple’s guide to
communication. Champaign, IL: Research Press.
Grant, P. M., & Beck, A. T. (2009). Defeatist beliefs as a mediator of cognitive impair-
ment, negative symptoms, and functioning in schizophrenia. Schizophrenia Bulletin, 35,
798–806.
Heighway, S. M., & Webster, S. K. (2008). S.T.A.R.S.: A social skills training guide for teaching
assertiveness, relationship skills, and sexual awareness. Arlington, TX: Future Horizons.
Heimberg, R. G., & Becker, R. E. (2002). Cognitive-behavioral group therapy for social phobia.
Hersen, M., & Bellack, A. S. (1976). A multiple-baseline analysis of social-skills training in
chronic schizophrenics. Journal of Applied Behavior Analysis, 9, 239–245.
Jacobson, N. S., & Christensen, A. (1998). Acceptance and change in couple therapy: A
therapist’s guide to transforming relationships. New York, NY: W. W. Norton.
Jacobson, N. S., & Margolin, G. (1979). Marital therapy: Strategies based on social learning
and behavior exchange principles. New York, NY: Brunner/Mazel.
Jakubowski, P., & Lange, A. J. (1978). The assertive option: Your rights and responsibilities.
Champaign, IL: Research Press.
Kelly, J. A., Murphy, D. A., Washington, C., Wilson, T., Koob, J., Davis, D., … Davantes,
B. (1994). The effects of HIV/AIDS intervention groups for high risk women in urban
clinics. American Journal of Public Health, 84, 1918–1922.
Kimber, B., Sandell, R., & Bremberg, S. (2008). Social and emotional training in Swedish
schools for the promotion of mental health: An effectiveness study of 5 years of interven-
tion. Health Education Research, 23, 931–940.
Laugeson, E. A., Frankel, F., Mogil, C., & Dillon, A. R. (2009). Parent-assisted social skills
training to improve friendships in teens with autism spectrum disorders. Journal of Autism
and Developmental Disorders, 39, 596–606.
Lazarus, A. A. (1966). Behavior rehearsal vs. nondirective therapy vs. advice in effecting
behavior change. Behaviour Research and Therapy, 4, 209–212.
Liberman, R. P. (2007). Dissemination and adoption of social skills training: Social validation
of an evidence-based treatment for the mentally disabled. Journal of Mental Health, 16,
595–623.
Liberman, R. P., DeRisi, W. J., & Mueser, K. T. (1989). Social skills training for psychiatric
patients. Needham Heights, MA: Allyn & Bacon.
Linehan, M. M. (1993). Skills training manual for treating borderline personality disorder. New
Maiuro, R. (1991). The evolution and treatment of anger and hostility in domestically violent
men. Revista Intercontinental de Psicologia y Educacion, 4, 165–189.
Matson, J. L. (2010). Social behavior and skills in children. New York, NY: Springer.
Matson, J. L., Mahan, S., & LoVullo, S. V. (2009). Parent training: A review of methods
for children with developmental disabilities. Research on Developmental Disabilities, 30,
961–968.
Matson, J. L., Sevin, J. A., & Box, M. L. (1995). Social skills in children. In W. O’Donohue
& L. Krasner (Eds.), Handbook of psychological skills training: Clinical techniques and
applications (pp. 36–53). Boston, MA: Allyn & Bacon.
McFall, R. M. (1982). A review and reformulation of the concept of social skills. Behavioral
Assessment, 4, 1–33.
Mesquita, A. R., Lyra, D. P. J., Brito, G. C., Balisa-Rocha, B. J., Aguiar, P. M., & de Almeida
Neto, A. C. (2010). Developing communication skills in pharmacy: A systematic review of
the use of simulated patient methods. Patient Education and Counseling, 78, 143–148.
Miller, W. R., & Rollnick, S. (2002). Motivational interviewing: Preparing people for change
(2nd ed.). New York, NY: Guilford Press.
Monti, P. M., Abrams, D. B., Kadden, R. M., & Cooney, N. L. (2002). Treating alcohol
dependence (2nd ed.). New York, NY: Guilford Press.
Mueser, K. T., Bellack, A. S., Douglas, M. S., & Wade, J. H. (1991). Prediction of social
skill acquisition in schizophrenic and major affective disorder patients from memory and
symptomatology. Psychiatry Research, 37 , 281–296.
Mueser, K. T., & Glynn, S. M. (1999). Behavioral family therapy for psychiatric disorders
(2nd ed.). Oakland, CA: New Harbinger.
Mueser, K. T., Noordsy, D. L., Drake, R. E., & Fox, L. (2003). Integrated treatment for dual
disorders: A guide to effective practice. New York, NY: Guilford Press.
Myles, B. S., Trautman, M. L., & Schelvan, R. L. (2004). The hidden curriculum: Practical
solutions for understanding unstated rules in social situations. Shawnee Mission, KS: Autism
Asperger Publishing Co.
Nezu, A. M., Nezu, C. M., & Perri, M. G. (1989). Problem-solving therapy for depression:
Therapy, research, and clinical guidelines. New York, NY: John Wiley & Sons, Inc.
Novaco, R. W. (1997). Remediating anger and aggression with violent offenders. Legal and
Criminology Psychology, 2, 77–88.
Pease, A., & Pease, B. (2006). The definitive book of body language: The hidden meaning behind
people’s gestures and expressions. New York, NY: Bantam.
Penn, D. L., Corrigan, P. W., Bentall, R. P., Racenstein, J. M., & Newman, L. (1997). Social
cognition in schizophrenia. Psychological Bulletin, 121, 114–132.
Poole, G. (2003). The complete book of questions: 1001 conversation starters for any occasion.
Grand Rapids, MI: Zondervan.
Popper, K. R. (1959). The logic of scientific discovery. New York, NY: Harper & Row.
Pratt, S. I., Bartels, S. J., Mueser, K. T., & Forester, B. (2008). Helping Older People
Experience Success (HOPES): An integrated model of psychosocial rehabilitation and
health care management for older adults with serious mental illness. American Journal of
Psychiatric Rehabilitation, 11, 41–60.
Pratt, S. I., Mueser, K. T., Smith, T. E., & Lu, W. (2005). Self-efficacy and psychoso-
cial functioning in schizophrenia: A mediational analysis. Schizophrenia Research, 78,
187–197.
Rapoport, E. M. (2009). ADHD and social skills: A step-by-step guide for teachers and parents.
Lanham, MD: Rowman & Littlefield Education.
Rector, N. A., Beck, A. T., & Stolar, N. (2005). The negative symptoms of schizophrenia: A
cognitive perspective. Canadian Journal of Psychiatry, 50, 247–257.
Reichow, B., & Volkmar, F. R. (2010). Social skills interventions for individuals with autism:
Evaluation for evidence-based practices within a best evidence synthesis framework.
Journal of Autism and Developmental Disorders, 40, 149–166.
Roberts, L. J., Shaner, A., & Eckman, T. A. (1999). Overcoming addictions: Skills training for
people with schizophrenia. New York, NY: Norton.
Salkovskis, P. M., Atha, C., & Storer, D. (1990). Cognitive-behavioural problem solving in the
treatment of patients who repeatedly attempt suicide. British Journal of Psychiatry, 157 ,
871–876.
Salter, A. (1949). Conditioned reflex therapy. New York, NY: Farrar, Strauss.
Samuels, J., Schudrich, W., & Altschul, D. (2009). Toolkit for modifying evidence-based practice
to increase cultural competence. Orangeburg, NY: Research Foundation for Mental Health.
Sayers, S. L., Curran, P. J., & Mueser, K. T. (1996). Factor structure and construct validity of
the Scale for the Assessment of Negative Symptoms. Psychological Assessment, 8, 269–280.
Sicile-Kira, C., & Grandin, T. (2004). Autism spectrum disorders: The complete guide to
understanding autism, Asperger’s syndrome, pervasive developmental disorder, and other
ASDs. New York, NY: Berkeley Publishing Group.
Smith, M. J. (1985). When I say no, I feel guilty: How to cope—Using the skills of systematic
assertive therapy. New York, NY: Bantam.
Smith, T. E., Hull, J. W., Romanelli, S., Fertuck, E., & Weiss, K. A. (1999). Symptoms and
neurocognition as rate limiters in skills training for psychotic patients. American Journal
of Psychiatry, 156, 1817–1818.
Strack, F., & Förster, J. (2009). Social cognition: The basis of human interaction. New York,
NY: Taylor and Francis.
Tauber, R., Wallace, C. J., & Lecomte, T. (2000). Enlisting indigenous community supporters
in skills training programs for persons with severe mental illness. Psychiatric Services, 51,
1428–1432.
Taylor, J. L., & Novaco, R. W. (2005). Anger treatment for people with developmental
disabilities: A theory, evidence and manual based approach by John L. Taylor and Raymond
W. Novaco. Chichester, England: John Wiley & Sons, Ltd.
Trower, P., Bryant, B., & Argyle, M. (1978). Social skills and mental health. London, England:
Methuen.
Tsang, H. W., Chan, A., & Wong, A. P. (2009). Vocational outcomes of an integrated
supported employment program for individuals with persistent and severe mental illness.
Journal of Behavior Therapy and Experimental Psychiatry, 40, 292–305.
Valenti-Hein, D., & Mueser, K. T. (1990). The dating skills program: Teaching social-sexual
skills to adults with mental retardation. Orland Park, IL: International Diagnostic Systems.
Wallace, C. J., Nelson, C. J., Liberman, R. P., Aitchison, R. A., Lukoff, D., Elder, J. P.,
& Ferris, C. (1980). A review and critique of social skills training with schizophrenic
patients. Schizophrenia Bulletin, 6, 42–63.
Wallace, C. J., Tauber, R., & Wilde, J. (1999). Teaching fundamental workplace skills to
persons with serious mental illness. Psychiatric Services, 50, 1147–1153.
Webster-Stratton, C., Reid, J., & Hammond, M. (2001). Social skills and problem-solving
training for children with early-onset conduct problems: Who benefits? Journal of Child
Psychology and Psychiatry, 42, 943–952.
White, S. W. (2011). Social skills training for children with Asperger syndrome and high-
functioning autism. New York, NY: Guilford Press.
Wing, J. K., & Brown, G. W. (1970). Institutionalism and schizophrenia. Cambridge, England:
Cambridge University Press.
Press.
Wright, J. H., Basco, M. R., & Thase, M. E. (2005). Learning cognitive-behavior therapy: An
illustrated guide. Washington, DC: American Psychiatric Publishing.
Wygant, D. (2012). Naked! How to find the perfect partner by revealing your true self . Carlsbad,
CA: Hay House.
13
Neurofeedback
Sarah Wyckoff
University of Tübingen and International Max Planck Research School, Germany
Niels Birbaumer
University of Tübingen, Germany, and Ospedale San Camillo, Venice, Italy
What is neurofeedback? Neurofeedback or electroencephalographic (EEG) biofeed-

back belongs to a family of therapeutic techniques known as biofeedback. As the
name implies, biofeedback therapy involves providing an individual with “feedback”
of biological information such as heart rate, respiration rate, skin conductance, hand
temperature, muscle activity, and brain activity. Neurofeedback is the practice of pro-
viding sensory feedback in an operant conditioning paradigm to modify or enhance
the activity of the central nervous system including EEG, event-related potentials,
slow cortical potentials (SCPs), and blood oxygenation level-dependent (BOLD) sig-
nal of cortical or subcortical origin. The visualization of brain signals gives individuals
the opportunity to gain awareness of their physiology and the information needed
to learn self-regulation or volitional control of specific brain activity for the purpose
of symptom reduction or performance enhancement. Despite having a short history,
several neurofeedback approaches have been developed and investigated for the treat-
ment of psychiatric and general medical conditions in patient populations of all ages.
This chapter begins with a brief discussion of the origins of brain signal recordings
and classical and operant conditioning and discusses the evolution of neurofeedback
therapy. Following this review, current feedback methods and technical requirements
are addressed. The chapter concludes with a discussion of therapeutic applications,
treatment rationale, and a review of neurofeedback-related research findings.
Historical Origins of Electroencephalography

and Conditioning
Scientists have been actively investigating brain signals and activation patterns since
the nineteenth century. Using a sensitive galvanometer, Richard Caton (1875) first

DOI: 10.1002/9781118528563.wbcbt13
reported observing electrical brain currents in live animals. A half-century later,

Hans Berger (1929) conducted one of the first known human EEG recordings and
published his discovery of rhythmic alpha wave activity. These early experiments
paved the way for modern electrophysiology and psychophysiology research. Over
the last hundred years, technological improvements in the acquisition and analysis
of brainwave activity have led to the discovery of distinct EEG wave patterns that
are linked to specific behavioral states and task conditions. Currently, the acquisition
and analysis of EEG activity is used as a neurological diagnostic procedure, a
guide for medication selection, and an assessment tool in cognitive behavioral and
psychophysiological research.
Spontaneous EEG rhythms are commonly defined into frequency bands defined as
delta (0.5–4 Hz), theta (4–8 Hz), alpha (8–12 Hz), sensorimotor rhythm or SMR
(12–15 Hz), beta (13–30 Hz), and gamma (30–100 Hz). The term SCP refers to
slow wave activity measured below 1 Hz. These slow oscillations cycle over several
seconds and belong to the family of event-related potentials (ERPs). EEG activity is
classified as synchronized or desynchronized and reflects the summation of excitatory
and inhibitory postsynaptic potentials in the pyramidal cells of the cerebral cortex, with
additional contributions from granular and glial cell activity (for reviews, see Lopes da
Silva, 1991; Speckmann & Elger, 1999). Surface EEG recordings capture large field
potentials generated by the coordinated action of glial networks (Fellin et al., 2009)
and the synchronous extracellular current flow of neurons with a similar spatial orien-
tation radial to the scalp. During relaxed eyes-closed conditions, synchronized high-
amplitude oscillations of slow EEG frequencies can be observed, while desynchronized
lower-amplitude oscillations of faster frequencies dominate during visual attention and
eyes-open conditions (Steriade, Gloor, Llinás, Lopes da Silva, & Mesulam, 1990).
Visuals of the basic EEG frequency bands and the mental state most commonly
associated with the prevalence of each band range are provided in Figure 13.1.
The historical time course for the discovery and investigation of classical and
operant conditioning paradigms paralleled that of EEG. Preceding Hans Berger’s
(1929) initial investigations of human brain activity, Ivan Pavlov (1927) worked to
establish the process of classical conditioning. In a series of experiments designed to
measure the salivary output of dogs relative to food presentation, Pavlov noted several
stimulus–response interactions. He observed that an unconditioned response was not
learned and occurred naturally in response to an unconditioned stimulus (salivating
at the sight of food), while a conditioned response could be learned and elicited
by a conditioned stimulus that was previously neutral until paired repeatedly with an
unconditioned response (salivating upon hearing the footsteps of the person delivering
the food) (Pavlov, 1927). While the process of classical conditioning described how
an environmental stimulus could trigger a response, it failed to account for all changes
in behavior or address the emergence of new behaviors.
The theory of operant conditioning emerged through the work of Edward
Thorndike and B. F. Skinner and addressed trial and error learning through conse-
quences. Based on Thorndike’s law of effect, which held that behaviors followed by a
pleasurable or rewarding consequence had a tendency to be repeated, whereas behav-
iors followed by an aversive consequence had a tendency to decrease, Skinner (1953)
developed the process of shaping animal behavior and learning through reinforcement
Neurofeedback 275
Bandwidth Bandwidth General

Waveform (3 second epoch)
name range descriptions
Raw EEG 0 – 45 Awake
Excitation
SCP < 1 Hz
thresholds
Deep sleep,
Delta 0.5 – 4 Hz
repair, coma
Drowsy,
Theta 4 – 8 Hz
creative
Relaxed,
Alpha 8 – 12 Hz no visual
processing
Motor
SMR 12 – 15 Hz relation,
alert
Cognitive
Beta 13 – 30 Hz
processing
Problem
Gamma 30 – 45 + Hz
solving
Figure 13.1 Table of basic frequency bandwidths and associated states. Adapted from Sherlin
(2009, p. 87).
or punishment. In operant conditioning, a reinforcer is designed to increase and

strengthen the probability that a desired behavior will be repeated by providing a plea-
surable consequence (positive) or removing an unpleasant consequence (negative).
Conversely, a punishment is designed to decrease or weaken the probability of a spe-
cific behavior occurring by providing an aversive consequence (positive) or removing a
pleasurable consequence (negative). Currently, the principles of classical and operant
conditioning are used as tools in animal learning research, investigated as etiological
components of psychiatric disorders, and applied in cognitive behavioral treatment.
Evolution of Neurofeedback
It was not until the 1930s when researchers began to investigate the possibility
of conditioning brainwave activity that the fields of EEG and classical and operant
conditioning would converge (see Sherlin et al., 2011, for a review). From the
1930s to the 1960s, researchers focused on the classical and operant condition-
ing of the alpha blocking response with many different styles of reinforcement. In
the 1960s the operant conditioning of state dependent alpha frequency amplitudes
was reported by Kamiya (1971). Shortly thereafter, Barry Sterman and colleagues
at UCLA reported the successful reinforcement of increased 11–15 Hz rhythmic
activity over the somatosensory cortex in cats (for review, see Sterman, 2000). Fol-
lowing the EEG conditioning paradigm, these same cats were included as subjects
in a study investigating the convulsive properties of rocket propellant. Although
nonconditioned cats in the study suffered convulsions after exposure to an established
dose of the toxic compound, the cats trained to enhance somatosensory (SMR)
activity serendipitously appeared to benefit from increased seizure thresholds. These
findings stimulated research in several laboratories and the resulting body of research
indicated that the operant conditioning of SMR brainwaves had the capacity to reduce
neuronal excitability, lessen the impact of transient neuronal discharges, and stabilize
brain state characteristics, thus countering the abnormal brain activity observed in
epileptic populations. Motivated by the potential applications of this new condition-
ing method, researchers and clinicians began to investigate the therapeutic effects
of “neurofeedback” brain training for epilepsy and attention-deficit/hyperactivity
disorder (ADHD). Following roughly the same timeline, researchers at the University
of Tübingen in Germany began developing EEG operant conditioning paradigms
for the regulation of theta brainwaves (Lutzenberger, Birbaumer, & Steinmetz,
1976) and SCP activity. In a series of experiments, clinical and control participants
underwent brain entrainment to learn voluntary control of positive and negative
SCP shifts over central brain sites (Birbaumer, Roberts, Lutzenberger, Rockstroh,
& Elbert, 1992; Elbert, Rockstroh, Lutzenberger, & Birbaumer, 1980), as well
as differentiation over right- versus left-hemispheric sites (Birbaumer et al., 1988;
Rockstroh, Elbert, Birbaumer, & Lutzenberger, 1990). The discovery that SCPs and
other brainwave components could be classified, conditioned, and retrained led to
the investigation of restorative or therapeutic applications for symptom reduction,
as well as assistive applications for thought translations and enhanced communica-
tion through brain–computer interface (BCI; Kübler et al., 1999; Kübler et al.,
2001; Wolpaw, Birbaumer, McFarland, Pfurtscheller, & Vaughan, 2002). The latest
generation of neurofeedback methods has focused on regulation of brain activa-
tion using the hemodynamic response and cerebral blood flow. Changes in cerebral
hemoglobin concentrations have been observed in a variety of motor and cognitive
tasks leading to the investigation of this signal as a neurofeedback and BCI parameter.
For neurofeedback applications, individuals are provided with information related
to changes in cerebral blood flow, specifically concentrations of oxyhemoglobin and
deoxyhemoglobin of BOLD signal, using real-time functional magnetic resonance
imaging (rtfMRI), hemoencephalography (HEG), and near-infrared spectroscopy
(NIRS). The therapeutic applications and treatment findings of EEG, SCP, HEG,
NIRS, and rtfMRI-based neurofeedback methods will be discussed later in the
chapter.
Neurofeedback 277
Basics of Neurofeedback
Over the last 50 years, the development of neurofeedback techniques and ther-
apeutic applications has seen tremendous growth. No longer is the investigation
of brain signal conditioning restricted to scientific researchers and university lab-
oratories. Technological advancements and improvements to amplifier recording
capabilities, electrode quality, signal processing, and artifact control have enhanced
the quality of recordings and reduced the cost of EEG acquisition and entrain-
ment devices. This has allowed neurofeedback applications to be investigated in a
variety of settings such as laboratories, hospitals, school environments, treatment
facilities, detention centers, and private practices by trained researchers, medical
professionals, school psychologists, social workers, and therapists. The condition-
ing of specific EEG frequencies and ratios, ERP, SCP, and BOLD signals has
been investigated for the treatment of neurodevelopmental, anxiety, mood, sub-
stance, dissociative, and psychotic disorders, as well as for epilepsy, migraine, stroke,
traumatic brain injury, and other medical conditions. Regardless of the equip-
ment used, the clinicians’ background, the patient population served, the signal
acquired, or the training method used, there are some standard principles of neu-
rofeedback training. In its simplest form, a neurofeedback clinician supplies the
individual in training with a rationale for treatment, real-time information on spe-
cific brain signals, specific training goals, and instantaneous feedback about his
or her training performance to shape behavior. The following sections address
some frequently asked questions and some basic information about neurofeedback
training.
What Is the Rationale for Neurofeedback Training?

The basis for clinical and therapeutic applications of neurofeedback is the principle
that specific mental states, cognitive processes, and disorder-related symptoms have
specific neurological correlates that can be measured, visualized, and retrained through
operant conditioning, resulting in physiological and behavioral improvements.
What Brain Information Is Provided and How Is It Collected?

Depending on the feedback method, brain signals are continuously acquired and
displayed on a computer screen within a few thousandths of a second for EEG
recordings to several seconds for NIRS, HEG, and rtfMRI data. For EEG, NIRS,
and HEG based methods, electrodes or optodes are placed on the head to record
electrical or BOLD signal activity, respectively. For rtfMRI neurofeedback, changes
in BOLD signal are observed during an MRI scanner sequence that acquires several
3D pictures of the brain every few seconds. All signals are filtered or preprocessed in
order to provide meaningful data to the clinician and trainee, as well as to establish
training parameters and baselines.
What Are the Specific Training Goals and How Are They Defined?
The specific training goals of neurofeedback depend on the condition treated,
training method, behavioral and neurological correlates, and assessment practices.
For example, EEG neurofeedback training for the treatment of ADHD may focus
on reducing theta and enhancing SMR or beta frequency amplitudes over central
electrode sites, whereas SCP-based training may focus on increasing the differentiation
between positive and negative potentials over central sites. NIRS and HEG feedback
may focus on increasing concentrations of oxyhemoglobin (oxyHb) in the frontal
lobe, while quantitative EEG (QEEG) informed protocol selection might indicate
the need for amplitude, coherence, or asymmetry training of a specific bandwidth
at various locations. It is important to remember that there is no “one size fits all”
protocol or “magic bullet” training. Pretreatment assessments should be conducted,
if possible, to individualize and guide training, to reduce negative training events, and
to serve as a baseline for determining treatment effects.
How Does the Operant Conditioning and Feedback Process Work?

In a series of training sessions, individuals receive feedback of their own brain activity
and develop regulation skills to change specific neurophysiological components. Con-
trolling for muscle, ocular, cardiac, and respiratory related artifacts, changes in brain
activity that occur in a desired direction are reinforced by auditory or visual feedback.
Brain signals are converted into game-like tasks in which points can be earned for
increasing or decreasing activity above or below a specific threshold on a thermometer
bar or by moving an object across the training screen in a specific direction.
Based on the principles of learning and operant conditioning, Sherlin and col-
leagues (2011) asserted that special consideration should be given to the speed of
reinforcement, type of reinforcement, shaping methods, specificity of training, sec-
ondary reinforcement, and generalization of skills when developing a neurofeedback
paradigm. They reported that neurofeedback protocols should employ the shortest
time delay possible (within 250–350 ms for EEG, around 1.5–8 s for BOLD)
and include discrete feedback to allow for post-reinforcement synchronization. In
order to avoid the potential of training or rewarding activity in the wrong direction,
emphasis was placed on shaping behavior by adjusting training thresholds in an a
priori direction, rather than with automatic calculation and updating of thresholds.
Training feedback should be tailored to reinforce specific behaviors and waveform
characteristics, avoiding possible artifacts. Consideration may be given to the use of
secondary rewards to enhance learning such as monetary rewards, tokens, and prizes.
Finally, generalization of self-regulation skills in daily life through transfer trials, visual
cues, and practice in role play and in vivo situations was encouraged.
Feedback Methods and Technical Requirements
The following sections discuss the details of EEG, SCP, and BOLD signal neurofeed-
back methods. An overview of each method is provided with emphasis on technical
Neurofeedback 279
requirements, data acquisition, signal processing, feedback generation, and diagnostic

requirements.
Electroencephalographic Neurofeedback
As previously discussed, EEG activity is organized into classic frequency bands (delta,
theta, alpha, SMR, beta, etc.) based on the number of cycles per second, waveform
characteristics, spatial distribution, and associated states or neurophysiological pro-
cesses. Spectral decomposition of the EEG through the application of the Fourier
transform allows for the separation of these frequency bands and the calculation of
activity within each band range. This information may be linked to various feedback
instruments and training parameters, allowing individuals the opportunity to visualize
specific components of brain activity and develop self-regulation strategies through
operant conditioning procedures.
EEG feedback training may employ monopolar, bipolar, multiple-channel, or
whole-head montages. The montage simply determines the manner in which elec-
trode pairs are connected to the EEG amplifier and the reference procedure for the
data output. In preparation for the training session, head measurements are taken to
ensure proper electrode placement. The skin is prepped with a mild abrasive cleaning
gel to remove oils and dead skin, and small electrodes (typically, silver/silver chloride)
are applied to the scalp with conductive paste. During training sessions, the client is
seated in front of a computer screen while EEG activity is continuously recorded and
instantaneously presented in the form of visual and auditory feedback. Most neuro-
feedback applications utilize the cortical EEG activity of the outer layers of the brain
for entrainment parameters; while low resolution brain electromagnetic tomography
(LORETA)-based neurofeedback applications provide feedback of current source den-
sities at deeper cortical levels (Congedo, Lubar, & Joffe, 2004). Visual feedback may
include a graphic representation of frequency band waveforms, averaged frequency
amplitudes, multiple band ratios, percentages of time under a specific threshold,
muscle artifacts amplitude, and so on (see Figure 13.2). The information provided to
the client should be meaningful and tailored to his or her specific training goals.
The training sessions last about an hour, including electrode application and clean-
up. The active brain training protocols typically last 30 to 45 minutes. The sessions
may be organized into multiple training blocks of continuous or discrete feedback.
Individuals learn to change their EEG activity through shaping procedures and the
manipulation of training thresholds in an a priori direction. When all training tasks
are met for a defined period, or fall within a specific standard deviation range of a
references database population as in z-scored training protocols (Thatcher, 2008), a
discrete reward is issued in the form of an auditory tone, feedback color change, or
point increase. To promote the generalization of newly acquired skills, individuals
may be provided with visual training cues to help them “recreate” training states
in classroom and work settings. Additionally, they may receive feedback of their
brain activity during specific problematic tasks; for example, during silent reading
or homework completion. Neurofeedback training schedules may include daily and
biweekly sessions. Length of treatment depends on the severity of the condition and
individual learning curves.
226 secs.left
Theta Beta
10.0 10.0
Theta threshold Beta threshold
7.5 7.5 78% 61%
5.0 5.0 T/B ratio EMG
2.70 3.66
2.5 2.5
0.0 0.0
+ − F + − F
EEG training signal
+ − F
10.0
5.0
0.0
−5.0
−10.0
T t 16′06′′ 16′07′′ 16′08′′ 16′09′′ 16′10′′
Figure 13.2 Theta-beta neurofeedback training screen.
Protocol selection may be guided by established research-based protocols, QEEG

analysis, and/or normative database comparisons. QEEG analysis is defined as the
mathematical processing of frequency and amplitude components of EEG, which may
be transformed into a variety of numerical measures, providing precise, quantitative
descriptions of many indices of brain function with or without normative database
comparisons (Hammond et al., 2004). Typically, QEEG data are derived from a
19-channel EEG recording utilizing the standardized International 10–20 system of
electrode placement. The EEG is recorded during standardized conditions, such as
eyes-closed, eyes-opened, reading, math, hyperventilation, or other tasks. The EEG
signal is digitized, artifacted to remove muscle movements, eye rolls and blinks,
electrocardiogram (EKG), and other corrupting factors. Finally, the refined data may
be compared to a variety of EEG normative database software and subjected to
spectral analysis using the fast Fourier transform (FFT) algorithm.
Individual QEEG recordings may be compared to a “normal” group or to a defined
“clinical” population, and a variety of statistical computations, such as relative and
absolute power, power ratios, coherence, phase lag, and hemispheric asymmetries, may
be calculated. When analyzing individual files to determine group differences and char-
acteristics, relative power (measurement of the percentage or proportion of total power
within each frequency band) may be the most useful measure. Relative power maps
and z scores minimize fluctuations observed in amplitude and frequency characteris-
tics due to interindividual differences. QEEG analysis yields a variety of color-coded
topographic maps and numerical tables with raw and standardized z scores, which
aid trained clinicians in the diagnostic process, identification of “signature” patterns
of electrical activity of the cerebral cortex within a specified population, selection of
Neurofeedback 281
neurofeedback protocols, and assessment of treatment outcomes. Although several

normative databases have been peer reviewed, cross-validated, and FDA registered, it
is important to note that QEEG and normative databases comparisons alone do not
diagnose a patient’s clinical problem and require a trained professional to evaluate for
training recommendations (Thatcher & Lubar, 2009).
Slow Cortical Potential Neurofeedback

As stated previously, SCPs are slow waveforms (below 1 Hz) embedded in oscillatory
EEG and classified as ERPs. ERPs do not occur spontaneously and are time locked
to a specific event. Depending on the processes under investigation, ERP paradigms
utilize cognitive, behavioral, and motor events to elicit a specific brain response. These
electrophysiological responses may be expressed and visualized through the averaging
of multiple presentations of a stimulus. More importantly, individuals can learn
voluntary control of these responses to optimize cognitive and behavioral correlates
through feedback and reinforcement.
SCP neurofeedback focuses on the conditioning of negative and positive polar-
izations in EEG activity recorded with a 128 Hz sampling rate, skin resistance of
5–10 k, time constant of 8–10 seconds, and a low frequency cutoff of 0.01 Hz.
These shifts reflect the regulatory mechanisms of cortical activation and inhibition
and are hypothesized to play a critical role in the preparatory distribution of sensory,
motor, and attentional resources. Lasting from a few hundred milliseconds to several
seconds, negative SCP shifts increase the firing probabilities of a cell assembly, while
positive SCP shifts inhibit this activity (see Birbaumer, 1999, for a review). Typically,
SCP feedback training employs a monopolar electrode placement with data recorded
at Cz, referenced to A1, and grounded to A2 mastoids. However, some studies and
independent clinicians have reported the use of bipolar and nonmidline placements.
Due to the negative impact of eye artifacts on the SCP signal, online correction for
electro-oculographic (EOG) components (blinks, horizontal and vertical movements)
is essential. EOG correction requires the placement of vertical and horizontal eye
electrodes and a short calibration phase. The electrode site preparation for SCP
training mirrors that described for EEG feedback, with the addition of the EOG
electrodes.
During a training session, the client is seated in front of a computer screen and
cued by a graphic symbol to “activate” or “deactivate” their brain activity. Within a
few milliseconds of the directional cue, the individual receives visual feedback about
the movement of his or her SCP activity (see Figure 13.3). The training sessions last
about an hour and are organized into multiple training blocks consisting of 30–40
trials, each with a baseline, feedback, and reward phase. During the baseline phase,
2 seconds of EEG activity are recorded and defined as a “relative zero” point. During
the 8-second feedback phase, the signal change (μV) from the relative baseline is
displayed. Successful activation and deactivation is reinforced with a visual reward,
such as a bursting sun or a smiley face icon. The negative and positive training
cues have a 50/50 distribution but may be altered for a 2:1 ratio to support the
enhancement of a specific potential. It is important to note that SCP training is
designed to support cognitive flexibility through bidirectional training of positive
Figure 13.3 Example of slow cortical potential feedback screens for “activation” task (neg-
ative shift, upper left panel), “deactivation” task (positive shift, upper right panel), visual
“reward” for successful trial (lower left panel), and “transfer” activation task (lower right
panel). Reproduced with permission from NeuroConn GmbH, Germany.
and negative shifts. Practitioners should avoid 100% reinforcement of activity in one
direction alone. To promote the generalization of self-regulation skills in everyday life
situations, 25% of all trials are presented as “transfer trials” in which visual feedback
is suspended during the active training phase but the level of success is indicated with
a visual reward (see Strehl, 2009, for a review). In research settings, SCP treatment
schedules have included 25–30 sessions and have utilized daily and biweekly training
sessions.
In general, SCP utilizes a standardized bidirectional neurofeedback training pro-
tocol. Other than the technical requirements discussed, there are no specific QEEG
diagnostic requirements for the selection of the training site, frequency bands,
or training thresholds. However, neurofeedback providers should have a clear
rationale for the use of this brain training method. Accordingly, SCP feedback
is appropriate for binary classification for BCI applications and as a treatment
for disorders characterized by impaired excitation thresholds, such as ADHD,
epilepsy, and migraine. As with any therapeutic intervention, pretreatment mea-
surements for neurofeedback training should include diagnostic interviews, discussion
of medical and family history, disorder-specific symptom questionnaires, and neu-
ropsychological testing such as continuous performance tasks and EEG/ERP to
detect hypothesis-related deficits and to serve as a baseline comparison for treatment
efficacy.
Neurofeedback 283
Blood Oxygenation Level-Dependent Signal Neurofeedback

The latest additions to the family of neurofeedback methods rely on measuring
the hemodynamic response. HEG/NIRS and rtfMRI methods provide information
related to BOLD signal changes as a neurofeedback parameter. Although BOLD
response is an indirect measure of neural activity, the correlation between BOLD
signal and electrical brain activity has been documented. Specifically, increases in
neuronal activity correspond with increase in BOLD response (Logothetis, 2002),
whereas negative BOLD response is coupled with decreased BOLD signal (Shmuel,
Augath, Oeltermann, & Logothetis, 2006). BOLD signal activity is influenced by
increases and decreases in deoxygenated hemoglobin concentrations resulting from
changes in cerebral blood volume, cerebral blood flow, and oxygen metabolism
following neural firing (Buxton, Uludağ, Dubowitz, & Liu, 2004).
Over the last two decades, fMRI research has shown BOLD signal differences
between healthy and psychiatric populations including individuals diagnosed with
schizophrenia, major depressive disorder, bipolar disorder, obsessive-compulsive dis-
order, posttraumatic stress disorder, and Alzheimer’s disease (see Habecker, Daniels,
& Renshaw, 2009, for a review). Multiple studies have demonstrated that human
participants can learn self-regulation of localized brain regions through rtfMRI feed-
back (see Sitaram, Caria, & Birbaumer, 2009, for a review) and HEG/NIRS feedback
(Kanoh, Murayama, Miyamoto, Yoshinobu, & Kawashima, 2009; Toomim et al.,
2004). While the majority of the studies focused on the utility of BOLD signal
regulation as an assistive BCI parameter, only a handful have specifically investi-
gated the cognitive, behavioral, and emotional effects of training BOLD signals for
restorative and clinical applications in pain perception, stroke rehabilitation, nicotine
dependence, emotional disorders (Caria, Sitaram, & Birbaumer, 2011), schizophrenia
(Ruiz et al., 2011), and impulsivity and sustained attention (Toomim et al., 2004).
Technological advancements in fMRI data acquisition and processing techniques
have allowed for the online or “real-time” fMRI analysis and feedback of the BOLD
signal from a targeted region of interest. As with EEG-based neurofeedback methods,
individuals using rtfMRI feedback are trained to modulate their own brain activity
based on the combination of contingent feedback and mental strategies. Real-time
fMRI neurofeedback utilizes a closed-loop system that is based on three components:
signal acquisition, signal analysis, and signal feedback (see Sitaram et al., 2009).
During signal acquisition, an individual is placed into an MRI scanner and a series
of brain images are acquired, measuring the increases and decreases of paramagnetic
load of blood flow to activated poles of neurons. Head padding and bite guard
are utilized to help prevent artifacts due to head movements; earplugs are provided
to reduce noise discomfort due to the scanner sequence sounds. The functional
images are exported to a host computer for online preprocessing of artifacts and signal
denoising and then used for incremental statistical analysis and generation of functional
maps of a region of interest. Using video projection and visualization software, the
calculated and baseline normalized differences in BOLD activity between target and
reference regions of interest are converted into a graduated thermometer display (see
Figure 13.4). Throughout the training protocol, the color-coded thermometer bar is
updated every 1.5 seconds with current fMRI data displaying increases and decreases
Scanner host computer
Scanner Real-time
echoplanar Brain
imaging images
sequence
Perl script for

transferring images
to fMRI-BCI
Participant fMRI-BCI
Visual feedback
Computer
-Preprocessing
-Feature selection
H
-Brain state classification
-Feedback generation
Figure 13.4 The University of Tübingen method for real-time fMRI brain state classification
system is comprised of the following subsystems: (1) image acquisition subsystem, which is
a modified version of the standard echo-planar imaging (EPI) sequence written in C and
executed on the scanner host computer, and (2) fMRI-BCI subsystem, which performs image
preprocessing, brain state classification, and visual feedback, implemented in C and Matlab
scripts (Mathworks, Natwick, MA) and executed on a 64-bit Windows desktop. A Perl-script
on the scanner host transfers the acquired images after every scan (at an interval of 1.5 s) to the
fMRI-BCI computer. Reproduced from R. Sitaram, S. Lee, S. Ruiz, M. Rana, R. Veit, & N.
Birbaumer (2011). Real-time support vector classification and feedback of multiple emotional
states. Neuroimage, 56, 753–765, with permission.
in activation. Training sessions are generally organized into alternating blocks of

activation and rest, extending for 30–60 seconds (Caria et al., 2011). The addition of
task-specific or feedback rating blocks may also be included to evaluate functional and
state-related changes following the regulation blocks. To generalize self-regulation
skills, transfer runs in which no fMRI feedback is provided are also included.
Unlike the instantaneous feedback of EEG activity (within a few hundred mil-
liseconds), hemodynamic coupling introduces a delay between neural activation and
BOLD signal changes. Despite the poor temporal resolution of fMRI, participants
in rtfMRI studies achieve control of BOLD response through operant conditioning.
This process of learning may be enhanced through participant education of training
strategies and signal time course delays (Caria et al., 2011). To improve learning
performance and reduce the risk of participants prematurely discontinuing successful
strategies due to feedback delays, participants are typically instructed to use cognitive,
Neurofeedback 285
emotional, or motor imagery strategies over several training blocks to influence the
feedback signal. Additionally, participants are informed of the 2- to 3-second delay
in the onset of BOLD signal increases and additional time delay of 1.5 seconds for
fMRI feedback processing steps.
HEG and NIRS imaging methods utilize light in the red and near-infrared range,
respectively, to determine cerebral oxygenation, blood flow, and metabolic status of
localized regions of the brain, producing a signal that is equivalent to the BOLD
signal (see Sitaram et al., 2009; Toomim et al., 2004, for a review). Based on the
observation that the properties of light passing through living tissue are influenced by
the functional state of tissue, HEG and NIRS applications use pairs of light sources
and light detectors (optodes) operating at two or more discrete wavelengths to
record changes in BOLD response. Specifically, these optodes are applied to the head,
separated at a distance of 2–7 cm, to allow continuous light to pass the intermediate
layers of the scalp, skull, and tissue at a depth of 1–3 cm. HEG utilizes a single pair
of optodes placed sequentially over FP1, Fz, and FP2 prefrontal brain sites and uses
alternating red (660 nm) and infrared (850 nm) light source wavelengths (Toomim
et al., 2004). NIRS applications utilize multiple pairs of optodes that may be applied
to several brain areas and use two near-infrared wavelength (between 700 and 1000
nm) light sources (Sitaram et al., 2009).
In both methods, the attenuation of the continuous light source signal recorded at
the detector optode yields qualitative differences in the concentrations of oxygenated
(oxyHb) and deoxygenated hemoglobin (deoxyHb). These signal changes can be
linked to a visual feedback instrument for the purposes of operant conditioning.
HEG studies have utilized multiple 10-minute continuous feedback training blocks
to increase oxyHb concentrations at various frontal training sites (Toomim et al.,
2004), whereas NIRS studies have utilized alternating activation and rest blocks in
which participants were directed to increase oxyHb concentrations though motor
imagery tasks during activation trials and to decrease oxyHb concentrations during
rest (Kanoh et al., 2009). As with rtfMRI neurofeedback methods, HEG/NIRS
feedback also has a 2- to 8-second time delay between the onset of the activation
task and the hemodynamic response in which increase in oxyHb can be observed.
The time delay issue is handled in the same way as with fMRI-based methods (via
directed training strategies and patient education). Currently, the majority of NIRS
studies have focused on BCI applications. However, several universities and research
groups have been developing NIRS neurofeedback studies to treat ADHD, stroke,
and traumatic brain injuries.
Clinical Applications and Research Findings
The following section focuses heavily on the review of neurofeedback research

findings for the treatment of ADHD. A summary of the DSM criteria, major neu-
rophysiological alterations, and a review of major treatment studies and outcomes is
provided. Additionally, a brief discussion of neurofeedback applications for other
psychiatric conditions, including anxiety disorder, dissociative disorder, learning
disorders, mood disorders, psychotic disorders, and substance-related disorders, is

presented.
Attention-Deficit/Hyperactivity Disorder
The Diagnostic and Statistical Manual of Mental Disorders (4th ed., text rev.; DSM-
IV-TR; American Psychiatric Association, 2000) category for attention deficit and
disruptive behaviors includes ADHD, conduct disorder (CD), and oppositional defiant
disorder (ODD). The core symptoms of ADHD include inattention, hyperactivity, and
impulsivity. Although ADHD is one of the most common disorders of childhood,
with an incidence of 7.5% by the age of 19 years (Barbaresi et al., 2004), the
prevalence of ADHD in the general adult population is estimated to be around
4–5% (Goodman & Thase, 2009). Significant treatment effects have been reported
using pharmacotherapy and psychological interventions for children and adults with
ADHD. Stimulant drugs have been found to work quickly and control the symptoms
of ADHD in about 75% of study participants (Connor, 2006; Nair & Moss, 2009).
Long-term investigations indicate the maintenance of core symptom reduction over 4
months to 5 years in childhood populations (Connor, 2006), but have not established
a clear-cut dose–response relationship for adult participants and find that most
individuals discontinue their medication (Torgeren, Gjervan, & Rasmussen, 2008).
In addition, side effects such as headache, anorexia, insomnia, nervousness, and nausea
(Connor, 2006; Jain et al., 2007) may contribute to decreased medication compliance
and the resurfacing of core symptoms.
Nonpharmacological interventions, including cognitive behavioral therapy,
metacognitive therapy, dialectical behavioral therapy, coaching cognitive reme-
diation, behavior modification, multimodal psychosocial treatment, school-based
programs, working-memory training, parent training, self-monitoring, and neuro-
feedback therapy, have been investigated for the treatment of ADHD symptoms
(Hodgson, Hutchinson, & Denson, 2012). Cognitive behavioral therapy has been
identified as the most efficacious psychological treatment for adults with ADHD
and symptoms of comorbid depression and anxiety (Vidal-Estrada, Bosch-Munso,
Noqueira-Moralis, Casas-Bruque, & Ramos-Quiroqa, 2012), whereas behavior
modification and neurofeedback interventions are the most efficacious psychological
treatments for children with ADHD. Neurofeedback therapy has emerged as
a medication-free alternative for the long-term treatment of ADHD. Several
neurophysiological models have been developed to account for the core symptoms
of ADHD and serve as the theoretical basis for the application of EEG, SCP, and
BOLD signal neurofeedback methods.
Investigation of spontaneous EEG in ADHD populations has revealed increased
theta and decreased alpha and/or beta frequencies in children (Mann, Lubar,
Zimmerman, Miller, & Muenchen, 1992; Monastra et al., 1999; Monastra & Lubar,
2001). Diagnosis-specific subtypes have also been identified, as children with inat-
tentive type ADHD tend to have significantly different levels of theta, alpha, and
beta from children with combined type, despite both groups differing significantly
from controls (Clarke, Barry, McCarthy, & Selikowitz, 1998). Adults with ADHD
often present with elevated theta/beta ratios (Bresnahan, Anderson, & Barry, 1999;
Neurofeedback 287
Bresnahan & Barry, 2002), or increased absolute theta and alpha power (Koehler
et al., 2009) with varying reductions in beta activity. Reductions in absolute delta and
midline beta power, as well as increased relative theta and enhanced beta power in the
right posterior region, have also been reported (Clarke et al., 2008). These studies
reflect the current “hypoarousal” model of ADHD, which focuses on the reduction
of excessive cortical slowing.
Rockstroh, Elbert, Lutzenberger, and Birbaumer (1990) observed impaired reg-
ulation of SCPs in children with attentional problems, while other ERP studies
indicate decreased amplitudes and prolonged latencies for p300 activity (Alexander
et al., 2008; Doehnert, Brandeis, Imhof, Drechsler, & Steinhausen, 2009; Johnstone,
Barry, & Anderson, 2001; Prox, Dietrich, Zhang, Emrich, & Ohlmeier, 2007;
Satterfield, Schell, & Nicholas, 1994) and decreased activation in cued contingent
negative variation (CNV) paradigms (Banaschewski et al., 2003; Mayer, Wyckoff,
Schulz, & Strehl, 2012; Sartory, Heine, Mueller, & Elvermann-Hallner, 2002).
These findings prompted researchers to classify ADHD as a disorder characteristic
of impaired excitation thresholds and deficits in the allocation of neurophysiologic
resources.
In a NIRS investigation of the Stroop color-word tasks, Negoro et al. (2010)
reported that participants with ADHD had significantly reduced oxyHb concentration
changes in the inferior prefrontal cortex compared to controls. Investigations of single
photon emission computed tomography (SPECT) images reveal that children with
ADHD have decreased regional cerebral blood flow (rCBF) in the orbitofrontal cortex
and middle frontal gyrus, with increased rCBF in the dorsomedial prefrontal and
somatosensory areas compared to healthy controls (Lee et al., 2005). Interestingly,
Lee and colleagues also reported that methylphenidate normalizes these imbalances
in rCBF. These findings support the application of HEG, NIRS, and rtfMRI feedback
methods to enhance BOLD signal concentrations and oxygen metabolism, which are
currently under investigation at the University of Tübingen, Germany.
The first investigations of neurofeedback for the treatment of ADHD began in
the 1970s. In a series of experiments, J. F. Lubar and colleagues began developing
and refining neurofeedback methods and treatment hypotheses (J. O. Lubar &
Lubar, 1984; J. F. Lubar & Shouse, 1976; J. F. Lubar, Swartwood, Swartwood, &
O’Donnell, 1995; Shouse & Lubar, 1979). Through their work, several research-
based protocols emerged, focusing on the enhancement of SMR (12–15 Hz) over
central electrode sites on the Rolandic cortex (C3, Cz, C4) and paired suppression
of theta (4–8 Hz) with enhancement of beta (16–20 Hz) over midline electrode
sites (Fz, Cz, Pz). Shortly after, researchers in Europe started investigating the
SCP protocols and rewarding the bidirectional shift and increased differentiation
of positive and negative shifts over the vertex (Cz). Finally, Toomim et al. (2004)
reported that individuals with ADHD, among other participants with psychological
impairments, were able intentionally to modulate cerebral blood oxygenation resulting
in the normalization of impulsivity subscores of the Test of Variables of Attention
(TOVA).
These protocols (see Table 13.1) have been investigated in a variety of A-B-A
designs (Heywood & Beale, 2003; Shouse & Lubar, 1979), multicase studies
(Alhambra, Fowler, & Alhambra, 1995; Kaiser & Othmer, 2000; J. O. Lubar &
Table 13.1 Summary of Neurofeedback Research Included in Attention-Deficit/Hyperactivity Disorder Treatment Meta-Analyses
Authors Study details Results

Fine et al., 1994* Participants: 71 ADHD, 8–11 yrs NF vs. Control: NF showed significant improvement on parent and laboratory
Study design: Randomized controlled trial test variables including Impulsive-Hyperactivity, Hyperactivity Index Scales,
Control group: Captain’s Log cognitive Hyperactive Scales, and the Home Situations Questionnaire M severity
training; no treatment score; Wide Range Assessment of Memory and Learning, Number/Letter
Protocol/placement: not provided, CZ Memory, Design Memory and Story Memory, and Stroop Test.
Rossiter & Participants: 23 ADHD (M = 12.9), NF and MED groups showed improvements on measures of inattention,
LaVaque, 1995 23 controls (M = 12.9) impulsivity, information processing, and variability on the TOVA, but no
Study design: Pre/post comparison difference on TOVA change scores between groups.
Comparison group: Stimulant medication
Protocol/placement: ↑ SMR / ↑ beta,
↓ theta, Cz or FCz-CPz
Linden et al., Participants: 9 ADHD, 9 controls, 5–15 yrs NF vs. Control: Posttreatment significant improvement (mean of 9 points) on
1996* Study design: Wait-list control the K-Bit IQ Composite than WL controls; NF significantly reduced parent
Protocol: ↑ beta / ↓ theta, Cz-Pz reports of inattentive behaviors.
Kaiser & Othmer, Participants: 1,089 patients (186 ADHD) Significant improvement on TOVA for attentiveness, impulse control, and
2000 Study design: Pre/post comparison response variability. Eighty-five percent of participants with moderate
Protocol/placement: ↑ beta/↓ theta, pretraining deficits had significant clinical improvement in one or more
C3 or C4 TOVA measures.
Palsson et al., Participants: 11 ADHD, 11 controls, 9–13 yrs NF vs. Game NF: Both groups improved on BASC and TOVA. BASC:
2001* Study design: Randomized controlled trial significant improvement for inattention, hyperactivity, internalizing scores;
Control group: Video game NF TOVA: significant/marginally significant improvements for errors of
(Sony PlayStation) omission, a measure of inattention, errors of commission, a measure of
Protocol/placement: ↑ SMR ↑ beta, ↓ impulsivity, total number of correct responses, and D prime, a measure of
theta ↓ alpha, Cz the ability to discriminate target stimuli from nontarget stimuli. Trends on
pre/post quantitative QEEG changes; both types of NF were reported to
improve children’s functioning substantially above the benefits of
background medication.
Monastra et al., Participants: 51 ADHD (M = 10), Posttreatment assessments with/without stimulant therapy (Ritalin) indicated
2002 49 controls (M = 10) significant improvement on the TOVA and ADDES; only NF group
Study design: Pre/post comparison sustained these gains when tested without Ritalin; QEEG-scan indicated
Comparison group: Stimulant medication significant reduction in cortical slowing only in NF group; Behavioral
Protocol/placement: ↑ beta / ↓ theta, measures indicated that parenting style exerted a significant moderating
Cz-CPz effect on the expression of behavioral symptoms at home but not at school.
Fuchs et al., 2003 Participants: 22 ADHD (M = 9.6), NF and MED were associated with improvements on all subscales of the
11 controls (M = 9.8) TOVA and speed/accuracy measures of the D2 Attention Endurance Test.
Study design: Pre/post comparison Significant reduction to core ADHD behaviors in both groups by both
Comparison group: Stimulant medication teachers and parents on the IOWA-Conners Behavior Rating Scale.
Protocol/placement: ↑ beta ↓ theta, C3 or C4
Heinrich et al., Participants: 13 ADHD (M = 11.1), NF vs. WL: NF only had ADHD symptomatology reduce by approximately
2004 9 controls (M = 10.5) 25%, impulsivity errors decrease, and CNV increase.
Study design: Wait-list control
Protocol/placement: SCP, Cz

Orlandi & Greco, Participants: 17 ADHD, 19 controls, NF vs. Game: NF only showed significant improvement on parent ratings and
2004* 9–11 yrs significant improvements on independent blinded-clinician ratings of
Study design: Randomized controlled trial symptom severity.
Control group: Game training
Protocol/placement: ↑ SMR or ↑ beta,
↓ theta, Cz
Rossiter, 2005 Participants: 31 ADHD, 31 controls EEG and MED group had significant TOVA tests of attention, impulse
Study design: Pre/post comparison control, speed processing, and variability in attention; Significant behavioral
Comparison group: Stimulant medication and attention score improvements for the NF group.
Protocol/placement: variable, ↑ SMR or ↑
beta, with ↓ delta, ↓ theta, or ↓ alpha,
C3 or C4
Kropotov et al., Participants: 86 ADHD (M = 11.4) For good performers, but not bad performers, the ERP GO/NOGO cues
2005 Study design: Pre/post comparison gained positive components evoked within 180–420 ms latency; Pre/post
Protocol/placement: ↑ beta/ ↑ SMR, ERP differences for good performers were distributed over frontal–central
C3-Fz and C4-Pz areas and appear to reflect an activation of frontal cortical areas associated
with beta training.
Xiong et al., 2005 Participants: 60 ADHD, >6 yrs Overall indexes of IVA were significantly improved among children with
Study design: Pre/post comparison predominantly inattentive, hyperactive, and combined subtype of ADHD.
Protocol/placement: ↑ SMR ↓ theta,
unreported placement
deBues, 2006* Participants: 53 ADHD, 7–11 yrs NF vs. SHAM: NF group had significantly better response control and
Study design: Randomized controlled trial attention on the IVA, and significantly lower parent-rated DSM-IV
Control group: Sham feedback inattentive symptoms and teacher-rated DSM-IV inattentive and
Protocol/placement: ↑ beta/SMR hyperactive-impulsive symptoms.
↓ theta, Fz
Levesque et al., Participants: 15 ADHD, 5 controls, NF vs. WL: NF only had significant improvement on Digit Span subtest of
2006 8–12 yrs WISC-R, IVA, CPRS-R scales of inattention and hyperactivity, and
Study design: Wait-list control Counting Stroop Task neutral and interference trials.
Protocol/placement: ↑ beta/SMR
↓ theta, Cz
Picard et al., Participants: 8 ADHD, 7 controls, NF vs. WL: NF only had significantly improved parent-rated hyperactive,
2006* 7–12 yrs inattentive, and global scores on the DBQ, and improved VCI scores on the
Study design: Wait-list control WISC.
Picard et al., Participants: 10 ADHD, 21 controls, NF vs. WL; NF had marginally/significantly improved hyperactive,
2006* 7–12 yrs inattentive, and global parent-DBQ and WISC-IV scores. NF vs. SHAM:
Study design: Randomized controlled trial NF had marginally/significantly improved hyperactive, inattentive, and
Control groups: Wait-list control, sham global parent-DBQ and VCI scores. WL vs. SHAM had no significant
feedback difference in parent-DBQ or VCI scores.

Strehl et al., 2006 Participants: 23 ADHD (M = 9.3) ADHD children learn to regulate negative SCP. NF had significant
Study design: Pre/post, randomized improvement on parent and teacher behavior rating scales, CPT attention
controlled trial test, and WISC IQ scores. Changes stable at 6-month follow-up; outcome
Comparison group: T/B feedback was predicted by the ability to produce negative potential shifts in transfer
(Leins et al., 2007) sessions without feedback.
Protocol/placement: SCP, Cz
Bakhshayesh, Participants: 18 ADHD (M = 9.6), 17 Theta/beta quotient significantly decreased after the NF training,
2011 controls (M = 9.0) EMG-amplitude significantly decreased after the EMG training. NF vs.
Study design: Randomized controlled trial EMG: NF group showed significant improvements in attention scores,
Control group: EMG intelligence scores, and behavior after training, EMG placebo group showed
Protocol/placement: ↑ beta ↓ theta, no significant improvements in any of the outcome variables except on the
FCz-CPz speed scale of the paper-pencil attention tests. At posttest 55.6% (n = 10) of
the NF and 23.5% (n = 4) of the EMG group no longer met criteria for
ADHD diagnosis.
Drechsler et al., Participants: 17 ADHD (M = 10.5), NF vs. Group Therapy: NF showed greater improvement on parent and
2007 13 controls (M = 11.2) teacher ratings of attention and cognition than therapy control.
Study design: Pre/post comparison Neuropsychological measures revealed similar improvements in both
Comparison group: Group therapy groups. Half of the NF group learned to regulate SCP negative shifts during
Protocol/placement: SCP, Cz a “transfer” condition without direct feedback; behavioral improvements of
this subgroup were moderately related to NF performance, whereas effective
parental support accounted better for some advantages of NF compared to
group therapy according to parents’ and teachers’ ratings.
Leins et al., 2007 Participants: 19 ADHD (M = 9.2) ADHD children learn to regulate EEG parameters; NF training produced
Study design: Pre/post, randomized significant improvement in parent and teacher behavior rating scales, CPT
controlled trial attention test, and WISC IQ scores. Changes stable at 6-month follow-up.
Comparison group: SCP feedback (Strehl
et al., 2006)
Protocol/placement: ↑ beta ↓ theta, Cz
McGrady et al., Participants: 31 ADHD, 7–12 yrs NF vs. WL: NF only showed significantly improved CTRS-R ADHD and
2007* Study design: Wait-list control Hyperactivity subscales, and on the GDS computer-based Distractibility
Protocol/placement: ↑ SMR/beta ↓ theta, task. Pre/post Tx improvement on the CTRS Hyperactivity Scales
Cz maintained until the end of the school year. Post-Tx EEG theta scores were
significantly correlated with post-Tx and FU CTRS-R Hyperactivity and
post-Tx CTRS-R ADHD and GDS Distractibility.
Gevensleben et al., Participants: 59 ADHD (M = 9.1), 35 NF vs. Attention training: NF group changes superior on parent and teacher
2009 controls (M = 9.4) ratings. Parent-rated FBB-HKS total score improvements reflect a medium
Study design: Randomized controlled trial effect size of 0.60. Comparable effects were obtained for the both NF
Control Group: Attention training protocols (theta/beta training, SCP training). Parental attitude toward the
Protocol/placement: SCP/↑ beta ↓ theta, treatment did not differ between NF and control group.
Cz
Holtmann et al., Participants: 20 ADHD (M = 10.3), 14 NF vs. Cognitive training: Both groups showed improvement on a Stop-Signal
2009* controls (M = 10.2) test, NF only had a significant reduction of impulsivity errors. On ERP
Study design: Randomized controlled trial measures, NF group had a marginally significant increase in N2-amplitude
Control group: Captain’s Log cognitive (an indicator of NoGo-N2 normalization). Parent-rated SNAP-IV
training inattention, hyperactivity, and impulsivity showed improvements over time
Protocol/placement: ↑ beta ↓ theta, Cz for both groups but no significant differences.
Urichuk et al., Participants: 20 ADHD, 17 controls, 7–15 NF vs. Sham: Both groups improved over the course of the project, but there
2009* yrs were no significant differences between groups. No significant changes for
Study design: Randomized controlled trial impulsivity or inattention levels of children on the TOVA for either group
Control group: Sham feedback were reported. Over time in both groups, parents reported children were
Protocol/placement: Unavailable doing better at the end, and children reported feeling more calm, being able
to concentrate better, having better sleep quality, and feeling less discomfort
in general.
Perreau-Linck Participants: 5 ADHD, 4 controls Note: One dropout in experimental group, one adverse effect from sham
et al., 2010* Study design: Randomized controlled trial feedback. NF vs. Sham: both showed significant improvements on several
Control group: Sham feedback CPRS-R subscales (Hyperactivity), with more overall improvement in the
Protocol/placement: ↑ SMR ↓ theta, C4 sham group. All participants showed improvement on at least one
neuropsychological measure, with more active-NF participants
demonstrating improvement on the Stroop Task Inhibition/Switching
Condition and more sham-NF participants showing more improvement on
the Stroop Task Inhibition Condition and the CPT-II Variability measure.
Note: ADDES = Attention Deficit Disorders Evaluation Scale; ADHD = attention-deficit/hyperactivity disorder; BASC = Behavior Assessment System for
Children–Monitor; CNV = contingent negative variation; CPRS-R = Conners’ Parent Rating Scales-Revised; CPT = Continuous Performance Test; CPT-II =
Continuous Performance Test-II; CTRS-R = Conners’ Teacher Rating Scales-Revised; DBQ = DuPaul Behavioral Questionnaire; EEG = electroencephalography;
EMG = electromyograph; ERP = event-related potential; FBB-HKS = German ADHD rating scale; GDS = Gordon Diagnostic System; IVA = Integrated Visual and
Auditory; NF = neurofeedback; QEEG = quantitative EEG; SMR = sensorimotor rhythm; SNAP-IV = Swanson, Nolan, and Pelham rating scale; TOVA = Tests of
Variable Attention; VCI = Verbal Comprehension Index; WISC = Wechsler Intelligence Scale for Children; WL = wait-list.
∗ Study details are those reported in Lofthouse et al. (2012).
Neurofeedback 295
Lubar, 1984; Thompson & Thompson, 1998), and pre/post designs (Boyd &
Campbell, 1998; J. F. Lubar et al., 1995; Mayer et al., 2012). These studies indicated
QEEG/spectral/amplitude changes in the protocol training direction, reduction of
core ADHD and comorbid mood symptoms, and improvements in classroom and
homework behaviors, analysis of pre-/post-TOVA, Wechsler Intelligence Scale for
Children-Revised (WISC-R), Wide Range Achievement Test 3 (WRAT-3), Attention
Deficit Disorders Evaluation Scale (ADDES), digit span assessments, medication
titration, parent and teacher behavior ratings, full-scale IQ, ERP amplitudes, and
error performance.
Two recent meta-analyses have reported the efficacy of neurofeedback as a non-
medication treatment alternative (see Table 13.1). Analysis of several randomized
controlled trials and pre/post studies indicated an overall medium effect size (Loft-
house, Arnold, Hersch, Hurt, & DeBeus, 2012) for the reduction of ADHD core
symptoms, a medium effect size for hyperactivity, and large effect sizes for inat-
tention and impulsivity (Arns, de Ridder, Strehl, Breteler, & Coenen, 2009). In
general, studies comparing neurofeedback to stimulant medication found comparable
effects for the reduction of core ADHD symptoms and improvements on subscales
of the TOVA and other neuropsychological tests (Fuchs, Birbaumer, Lutzenberger,
Gruzelier, & Kaiser, 2003; Rossiter, 2005; Rossiter & La Vaque, 1995), with only
the neurofeedback group maintaining treatment gains after discontinuation of med-
ication (Monastra, Monastra, & George, 2002). Pre/post investigations of various
feedback methods indicated the learning of self-regulation skills for training param-
eters, reduction of core ADHD symptoms on parent and teacher behavior reports,
IQ gains, enhanced ERP activity, and improvements on continuous performance
tasks and other neuropsychological tests (Kropotov et al., 2005; Leins et al., 2007;
Palsson et al., 2001; Strehl, Leins, Goth, Klinger, & Birbaumer, 2006; Xiong,
Shi, & Xu, 2005). Neurofeedback also showed greater improvements on treatment
outcomes compared to wait-list controls (Heinrich, Gevensleben, Freisleder, Moll,
& Rothenberger, 2004; Levesque, Beauregard, & Mensour, 2006; Linden, Habib,
& Radojevic, 1996; McGrady, Prodente, Fine, & Donlin, 2007; Picard, Moreau,
Guay, & Achim, 2006). Finally, neurofeedback therapy showed superior therapeutic
effects or performance enhancement on some assessment variables compared to com-
puter training for attentional and cognitive skills (Fine, Goldman, & Sanford, 1994;
Gevensleben et al., 2009; Holtmann et al., 2009; Orlandi & Greco, 2004), elec-
tromyograph biofeedback (Bakhshayesh, Hansch, Wyschkon, Rezai, & Esser, 2011),
group therapy (Drechsler et al., 2007), and sham feedback (deBues, 2006; Lans-
bergen, Van Dongen-Boomsma, Buitelaar, & Slaats-Willemse, 2011; Perreau-Linck,
Lessard, Levesque, & Beauregard, 2010; Urichuk et al., 2009).
The current body of research supports the use of neurofeedback applications in the
treatment of ADHD. Neurofeedback has been shown to have comparable effects to
stimulant medication, with long-term effects beyond medication titration. Follow-up
studies indicated that the improvements to core ADHD symptoms and the ability to
self-regulate specific brain parameters remain stable after 6-month to 2-year follow-up
(Gani, Birbaumer, & Strehl, 2008; Gevensleben et al., 2010; Leins et al., 2007;
Strehl et al., 2006). Although promising, additional research and placebo-controlled
investigations are needed.
Other Therapeutic Applications

While the therapeutic application of neurofeedback for psychiatric disorders has
been most widely investigated for ADHD, it has also aided in the treatment of
anxiety, depression, dissociative disorders, learning disorders, psychotic disorders, and
substance-related disorders.
Anxiety disorders. Over the last 35 years, clinicians have been investigating the
therapeutic effects of neurofeedback for anxiety disorders. Specifically, generalized
anxiety disorder (GAD), obsessive-compulsive disorder (OCD), and posttraumatic
stress disorder (PTSD) have been investigated (see Moore, 2005). Several proto-
cols have emerged for the training of GAD, including theta or alpha suppression
with/without beta enhancement (Kerson, Sherman, & Kozlowski, 2009; Rice,
Blanchard, & Purcell, 1993; Thomas & Sattlberger, 1997), theta or alpha enhance-
ment with/without beta enhancement (Passini, Watson, Dehnel, Herder, & Watkins,
1977; Rice et al., 1993; Vanathy, Sharma, & Kumar, 1998; C. G. Watson & Herder,
1980; B. W. Watson, Woolley-Hart, & Timmons, 1979), and alpha symmetry train-
ing (Kerson et al., 2009). The use of these neurofeedback protocols has led to the
reduction of anxiety symptoms, improvements on the Minnesota Multiphasic Person-
ality Inventories (MMPI and MMPI-2), and reductions on the State-Trait Anxiety
Inventory (STAI), Psychosomatic Symptom Checklist, and Brief Psychiatric Rating
Scale.
For the treatment of PTSD, alpha-theta enhancement protocols have been utilized
and led to symptom reduction, medication titration, relapse prevention, and improve-
ments on the MMPI (Peniston & Kulkosky, 1991). For the treatment of OCD, alpha
enhancement (Mills & Solyom, 1974) was shown to reduce rumination behavior
during training sessions, and QEEG guided protocols (Hammond, 2003; Sürmeli &
Ertem, 2011) led to improvements on the Yale–Brown Obsessive Compulsive Scale
(Y-BOCS) and MMPI. Current investigations at Yale University School of Medicine
have focused on the application of rtfMRI feedback to train OCD patients to develop
control of BOLD signal activity in a region of the orbitofrontal cortex associated with
contamination anxiety (Hampson et al., 2012).
Depression. Early research in the application of neurofeedback protocols for depression

focused on comorbid substance abuse and mood disorders. Saxby and Peniston
(1995) applied the alpha-theta enhancement protocol to a group of 14 alcoholic
outpatients with comorbid depression. Following 20 sessions of training, the patients
reported a sharp decrease in symptoms on the Beck Depression Inventory (BDI)
and significant reductions in symptoms on the Millon Clinical Multiaxial Inventory
including schizoid, avoidant, dependent, histrionic, passive-aggressive, schizotypal,
borderline, anxiety, somatoform, hypomanic, dysthymic, alcohol and drug abuse,
psychotic thinking, and psychotic depression. Additional research has focused on the
issue of alpha asymmetry in depressed patients. Using a protocol designed to modify
frontal alpha asymmetries (F4—F3/F4 + F3—referenced to Cz), a series of case
studies (Baehr, Rosenfeld, & Baehr, 1997; Earnest, 1999; Rosenfeld, Baehr, Baehr,
Gotlib, & Ranganath, 1996) reported symptom reductions and MMPI improvements
Neurofeedback 297
in depressed adolescent and adult patients who were successful in regulating alpha
symmetry. In a follow-up study, posttreatment changes in depression scores and
asymmetries were stable and enduring from 1 to 5 years following treatment cessation
(Baehr, Rosenfeld, & Baehr, 2001).
A recent randomized controlled trial investigated the utility of alpha asymmetry
training compared to a psychotherapy placebo condition, reporting that 10 sessions
of asymmetry training induced right frontal alpha increases exclusively in the train-
ing group and led to a reduction in depressive symptoms (Choi et al., 2011).
Finally, Dias and van Deusen (2011) recently combined the alpha asymmetry and
alpha-theta training protocols of depression research with the beta reduction pro-
tocols common to anxiety training. Following 10 sessions of training focused on
enhancing right alpha asymmetry, increasing the beta/theta relationship on the left
prefrontal cortex, and reducing high-beta activity over the entire prefrontal cortex,
Dias and van Deusen reported mood enhancement and significant changes in self-
report of depressive symptoms of a pilot participant. Further research is needed to
investigate the utility of this protocol for treatment of comorbid depression and
anxiety.
Dissociative identity disorder. Manchester, Allen, and Tachiki (1998) investigated the
efficacy of occipital alpha-theta training in 11 female patients with a diagnosis of
dissociative identity disorder. Following 30 neurofeedback training sessions and 10
neurofeedback-related group therapy sessions, all patients were assessed as “unified”
and scored within normal limits on the Dissociative Experience Scales through a
1-year follow-up.
Learning disorders. The application of neurofeedback therapy has been investigated

for a variety of learning disabilities including dyslexia, reading disabilities, and Down
syndrome. In a series of studies, Tansey (1984, 1991) reported the positive impact
of SMR enhancement over the Rolandic cortex for the reduction and remediation
of learning disabilities, improvement of EEG abnormalities, and normalization of
WISC-R performance. In a matched-group placebo-controlled design, Fernandez
et al. (2003) reported similar findings, indicating that children who learned to
decrease theta/alpha ratios with contingent feedback had significant improvements
on the TOVA, WISC, and EEG parameters compared to control participants who
received noncontingent feedback. At a 2-year follow-up, these gains persisted for the
contingent feedback group, resulting in long-term remission of learning disabilities
(Becerra et al., 2006).
In a case study, Fleischman and Othmer (2005) reported IQ gains following
neurofeedback therapy for mild developmental delay. Breteler, Arns, Peters, Giep-
mans, and Verhoeven (2010) reported that children with dyslexia showed significant
improvements in spelling following neurofeedback therapy compared to remedial
education alone. QEEG changes, along with improvements in speech, memory, and
coordination, were also reported following QEEG guided neurofeedback therapy for
children with Down syndrome (Sürmeli & Ertem, 2007). Finally, in a randomized
control trial, Orlando and Rivera (2004) reported that QEEG-guided neurofeedback
resulted in superior improvements on reading and reading composition scores, verbal
IQ, and full-scale IQ scores for a group of middle school children with learning
disabilities compared to a treatment-as-usual peer cohort.
Schizophrenia. The initial investigation of neurofeedback training as a treatment for

schizophrenia focused on the application of SCP feedback. Schneider et al. (1992)
first reported that patients with schizophrenia were able to learn self-regulation and
differentiation of SCP shifts after 20 sessions. Later, Gruzelier et al. (1999) developed
an SCP asymmetry reversal protocol with bipolar electrode placements over the
sensory motor strip. The ability to shift negativity to the left and right correlated
with positive and negative symptoms of schizophrenia. After 10 or more sessions,
some participants showed a reduction of anxiety and depression symptoms on the
Positive and Negative Symptom Scale (PANSS). In a case study of a patient suffering
20 years with paranoid schizophrenia, QEEG guided neurofeedback was associated
with reductions in bilateral hand tremors, repetitive demands, verbal or violent
outbursts, physical altercations, and in-room restraints (Bolea, 2010). Increases in
positive statements, communication, helping behaviors, and self-grooming behaviors
were also reported. The most recent investigations have focused on the use of rtfMRI
feedback. Ruiz et al. (2011) trained patients with schizophrenia to increase BOLD
signal activity in the bilateral anterior insula resulting in better performance on a face
emotion recognition task.
Substance abuse. Currently, brain imaging data and neurofeedback studies support
the enhancement of occipital alpha-theta frequencies for alcohol dependence, or
alpha-theta enhancement in tandem with beta training for mixed substance abuse
disorders (see Sokhadze, Cannon, & Trudeau, 2008, for a review). Peniston and
Kulkosky (1989) conducted the first randomized controlled trial investigating the
use of alpha-theta training for the treatment of alcoholism. After completion of a
hand temperature-training phase, the study participants completed 15 sessions of
eyes-closed alpha-theta training and showed reductions on BDI assessments and
lower levels of beta-endorphins as compared to a treatment-as-usual control group.
At a 13-month follow-up, significantly more alcoholics maintained sobriety than
did individuals who did not receive the neurofeedback training. Similar findings
were reported in a series of replication studies (Bodenhamer-Davis & Callaway,
2004; Kelly, 1997; Saxby & Peniston, 1995). An investigation by Fahrion (1995)
applied the alpha-theta protocol to prisoners suffering with addictions and identified
differential effects based on age, race, and drug of choice, leading to modifications to
the traditional protocol (Fahrion, 2002).
Schneider et al. (1993) reported that the successful regulation of SCP shifts
resulted in relapse prevention. Due to the comorbid nature of ADHD and substance
abuse, Scott, Kaiser, Othmer, and Sideroff (2005) incorporated a series of SMR-
beta enhancement training sessions prior to alpha-theta training and reported that
neurofeedback participants exclusively showed normalization of attentional variables
and had superior gains on the MMPI-2 compared to control participants. The use of
beta enhancement protocols in addition to alpha-theta training has also been effective
in treating crack cocaine dependence (Burkett, Cummins, Dickson, & Skolnick,
2005) with results indicating that neurofeedback led to better community integration
Neurofeedback 299
into housing, schools, and workforce, as well as reductions in depressive and anxious
symptoms, arrest rates, and relapse one year posttreatment. Nicotine dependence is the
latest substance abuse issue to be treated with neurofeedback methods. Research teams
have been investigating the use of rtfMRI to isolate and reward the modification of
brain regions associated with the processing of smoking-related information (Hartwell
et al., 2012).
Neurofeedback in Cognitive Behavioral Therapy
Neurofeedback therapy is a behavior modification strategy that can be incorporated

into cognitive behavioral therapy (CBT) and multimodal interventions for the treat-
ment of psychiatric disorders. In the context of CBT interventions, neurofeedback
works in a bottom-up fashion to address the neurophysiological components that
drive psychiatric symptoms. CBT interventions target symptoms in a top-down fash-
ion to assist participants to identify, develop, and utilize cognitive strategies that
support neurofeedback training goals. For example, neurofeedback protocols are
easily integrated into the CBT case conceptualization of adult ADHD outlined by
Ramsay and Rostain (2008). This approach focuses on the awareness of neurobio-
logical and environmental interactions, developmental experiences, cognitive schemas
and core beliefs, compensatory strategies, and situation-specific automatic thoughts,
emotions, and behaviors (Ramsay & Rostain, 2008). Prior to treatment, clinicians
address the neurobiological components of ADHD through psychoeducation, neu-
ropsychological testing, ERP protocols, and QEEG analysis to guide training and
establish a pretreatment baseline. Neurofeedback training protocols are designed to
address the specific neurobiological deficits and may utilize EEG or SCP feedback
methods. Elevated theta/beta ratios may be inhibited to promote greater executive
functioning and cortical arousal, or the enhanced differentiation of SCP shifts may be
rewarded to promote cortical flexibility and regulation of neuronal activity thresholds.
During the neurofeedback intake, clinicians investigate the developmental course and
current symptom picture of the participant, along with positive and negative cognitive
schemas and core beliefs. The impact of ADHD symptoms in the realm of work,
school, and relationships is discussed and individualized progress logs are developed
to promote and track behavioral changes.
During neurofeedback training sessions, clinicians help the participant identify
cognitive distortions that may have a negative impact on his or her training per-
formance. For example, if a participant has several successful SCP training blocks
followed by an unsuccessful training block, he or she may become frustrated or
discouraged and engage in all-or-nothing thinking (“I did terrible on this training
block. This treatment will never help me”) or overgeneralization (“I cannot expect to
stay focused in a lecture, if I cannot focus during a neurofeedback session”). These
thoughts may trigger feelings of inadequacy or physical stress, which may in turn
lead to additional session failures and/or avoidance behaviors such as arriving late to
training sessions and missing or rescheduling appointments. To prevent this outcome,
training performance should be discussed following each session in order to help the
participant identify successful and unsuccessful strategies, recognize positive training
parameters, dispute cognitive distortions and negative self-statements, and redirect

training behaviors.
Outside of training sessions, participants often have “homework” tasks to help
generalize their neurofeedback self-regulation skills. This is typically done using
DVD training simulations or wallet-sized cue cards with a picture of the training
screen. Participants are asked to practice regulating the specific training parameters or
recreating the training mental state before or during problem situations (i.e., before
lectures or meetings, while reading, during homework assignments, etc.). These
exercises may also be incorporated into CBT thought log assignments and/or behavior
activation tasks to address self-defeating behaviors such as procrastination. Once task-
specific automatic thoughts have been processed and the task has been broken down
into manageable steps, the participant is encouraged to visualize the training session
and begin the task in a focused mental state. In the event that the participant becomes
distracted or off-task, the exercise can be used as a redirection strategy.
Conclusion
This chapter provided a brief discussion of the origins of brain signal recordings,
the development of classical and operant conditioning paradigms, and the evolution
of neurofeedback therapy. Neurofeedback is the practice of providing individuals
with specific feedback of brain activity in an operant conditioning paradigm to
modify behavior, reduce disorder-specific symptoms, and enhance overall functioning.
Operant conditioning of EEG, SCPs, and BOLD signal activity has been effective
in the treatment and symptom reduction of ADHD, GAD, OCD, PTSD, major
depressive disorder, dissociative identity disorder, learning disabilities, schizophrenia,
and substance-related disorders. Neurofeedback therapy is a bottom-up approach
to symptom reduction and may be integrated into CBT protocols and multimodal
treatment plans. The information provided should give readers a solid foundation
and understanding of the various neurofeedback methods, technical requirements,
and clinical applications. The current body of work related to this noninvasive
nonpharmacological treatment is promising, but additional research and randomized
control trials are needed.
Acknowledgements
This work was supported by the Deutsche Forschungsgemeinschaft (DFG, #

BI 195/69-1) and Bundesministerium für Bildung und Forschung (BMBF, #
01GQ0831).
References
Alexander, D. M., Hermens, D. F., Keage, H. A., Clark, C. R., Williams, L. M., Kohn,
M. R., … Gordon, E. (2008). Event-related wave activity in the EEG provides new
marker of ADHD. Clinical Neurophysiology, 119, 163–179.
Neurofeedback 301
Alhambra, M. A., Fowler, T. P., & Alhambra, A. A. (1995). EEG biofeedback: A new treatment
option for ADD/ADHD. Journal of Neurotherapy, 1, 39–43.
Arns, M., de Ridder, S., Strehl, U., Breteler, M., & Coenen, A. (2009). Efficacy of neuro-
feedback treatment in ADHD: The effects on inattention, impulsivity and hyperactivity:
A meta-analysis. Clinical EEG and Neuroscience, 40, 180–189.
Baehr, E., Rosenfeld, J. P., & Baehr, R. (1997). The clinical use of an alpha asymmetry protocol
in the neurofeedback treatment of depression: Two case studies. Journal of Neurotherapy,
2, 10–23.
Baehr, E., Rosenfeld, J. P., & Baehr, R. (2001). Clinical use of an alpha asymmetry neurofeed-
back protocol in the treatment of mood disorders: Follow-up study one to five years post
therapy. Journal of Neurotherapy, 4, 11–18.
Bakhshayesh, A. R., Hansch, S., Wyschkon, A., Rezai, M. J., & Esser, G. (2011). Neurofeedback
in ADHD: A single-blind randomized controlled trial. European Child and Adolescent
Banaschewski, T., Brandeis, D., Heinrich, H., Albrecht, B., Brunner, E., & Rothenberger, A.
(2003). Association of ADHD and conduct disorder: Brain electrical evidence for the
existence of a distinct subtype. Journal of Child Psychology and Psychiatry, 44, 256–376.
Barbaresi, W., Katusic, S., Colligan, R., Weaver, A., Pankratz, V., Mrazek, D., & Jacobsen, S.
(2004). How common is attention-deficit/hyperactivity disorder? Towards resolution of
the controversy: Results from a population-based study. Acta Paediatrica Supplement,
445, 55–59.
Becerra, J., Fernandez, T., Harmony, T., Caballero, M. I., Garcia, F., Fernandez-Bouzas, A., …
Prado-Alcala, R. A. (2006). Follow-up study of learning disabled children treated with
neurofeedback or placebo. Clinical EEG & Neuroscience, 37 , 198–203.
Berger, H. (1929). Uber das Elektrenkephalogramm des Menschen, 1st report. Archiv für
Psychiatrie und Nervenkrankheiten, 87 , 527–570.
Birbaumer, N. (1999). Slow cortical potentials: Plasticity, operant control, and behavioral
effects. Neuroscientist, 5, 74–78.
Birbaumer, N., Lang, P., Cook, E., Elbert, T., Lutzenberger, W., & Rockstroh, B. (1988).
Slow brain potentials, imagery and hemispheric differences. International Journal of
Birbaumer, N., Roberts, L., Lutzenberger, W., Rockstroh, B., & Elbert, T. (1992). Area-
specific self-regulation of slow cortical potentials on the sagittal midline and its effects on
behavior. Electroencephalography and Clinical Neurophysiology, 84, 353–361.
Bodenhamer-Davis, E., & Callaway, T. G. (2004). Extended follow-up of Peniston protocol
results with chemical dependency. Journal of Neurotherapy, 8, 135.
Bolea, A. S. (2010). Neurofeedback treatment of chronic inpatient schizophrenia. Journal of
Neurotherapy, 14, 47–54.
Boyd, W. D., & Campbell, S. E. (1998). EEG biofeedback in the schools: The use of EEG
biofeedback to treat ADHD in a school setting. Journal of Neurotherapy, 2, 65–71.
Bresnahan, S. M., Anderson, J. W., & Barry, R. J. (1999). Age-related changes in quantitative
EEG in attention-deficit/hyperactivity disorder. Biological Psychiatry, 46, 1690–1697.
Bresnahan, S. M., & Barry, R. J. (2002). Specificity of quantitative EEG analysis in adults with
attention deficit hyperactivity disorder. Psychiatry Research, 112, 133–144.
Breteler, M. H., Arns, M., Peters, S., Giepmans, I., & Verhoeven, L. (2010). Improvements in
spelling after QEEG-based neurofeedback in dyslexia: A randomized controlled treatment
study. Applied Psychophysiology & Biofeedback, 35, 5–11.
Burkett, V. S., Cummins, J. M., Dickson, R. M., & Skolnick, M. (2005). An open clinical trial
utilizing real-time EEG operant conditioning as an adjunctive therapy in the treatment of
crack cocaine dependence. Journal of Neurotherapy, 9, 27–48.
Buxton, R. B., Uludağ, K., Dubowitz, D. J., & Liu, T. T. (2004). Modeling the hemodynamic
response to brain activation. Neuroimage, 23 (Suppl. 1), S220–S233.
Caton, R. (1875). The electric currents of the brain. British Medical Journal, 2, 278.
Caria, A., Sitaram, R., & Birbaumer, N. (2011). Real-time fMRI: A tool for local brain regula-
tion. Neuroscientist. Advance online publication. doi:10.1177/1073858411407205
Choi, S. W., Chi, S. E., Chung, S. Y., Kim, J. W., Ahn, C. Y., & Kim, H. T. (2011). Is alpha
wave neurofeedback effective with randomized clinical trials in depression? A pilot study.
Neuropsychobiology, 63, 43–51. doi:10.1159/000344490
Clarke, A. R., Barry, R. J., Heaven, P. C., McCarthy, R., Selikowitz, M., & Bryne, M. K.
(2008). EEG in adults with attention-deficit/hyperactivity disorder. International Journal
of Psychophysiology, 70, 173–183.
Clarke, A. R., Barry, R. J., McCarthy, R., & Selikowitz, M. (1998). EEG analysis in attention-
deficit/hyperactivity disorder: A comparative study of two subtypes. Psychiatry Research,
81, 19–29.
Congedo, M., Lubar, J. F., & Joffe, D. (2004). Low-resolution electromagnetic tomography
neurofeedback. IEEE Transactions on Neural Systems and Rehabilitation Engineering, 12,
387–397.
Connor, D. F. (2006). Stimulants. In R. A. Barkley (Ed.), Attention-deficit hyperactivity
disorder: A handbook for diagnosis and treatment (3rd ed., pp. 608–647). New York, NY:
Guilford Press.
deBues, R. (2006, May). Progress in efficacy studies of EEG biofeedback for AHD. Paper presented
at the meeting of the American Psychiatric Association, Toronto, Canada.
Dias, A. M., & van Deusen, A. (2011). A new neurofeedback protocol for depression. Spanish
Journal of Psychology, 14, 374–384.
Doehnert, M., Brandeis, D., Imhof, K., Drechsler, R., & Steinhausen, H. C. (2009). Mapping
attention-deficit/hyperactivity disorder from childhood to adolescence: No neurophysi-
ologic evidence for a developmental lag of attention but some for inhibition. Biological
Psychiatry, 67 , 608–616.
Drechsler, R., Straub, M., Doehnert, M., Heinrick, H., Steinhausen, H. C., & Brandeis, D.
(2007). Controlled evaluation of a neurofeedback training of slow cortical potentials in
children with attention deficit/hyperactivity disorder (ADHD). Behavioral and Brain
Functions, 3, 35. doi:10.1186/1744-9081-3-35
Earnest, C. (1999). Single case study of EEG asymmetry biofeedback for depression: An
independent replication in an adolescent. Journal of Neurotherapy, 3, 28–35.
Elbert, T., Rockstroh, B., Lutzenberger, W., & Birbaumer, N. (1980). Biofeedback of
slow cortical potentials. I. Electroencephalography & Clinical Neurophysiology, 48,
293–301.
Fahrion, S. L. (1995). Human potential and personal transformation. Subtle Energies, 6,
55–88.
Fahrion, S. L. (2002, February). Group biobehavioral treatment of addiction. Paper presented
at the 4th meeting on the Neurobiology of Criminal and Violent Behavior, Research
and Clinical Applications of Neurofeedback for Offender Populations with Substance Use
Disorders, Scottsdale, AZ.
Fellin, T., Halassa, M. M., Terunuma, M., Succol, F., Takano, H., Frank, M., … Haydon, P. G.
(2009). Endogenous nonneuronal modulators of synaptic transmission control cortical
slow oscillations in vivo. Proceedings of the National Academy of Sciences of the United
States of America, 106, 15037–15042.
Neurofeedback 303
Fernandez, T., Herrera, W., Harmony, T., Diaz-Comas, L., Santiago, E., Sanchez, L., …
Valdes, P. (2003). EEG and behavioral changes following neurofeedback treatment in
learning disabled children. Clinical Electroencephalography, 34, 145–150.
Fine, A. H., Goldman, L., & Sanford, J. (1994, August). Innovative techniques in the
treatment of ADHD: An analysis of the impact of EEG biofeedback training and a
cognitive computer generated training. Paper presented at the meeting of the American
Psychological Association, Los Angeles, CA.
Fleischman, M. J., & Othmer, S. (2005). Case study: Improvements in IQ score and main-
tenance of gains following EEG biofeedback with mildly developmentally delayed twins.
Journal of Neurotherapy, 9, 35–46.
Fuchs, T., Birbaumer, N., Lutzenberger, W., Gruzelier, J. H., & Kaiser, J. (2003).
Neurofeedback treatment for attention deficit/hyperactivity disorder in children: A
comparison with methylphenidate. Applied Psychophysiology and Biofeedback, 28, 1–12.
doi:10.1023/A:1022353731579
Gani, C., Birbaumer, N., & Strehl, U. (2008). Long term effects after feedback of slow cor-
tical potentials and theta-beta-amplitudes in children with attention-deficit/hyperactivity
disorder. International Journal of Bioelectromagnetics, 10, 209–323.
Gevensleben, H., Holl, B., Albrecht, B., Schlamp, D., Kratz, O., Studer, P., … Hartmut, H.
(2010). Neurofeedback training in children with ADHD: 6-month follow-up of a
randomized controlled trial. European Child and Adolescent Psychiatry, 19, 715–724.
doi:10.1007/s00787-010-0109-5
Gevensleben, H., Holl, B., Albrecht, B., Vogel C., Schlamp, D., Kratz, O., … Heinrich, H.
(2009). Is neurofeedback an efficacious treatment for ADHD? A randomized controlled
clinical trial. Journal of Child Psychology and Psychiatry, 50, 780–789.
Goodman, D. W., & Thase, M. E. (2009). Recognizing ADHD in adults with comorbid mood
disorders: Implications for identification and management. Postgraduate Medicine, 121,
20–30.
Gruzelier, J., Hardman, E., Wild, J., Zaman, R., Nagy, A., & Hirsch, S. (1999). Learned control
of interhemispheric slow potential negativity in schizophrenia. International Journal of
Psychophysiology, 34, 341–348.
Habecker, E. L., Daniels, M. A., & Renshaw, P. F. (2009). fMRI in psychiatric disorders.
In M. Filippi (Ed.), fMRI techniques and protocols (pp. 615–656). New York, NY and
London, England: Humana Press. doi:10.1007/978-1-60327-919-2_21
Hammond, D. C. (2003). QEEG-guided neurofeedback in the treatment of obsessive-
compulsive disorder. Journal of Neurotherapy, 7 , 25–52.
Hammond, D. C., Walker, J., Hoffman, D., Lubar, J. F., Trudeau, D., Gurnee, R., & Horvat, J.
(2004). Standards for the use of quantitative electroencephalography (QEEG) in neuro-
feedback: A position paper of the International Society for Neuronal Regulation. Journal
of Neurotherapy, 8, 5–27.
Hampson, M., Stocia, T., Saksa, J., Scheinost, D., Qiu, M., Bhawnani, J., … Constable, T.
(2012). Real-time fMRI biofeedback targeting the orbitofrontal cortex for contamination
anxiety. Journal of Visualized Experiments, 59. doi:10.3791/3535
Hartwell, K. J., Prosciandaro, J. J., Borckardt, J., Li, X., George, M. S., & Brady, K. T.
(2012). Real-time fMRI in the treatment of nicotine dependence: A conceptual
review and pilot studies. Psychology of Addictive Behaviors. Advance online publication.
doi:10.1037/a0028215
Heinrich, H., Gevensleben, H., Freisleder, F. J., Moll, G. H., & Rothenberger, A. (2004).
Training of slow cortical potentials in ADHD: Evidence for positive behavioral and
neurophysiological effects. Biological Psychiatry, 55, 772–775.
Heywood, C., & Beale, I. (2003). EEG biofeedback vs. placebo treatment for attention-
deficit/hyperactivity disorder: A pilot study. Journal of Attention Disorders, 7 , 43–55.
doi:10.1177/108705470300700105
Hodgson, K., Hutchinson, A. D., & Denson, L. (2012). Nonpharmacological treatments
for ADHD: A meta-analytic review. Journal of Attention Disorders. Advance online
publication.
Holtmann, M., Grasmann, D., Cionek-Szpak, E., Hager, V., Panzer, N., Beyer, A., & Stadler, C.
(2009). Specific effects of neurofeedback on impulsivity in ADHD. Kindheit und Etwick-
lung, 18, 95–104.
Jain, U., Hechtman, L., Weiss, M., Ahmed, T. S., Reiz, J. L., Donnelly, G. A., … Darke, A. C.
(2007). Efficacy of a novel biphasic controlled-released methylphenidate formula in adults
with attention-deficit/hyperactivity disorder: Results of a double blind, placebo-controlled
crossover study. Journal of Clinical Psychiatry, 68, 268–277.
Johnstone, S. J., Barry, R. J., & Anderson, J. W. (2001). Topographic distribution and
development time course of auditory event-related potentials in two subtypes of attention
hyperactivity disorder. International Journal of Psychophysiology, 42, 73–94.
Kaiser, D. A., & Othmer, S. (2000). Effect of neurofeedback on variables of attention in a large
multi-center trial. Journal of Neurotherapy, 4, 5–15.
Kamiya, J. (1971). Biofeedback training in voluntary control of EEG alpha rhythms. California
Medicine, 115, 44.
Kanoh, S., Murayama, Y. M., Miyamoto, K., Yoshinobu, T., & Kawashima, R. (2009). A
NIRS-based brain-computer interface system during motor imagery: System development
and online feedback training. Conference proceedings: Annual International Conference of
the IEEE Engineering in Medicine and Biology Society, 594–597.
Kelly, M. J. (1997). Native Americans, neurofeedback, and substance abuse theory: Three year
outcome of alpha/theta neurofeedback training in the treatment of problem drinking
among Dine (Navajo) people. Journal of Neurotherapy, 2, 24–60.
Kerson, C., Sherman, R. A., & Kozlowski, G. P. (2009). Alpha suppression and sym-
metry training for generalized anxiety symptoms. Journal of Neurotherapy, 13,
146–155.
Koehler, S., Lauer, P., Schreppel, T., Jacob, C., Heine, M., Boreatti-Hummer, A., …
Herrmann, M. J. (2009). Increased EEG power density in alpha and theta bands in
adult ADHD patients. Journal of Neural Transmission, 116, 97–104.
Kropotov, J. D., Grin-Yastenko, V. A., Pomarev, V. A., Chutko, L. S., Yakovenko, E. A., &
Nikishene, I. S. (2005). ERP correlates of EEG relative beta training in ADHD children.
International Journal of Psychophysiology, 55, 23–34.
Kübler, A., Kotchoubey, B., Hinterberger, T., Ghanayim, N., Perelmouter, J., Schauer, M., …
Birbaumer, N. (1999). The thought translation device: A neurophysiological approach to
communication in total motor paralysis. Experimental Brain Research, 124, 223–232.
Kübler, A., Neumann, N., Kaiser, J., Kotchoubey, B., Hinterberger, T., & Birbaumer, N. P.
(2001). Brain-computer communication: Self-regulation of slow cortical potentials for
verbal communication. Archives of Physical Medicine and Rehabilitation, 82, 1533–1539.
Lansbergen, M. M., Van Dongen-Boomsma, M., Buitelaar, J. K., & Slaats-Willemse, D.
(2011). ADHD and EEG-neurofeedback: A double-blind randomized placebo controlled
feasibility study. Journal of Neurotransmission, 118, 275–284.
Lee, J. A., Kim, B. N., Hang, E., Lee, D. S., Kim, Y. K., Chung, J. K, … Cho, S. C. (2005).
Regional cerebral blood flow in children with attention deficit hyperactivity disorder:
Comparison before and after methylphenidate treatment. Human Brain Mapping, 24,
157–164.
Neurofeedback 305
Leins, U., Goth, G., Hinterberger, T., Klinger, C., Rumpf, N., & Strehl, U. (2007). Neu-
rofeedback for children with ADHD: A comparison of SCP and theta/beta protocols.
Applied Psychophysiology and Biofeedback, 24, 213–233.
Levesque, J., Beauregard, M., & Mensour, B. (2006). Effects of neurofeedback training on
the neural substrates of selective attention in children with attention-deficit/hyperactivity
disorder: A functional magnetic imaging study. Neuroscience Letters, 394, 216–221.
Linden, M., Habib, T., & Radojevic, V. (1996). A controlled study of the effects of EEG
biofeedback on cognition and behavior of children with attention deficit disorders and
learning disabilities. Biofeedback and Self-Regulation, 21, 35–49.
Lofthouse, N., Arnold, L. E., Hersch, S., Hurt, E., & DeBeus, R. (2012). A review of neuro-
feedback treatment for pediatric ADHD. Journal of Attention Disorders, 16, 351–372.
Logothetis, N. K. (2002). The neural basis of the blood-oxygen-level-dependent functional
magnetic resonance imaging signal. Philosophical Transactions of the Royal Society of
London. Series B: Biological Sciences, 357 , 1003–1037.
Lopes da Silva, F. (1991). Neural mechanism underlying brain waves: From neural membranes
to networks. Electroencephalography and Clinical Neurophysiology, 79, 81–93.
Lubar, J. F., & Shouse, M. N. (1976). EEG and behavioral changes in a hyperkinetic child
concurrent with training of sensorimotor rhythm (SMR): A preliminary report. Biofeedback
and Self-Regulation, 1, 293–306.
Lubar, J. F., Swartwood, M. O., Swartwood, J. N., & O’Donnell, P. H. (1995). Evaluation
of the effectiveness of EEG neurofeedback training for ADHD in a clinical setting as
measured by changes in TOVA scores, behavioral rating, and WISC-R performance.
Biofeedback & Self-Regulation, 20, 83–99.
Lubar, J. O., & Lubar, J. F. (1984). Electroencephalographic biofeedback of SMR and
beta for treatment of attention deficit disorders in a clinical setting. Biofeedback and
Lutzenberger, W., Birbaumer, N., & Steinmetz, P. (1976). Simultaneous biofeedback of heart
rate and frontal EMG as pretraining for the control of EEG theta activity. Biofeedback
Manchester, C., Allen, T., & Tachiki, K. H. (1998). Treatment of dissociative identity disorder
with neurotherapy and group self-exploration. Journal of Neurotherapy, 5, 33–44.
Mann, C. A., Lubar, J. F., Zimmerman, A. W., Miller, C. A., & Muenchen, R. A. (1992). Quan-
titative analysis of EEG in boys with attention-deficit-hyperactivity disorder: Controlled
study with clinical implications. Pediatric Neurology, 8, 30–36.
Mayer, K., Wyckoff, S., Schulz, U., & Strehl, U. (2012). Neurofeedback for
adult attention-deficit/hyperactivity disorder: Investigation of slow cortical poten-
tial neurofeedback: Preliminary results. Journal of Neurotherapy, 16, 37–45.
doi:10.1080/10874208.2012.650113
McGrady, A., Prodente, C., Fine, T., & Donlin, J. (2007, February). Neurofeedback in children
with behavioral and emotional problems. Paper presented at the annual meeting of the
Association for Applied Psychophysiology & Biofeedback, Monterey, CA.
Mills, G. K., & Solyom, L. (1974). Biofeedback of EEG alpha in the treatment of obsessive
ruminations: An exploration. Journal of Behavioral Therapy and Experimental Psychiatry,
5, 37–41.
Monastra, V. J., & Lubar, J. F. (2001). The development of a quantitative electroencephalog-
raphy scanning process for attention deficit-hyperactivity: Reliability and validity studies.
Neurophysiology, 15, 136–144.
Monastra, V. J., Lubar, J. F., Linden, M., VanDeusen, P., Green, G., Wing, W., … Fenger, T. N.
(1999). Assessing attention deficit attention-deficit/hyperactivity disorder via quantitative
electroencephalography. Neurophysiology, 13, 424–433.
Monastra, V. J., Monastra, D. M., & George, S. (2002). The effects of stimulant ther-
apy, EEG biofeedback, and parenting style on the primary symptoms of attention-
deficit/hyperactivity disorder. Applied Psychophysiology and Biofeedback, 27 , 231–249.
Moore, N. (2005). The neurotherapy of anxiety disorders. Journal of Adult Development, 12,
147–154. doi:10.1007/s10804-005-7031-y
Nair, R., & Moss, S. B. (2009). Management of attention-deficit hyperactivity disorder in
adults: Focus on methylphenidate hydrochloride. Neuropsychiatric Disease and Treatment,
5, 421–431.
Negoro, H., Sawada, M., Lita, J., Ota, T., Tanka, S., & Kishimoto, T. (2010). Prefrontal
dysfunction in attention-deficit/hyperactivity disorder as measured by near-infrared spec-
troscopy. Child Psychiatry and Human Development, 41, 193–203.
Orlandi, M. A., & Greco, D. (2004, August). A randomized, double-blind clinical trial of EEG
neurofeedback treatment for attention-deficit/hyperactivity disorder. Paper presented at the
meeting of the International Society for Neuronal Regulation, Fort Lauderdale, FL.
Orlando, P. C., & Rivera, R. O. (2004). Neurofeedback for elementary students with identified
learning problems. Journal of Neurotherapy, 8, 5–19.
Palsson, O. S., Pope, A. T., Ball, J. D., Turner, M. J., Nevin, S., & deBeus, R. (2001,
March). Neurofeedback videogame ADHD technology: Results of the first concept study.
Paper presented at the annual meeting of the Association for Applied Psychophysiology
& Biofeedback, Research Triangle Park, NC.
Passini, F. T., Watson, C. G., Dehnel, L., Herder, J., & Watkins, B. (1977). Alpha wave
biofeedback training therapy in alcoholics. Journal of Clinical Psychology, 33, 292–299.
Pavlov, I. P. (1927). Conditioned reflexes: An investigation of the physiological activity of the
cerebral cortex (G. V. Anrep, Ed. & Trans.). London, England: Oxford University Press.
Peniston, E. G., & Kulkosky, P. J. (1989). Alpha-theta brainwave training and beta endor-
phin levels in alcoholics. Alcoholism: Clinical and Experimental Results, 13, 271–279.
doi:10.1111/j.1530-0277.1989.tb00325.x
Peniston, E. G., & Kulkosky, P. J. (1991). Alpha-theta brainwave neurofeedback
therapy for Vietnam veterans with combat-related posttraumatic stress disor-
der. Medical Psychotherapy: An International Journal, 4, 47–60. Retrieved from
http://www.neurodynamic.info/uploads/Peniston_2_1_.pdf
Perreau-Linck, E., Lessard, N., Levesque, J., & Beauregard, M. (2010). Effects of neuro-
feedback training on inhibitory capacities in ADHD children: A single blind randomized
placebo-controlled study. Journal of Neurotherapy, 14, 229–242.
Picard, C., Moreau, G., Guay, M. C., & Achim, A. (2006, September). Double double-blind
sham study of neurofeedback treatment in children with ADHD. Paper presented at the
meeting of the International Society for Neurofeedback and Research, Atlanta, GA.
Prox, V., Dietrich, D. E., Zhang, Y., Emrich, H. M., & Ohlmeier, M. D. (2007). Attentional
processing in adults with ADHD as reflected by event-related potentials. Neuroscience
Letters, 419, 236–241.
Ramsay, J. R., & Rostain, A. L. (2008). Cognitive-behavioral therapy for adult ADHD: An
integrative psychosocial and medical approach. New York, NY: Taylor & Francis.
Rice, K. M., Blanchard, E. B., & Purcell, M. (1993). Biofeedback treatments of generalized
anxiety disorder: Preliminary results. Biofeedback and Self-Regulation, 18, 93–105.
Rockstroh, B., Elbert, T., Birbaumer, N., & Lutzenberger, W. (1990) Biofeedback-produced
hemispheric asymmetry of slow cortical potentials and its behavioral effects. International
Journal of Psychophysiology, 9, 151–165.
Rockstroh, B., Elbert, T., Lutzenberger, W., & Birbaumer, N. (1990) Biofeedback: Evaluation
and therapy in children with attentional dysfunctions. In A. Rothenberger (Ed.), Brain
and behavior in child psychiatry (pp. 345–355). Berlin, Germany: Springer.
Neurofeedback 307
Rosenfeld, J. P., Baehr, E., Baehr, R., Gotlib, I. H., & Ranganath, C. (1996). Preliminary
evidence that delay changes in frontal asymmetry correlate with changes in affect in
therapy sessions. International Journal of Psychophysiology, 23, 137–141.
Rossiter, T. (2005). The effectiveness of neurofeedback and stimulant drugs in treating
AD/HD: Part II. Replication. Applied Psychophysiology & Biofeedback, 29, 233–243.
Rossiter, T. R., & La Vaque, T. J. (1995). A comparison of EEG biofeedback and psychos-
timulants in treating attention deficit/hyperactivity disorders. Journal of Neurotherapy, 1,
48–59.
Ruiz, S., Lee, S., Soekadar, S. R., Caria, A., Veit, R., Kircher, T., … Sitaram, R. (2011).
Acquired self-control of insula cortex modulates emotion recognition and brain network
connectivity in schizophrenia. Human Brain Mapping. Advance online publication.
doi:10.1002/hbm.21427
Sartory, G., Heine, A., Mueller, B. W., & Elvermann-Hallner, A. (2002). Event-
and motor-related potentials during the continuous performance task in attention-
deficit/hyperactivity disorder. Journal of Psychophysiology, 16, 97–106.
Satterfield, J. H., Schell, A. M., & Nicholas, T. (1994). Preferential neural processing of
attended stimuli in attention deficit hyperactivity disorder and normal boys. Psychophysiol-
ogy, 31, 1–10.
Saxby, E., & Peniston, E. G. (1995). Alpha-theta brainwave neurofeedback training: An
effective treatment for male and female alcoholics with depressive symptoms. Journal of
Schneider, F., Elbert, T., Heimann, H., Welker, A., Stetter, F., Mattes, R., … Mann, K. (1993).
Biofeedback & Self-Regulation, 18, 23–32.
Schneider, F., Rockstroh, B., Heinmann, H., Lutzenberger, W., Mattes, R., Elbert, T., …
Bartels, M. (1992). Self-regulation of slow cortical potentials in psychiatric patients:
Schizophrenia. Biofeedback and Self-Regulation, 17 , 277–292.
Scott, W., Kaiser, D., Othmer, S., & Sideroff, S. I. (2005). Effects of an EEG biofeedback
protocol on a mixed substance abusing population. American Journal of Drug and Alcohol
Abuse, 31, 455–469.
Sherlin, L. H. (2009). Diagnosing and treating brain function through the use of low resolution
brain electromagnetic tomography (LORETA). In T. H. Budzynski, H. K. Budzynski,
J. R. Evens, & A. Abarbanel (Eds.), Introduction to quantitative EEG and neurofeedback:
Advanced theory and applications (2nd ed., pp. 83–102). Oxford, England: Elsevier.
Sherlin, L. H., Arns, M., Lubar, J., Heinrich, H., Kerson, C., Strehl, U., & Sterman, M. B.
(2011). Neurofeedback and basic learning theory: Implications for research and practice.
Journal of Neurotherapy, 15, 292–304.
Shmuel, A., Augath, M., Oeltermann, A., & Logothetis, N. K. (2006). Negative functional
MRI response correlates with decreases in neuronal activity in monkey visual area V1.
Nature Neuroscience, 9, 569–577.
Shouse, M. N., & Lubar, J. F. (1979). Operant conditioning of EEG rhythms and Ritalin in
the treatment of hyperkinesias. Biofeedback & Self-Regulation, 4, 299–311.
Sitaram, R., Caria, A., & Birbaumer, N. (2009). Hemodynamic brain-computer interfaces for
communication and rehabilitation. Neural Networks, 22, 1320–1238.
Sitaram, R., Lee, S., Ruiz, S., Rana, M., Veit, R., & Birbaumer, N. (2011). Real-time support
vector classification and feedback of multiple emotional states. Neuroimage, 56, 753–765.
Skinner, B. F. (1953). Science and human behavior. New York, NY: Free Press.
Sokhadze, E. M., Cannon, R. L., & Trudeau, D. L. (2008). EEG biofeedback as a treatment
for substance use disorders: Review, rating of efficacy, and recommendations for further
research. Applied Psychophysiology & Biofeedback, 33, 1–28.
Speckmann, E. J., & Elger, C. E. (1999). Introduction to the neurophysiological basis of

the EEG and DC potentials. In E. Niedermeyer & F. Lopes da Silva (Eds.), Electroen-
cephalography: Basic principles, clinical applications, and related fields (4th ed., pp. 13–27).
Baltimore, MD: Williams & Wilkins.
Steriade, M., Gloor, P., Llinás, R. R., Lopes da Silva, F., & Mesulam, M. M. (1990).
Basic mechanisms of cerebral rhythmic activities. Electroencephalography and Clinical
Neurophysiology, 76, 481–508.
Sterman, M. B. (2000). Basic concepts and clinical findings in the treatment of seizure disorders
with EEG operant conditioning. Clinical Electroencephalography, 31, 45–55.
Strehl, U. (2009). Slow cortical potentials neurofeedback. Journal of Neurotherapy, 13,
117–126. doi:10.1080/10874200902885936
Strehl, U., Leins, U., Goth, G., Klinger, C., & Birbaumer, N. (2006). Physiological regulation
of slow cortical potentials: A new treatment for children with ADHD. Pediatrics, 118,
1530–1540.
Sürmeli, T., & Ertem, A. (2007). EEG neurofeedback treatment of patients with Down
syndrome. Journal of Neurotherapy, 11, 63–68.
Sürmeli, T., & Ertem, A. (2011). Obsessive-compulsive disorder and the efficacy of qEEG-
guided neurofeedback treatment: A case series. Clinical EEG and Neuroscience, 42,
195–201.
Tansey, M. A. (1984). EEG sensorimotor rhythm biofeedback training: Some effects on the
neurological precursors of learning disabilities. International Journal of Psychophysiology,
3, 85–89.
Tansey, M. A. (1991). Wechsler (WISC-R) changes following treatment of learning disabilities
via EEG biofeedback in a private practice setting. Australian Journal of Psychology, 43,
147–153.
Thatcher, R. W. (2008, April). Z-score EEG biofeedback: Conceptual foundations. Neuro-
Connections Newsletter, pp. 9, 11, 20.
Thatcher, R. W., & Lubar, J. F. (2009). History of the scientific standards of QEEG normative
databases. In T. Budzinsky, H. Budzinsky, J. Evans, & A. Abarbanel (Eds.), Introduction
to QEEG and neurofeedback: Advanced theory and applications (2nd ed., pp. 29–59).
New York, NY: Elsevier.
Thomas, J. E., & Sattlberger, B. A. (1997). Treatment of chronic anxiety disorder with
neurotherapy: A case study. Journal of Neurotherapy, 2, 14–19.
Thompson, L., & Thompson, M. (1998). Neurofeedback combined with training in metacog-
nitive strategies: Effectiveness in students with ADD. Applied Psychophysiology and
Biofeedback, 23, 243–263.
Toomim, H., Mize, W., Kwong, P. C., Toomim, M., Marsh, R., Kozlowski, G. P., …
Remond, A. (2004). Intentional increase of cerebral blood oxygenation using hemoen-
cephalography (HEG). Journal of Neurotherapy, 8, 5–31.
Torgeren, T., Gjervan, B., & Rasmussen, K. (2008). Treatment of adult ADHD: Is current
knowledge useful to clinicians? Neuropsychiatric Disease and Treatment, 4, 177–186.
Urichuk, L., Hnatko, G., Baydala, L. Wilkman, E., Hoover, H. J., Vohra, S., & Schachter, H.
(2009, September). Neurofeedback treatment of ADHD: A feasibility study. Paper pre-
sented at the meeting of the Canadian Psychiatry Association, St John’s, Canada.
Vanathy, S., Sharma, P. S. V. N., & Kumar, K. B. (1998). The efficacy of alpha and theta
neurofeedback training in treatment of generalized anxiety disorder. Indian Journal of
Vidal-Estrada, R., Bosch-Munso, R., Noqueira-Moralis, M., Casas-Bruque, M., & Ramos-
Quiroqa, J. A. (2012). Psychological treatment of attention deficit hyperactivity disorder
in adults: A systematic review. Actas Espanolas de Psiquiatria, 40, 147–154.
Neurofeedback 309
Watson, B. W., Woolley-Hart, A., & Timmons, B. H. (1979). Biofeedback instruments for the
management of anxiety and for relaxation training. Journal of Biomedical Engineering, 1,
58–62.
Watson, C. G., & Herder, J. (1980). Effectiveness of alpha biofeedback therapy: Negative
results. Journal of Clinical Psychology, 36, 508–513.
Wolpaw, J. R., Birbaumer, N., McFarland, D. J., Pfurtscheller, G., & Vaughan, T. M. (2002).
Brain-computer interfaces for communication and control. Clinical Neurophysiology, 113,
767–791.
Xiong, Z., Shi, S., & Xu, H. (2005). Controlled study of the effectiveness of EEG biofeedback
training on children with attention deficit hyperactivity disorder. Journal of Huazhong
University of Science and Technology, 25, 368–370.
14
Homework Assignments and
Self-Monitoring
Nikolaos Kazantzis
La Trobe University, Australia
Frank M. Dattilio
Amy Cummins and Xavier Clayton

La Trobe University, Australia
Introduction
Aaron T. Beck’s (1976) model of psychopathology centers on the role of dysfunctional

cognition in understanding emotional distress and impaired behavior. The theory is
extended to the practice of cognitive therapy, now commonly referred to as cognitive
behavior therapy (CBT), in which therapeutic interventions are aimed at helping
patients change the content and process of their thinking, including the ability to
question, evaluate, and gain distance from thoughts and to develop flexibility in
their beliefs, rules, and assumptions (A. T. Beck, Rush, Shaw, & Emery, 1979).
These cognitive skills enable patients to truly engage with each moment and maintain
a present focus even during situations that are upsetting or otherwise emotionally
challenging. Extensive research has demonstrated the effectiveness of CBT for helping
individuals with a wide variety of mental health conditions to lead more fulfilling lives
(A. T. Beck & Dozois, 2011). The application of A. T. Beck’s model in CBT requires
a great emphasis on the manner in which the therapist interacts with the patient
(J. S. Beck, 2005; Kazantzis, J. S. Beck, Dattilio, Dobson, & Rapee, in press;
Leahy, 2001). Patients’ cognitions are central to understanding their engagement
in the therapeutic process, their view of the therapist, their expectations regarding
the outcome of therapy, and their engagement with therapeutic techniques between
sessions. Of course, it would be misleading to suggest that cognitions are the sole
focus of clinical attention in CBT. Cognitive change is also achieved via the acquisition

DOI: 10.1002/9781118528563.wbcbt14
of emotional, behavioral, and physiologically focused skills in CBT (Dobson, 2010).

The point is that the same patient cognitions that contribute to the development
and maintenance of psychopathology are present in the patient’s view of the therapy
process.
Homework assignments have been considered crucial to the practice of CBT
because they serve to strengthen gains made from one session to the next (A. T. Beck
et al., 1979; J. S. Beck & Tompkins, 2007). Extending from the initial work with
mood disorders (A. T. Beck et al., 1979), homework is now routinely incorporated
in CBT formulations for a variety of clinical conditions, including, but not limited to,
generalized anxiety disorder (Barlow, Esler, & Vitali, 1998; M. G. Newman et al.,
2011; Wetherell, Gatz, & Craske, 2003), posttraumatic stress disorder (Felmingham
& Bryant, 2012; Resick, Williams, Suvak, Monson, & Gradus, 2012), panic disorder
(Barlow et al., 1998; Gloster et al., 2011; Vincelli et al., 2003), obsessive-compulsive
disorder (Simpson et al., 2011), borderline personality disorder (Linehan, 1993), and
relapse prevention for alcohol abuse and dependence (Dimeff & Marlatt, 1995).
What Is Homework, and What Is Homework Not?
Stemming from the educational model, the extension of therapy to the everyday
situations in which the patients’ problems exist reflects a basic principle of learning
and skill acquisition, namely, that practice is important for learning (Kazantzis, Arntz,
Borkovec, Holmes, & Wade, 2010). Psychotherapeutic homework assignments can
encompass a broad range of creative activities or tasks (Lambert, Harmon, & Slade,
2007). In the treatment of CBT for depression, for example, a range of potential
homework assignments are frequently assigned and often include self-monitoring
sheets, behavioral activation schedules, arousal reduction, and the use of thought
records (Thase & Callan, 2006).
We can define therapeutic homework as therapeutic activities completed between
consultation sessions, which are collaboratively designed by the therapist and
patient to assist with progress toward therapeutic goals (A. T. Beck et al., 1979;
J. S. Beck, 2011). However, homework is much more than that. It is also an impor-
tant relational process that draws upon the patient’s and therapist’s efforts to work as
a collaborative team to devise empirical tests of the patient’s experience (i.e., through
monitoring; see Dattilio & Hanna, 2012). It is through this unique experimentation
with specific techniques and ways of relating that change takes place (Kazantzis,
Petrik, & Cummins, 2012).
Socializing Patients to Homework
One of the challenges for the practitioner in socializing patients during the early
phase of CBT is to communicate the learning principle clearly. Homework can be
introduced through the notion of “self-practice,” “self-therapy,” or “experiments,”
and by distinguishing this from one’s recollection of school homework, which is
graded on a pass/fail basis and usually is assigned by a teacher without input
Homework Assignments and Self-Monitoring 313
from the student (Kazantzis, 2011). If we are practicing CBT in a manner true
to the tenets of collaborative empiricism, any result is useful since it provides
important information about the patients’ problems and represents “data” for the
case formulation. In essence, it becomes “grist for the therapeutic mill.” Moreover,
unlike school homework, CBT assignments are not unilaterally assigned, but rather
result from a collaboration between therapist and patient, and ultimately the patient
may design his or her own tasks. Thus, our first recommendation is that practitioners
avoid using the term “homework” with patients. We advocate for a discussion of
the patient’s previously rewarding learning experiences, and use their language and
metaphors about learning to convey the importance of therapeutic homework.
As patients practice therapeutic techniques and find them helpful, they can apply
them in different ways to other aspects of their lives. Some patients quickly adapt the
homework, or take its central elements or gist, and apply it in a totally unique way. In
order for CBT to be helpful to patients in the long term, it should encourage a level
of adaptation and generalization with therapeutic assignments in the short term.
As one example, John developed skills in monitoring his pleasure and sense of
accomplishment through the day, as part of his initial therapeutic work on depression.
He found it helpful to ask himself, “What is my level of sadness in this situation?” and
“How high is my feeling of contentment right now?” This was something that he
practiced throughout the course of his therapy. Ideally, we want our patients to take
the techniques that they find helpful in therapy, and embrace them as a part of their
daily thinking (i.e., to develop complex reasoning about the application of techniques;
Kazantzis & Daniel, 2009). In this way, the skills honed through homework practice
become a part of the fabric of their general skill base and contribute to their overall
well-being. Thus, when socializing patients to CBT, it is important to convey that
homework tasks are an extension of the in-session work which will ultimately support
patients in maintaining their well-being long after they conclude therapy.
Managing Therapist Expectations and Reactions
One challenge for practitioners is that most patients, at least sometimes, do not
engage with their therapeutic homework assignments. A larger problem, however,
and one that stems from the same source, involves therapists’ expectations of their
patients. When we adopt the medical model, we expect our patients to “adhere” or
“comply” with homework as planned, and these notions fall short of capturing the
complexity of everyday clinical practice, because many patients benefit from partially
completed homework, and some patients can complete more homework than was
discussed, but only derive a small benefit. A more useful way of evaluating patients’
between-session therapeutic work is to consider the practical difficulty of the task,
the situational obstacles to its completion, and the degree of skill gained from the
actual activity (Fehm & Mrose, 2008; Schmidt & Woolaway-Bickel, 2000; Simpson
et al., 2010; Simpson et al., 2011; Westra & Dozois, 2006). These considerations
form a broader concept of engagement which, when adopted in place of achieving
compliance, helps therapists to manage their own expectations about what is possible
for patients. If a patient has not engaged with the homework, or is only partially
engaged, the therapist should focus on the quality of the work done and the learning
that has resulted, being sure to frame all attempts as successes and connecting their
verbal praise with work done.
Sophie, an experienced cognitive therapist, often experiences disappointment with
her patients’ lack of homework completion, despite doing everything that is requested
of her as a therapist. She often feels annoyed when she hears the excuse, “I forgot.”
When therapists are asked for “adaptive therapist emotions and attitudes” in the
use of therapeutic homework during professional workshops on enhancing the use
of homework in CBT, the list usually comes sluggishly—“enthusiasm,” “empathy,”
and “patience.” These adjectives are among the most commonly identified adaptive
experiences. Yet, when therapists are asked what they would hypothesize to be the
most commonly identified experiences among CBT practitioners, they produce a much
different list: “anger,” “frustration,” “annoyance,” “disappointment,” “anxiety,”
“guilt.” Such lists have been remarkably consistent among different practitioner
groups in many different countries. Homework noncompliance is a problem for the
practice of CBT worldwide, for several reasons it seems.
As a self-reflection exercise, it may be helpful to think of a recent experience of
a patient who did not engage with a therapeutic homework task. What emotion did
you feel? And as you had that emotion, what went through your mind? What did this
experience mean to you as a clinician?
Despite the potential for such experiences, there are also CBT practitioners who
say that they love the role of homework in therapy. They practice creatively, and see
the integration of homework as just another expression of their ability to fuse the
process of case conceptualization with the specific technique or treatment strategy in
a manner suitable for the particular patient sitting in their consultation room. Such
practitioners could not imagine using CBT without homework and would consider it
foolish to do so. As it turns out, they are right.
The State of Empirical Evidence for Therapeutic Homework
Homework assignments have been investigated more than any other therapeutic
process in CBT (Persons, Davidson, & Tompkins, 2000), and their effects have
been evaluated in several ways. One group of studies contrasted therapy conditions
with and without the use of homework assignments and compared their therapeutic
outcomes, generally operationalized as symptom reduction. Interestingly, only some
of these studies have demonstrated an advantage for the “homework” conditions
when reviewing the findings at the conventional p < .05 criterion for statistical
significance, which led many researchers through the 1980s and 1990s to debate the
necessity of homework in CBT (e.g., Zettle & Hayes, 1987). However, the advent
of quantitative review methods afforded some clarification. It turns out that these
studies had low statistical power (a 58% chance of detecting a large effect size, a 32%
chance of detecting a medium effect size, and only a 9% chance of detecting a small
effect size; see Kazantzis, 2000).
Meta-analyses also confirmed that when all the studies were aggregated and
analyzed, the difference in outcome between “homework” and “no-homework”
conditions was actually substantial (d = 0.77 in Kazantzis, Deane, & Ronan, 2000;
and d = 0.63 in Kazantzis, Whittington, & Dattilio, 2010). To interpret the more
conservative effect size of 0.63, this would mean that if we were to randomly assign
200 patients to comparable therapy conditions, with 100 assigned to therapy with
homework, and 100 to therapy without homework, we would expect 63% and 37%
of patients to improve, respectively. (This calculation is based on Rosenthal’s [1991]
binomial effect size display, but see McGraw, 1991, for its limitations.)
Research has also addressed the questions: “Do practitioners actually use home-
work, and if so, what do they think of it?” These are important questions as there may
be many barriers to the implementation of the evidence base (Garland, Brookman-
Frazee, & Chavira, 2010). Surveys among practitioners in Australia (Deane, Glaser,
Oades, & Kazantzis, 2005), Canada (Carroll, Nich, & Ball, 2005), Germany (Fehm &
Kazantzis, 2004; Helbig & Fehm, 2004), New Zealand (Kazantzis, Busch, Ronan, &
Merrick, 2007; Kazantzis & Deane, 1999), and the United States (Kazantzis,
Lampropoulos, & Deane, 2005) have found that the majority of practitioners surveyed
reported that therapeutic homework was “generally” or “almost always” incorporated
into their therapy sessions. Interestingly, the use of between-session therapeutic tasks
has been reported among those identifying a range of theoretical orientations. For
example, Kazantzis et al. (2005) found that in a diverse sample of psychologists,
comprised of individuals who identified their primary orientation as CBT (39%) or
psychodynamic/analytic (24%), a high proportion (68%) reported regular homework
use. The proposition that homework assignments are now incorporated into a range
of different therapies is not limited to these data. Experts from a range of therapeutic
approaches have outlined how homework facilitates change mechanisms in, among
others, acceptance and commitment therapy (Twohig, Pierson, & Hayes, 2007),
behavior therapy (Ledley & Huppert, 2007), brief strategic family therapy (Robbins,
Szapocznik, & Pe’rez, 2007), client-centered therapy (Witty, 2007), cognitive ther-
apy (J. S. Beck & Tompkins, 2007), emotion-focused experiential therapy (Ellison &
Greenberg, 2007), interpersonal psychotherapy (Young & Mufson, 2007),
personal construct therapy (Neimeyer & Winter, 2007), and psychodynamic therapy
(Stricker, 2007).
Another branch of the empirical literature has sought to explore a closely
related, but different, research question: “Is there a positive correlation between
patient homework ‘compliance’ and treatment outcome?” Answering this research
question in the affirmative provides us with valuable information about the relation
(or association) between the two variables, but does not enable us to ascertain the
direction of causality (Kaplan & Saccuzzo, 2008). Compliance with homework may
lead to symptom reduction, but it is equally plausible that symptom reduction may
encourage greater compliance with homework. There has been some confusion about
what constitutes a causal effect in this research area. For example, Burns and Spangler
(2000) reported that homework compliance had a causal effect on treatment out-
come, based on an application of structural equation modeling (SEM) to examine the
correlation between homework compliance and symptom reduction in the treatment
of depression. As Kazantzis, Ronan, and Deane (2001) noted, although this is an
exceptional illustration of the utility of SEM, these data were unable to demonstrate
that homework compliance caused symptom reduction. Prospective, experimental

research remains the gold standard for determining causality (Urbina, 2004).
The relationship between homework compliance and treatment outcome
has been examined in the context of CBT for depression (Addis & Jacobson,
2000; Brothers, Yang, Strunk, & Anderson, 2011; Coon & Thompson, 2003;
Cowan et al., 2008; Neimeyer, Kazantzis, Kassler, Baker, & Fletcher, 2008;
Startup & Edmonds, 1994), anxiety-related disorders (Hughes & Kendall, 2007;
M. G. Newman et al., 2011; Westra, Dozois, & Marcus, 2007; Woods, Chambless, &
Steketee, 2002), substance use (Carroll et al., 2005; Gonzalez, Schmitz, & DeLaune,
2006; Witkiewitz & Bowen, 2010), psychotic symptoms (Dunn, Morrison, &
Bentall, 2002), hoarding (Tolin, Frost, & Steketee, 2007), and body image distress
(Cash & Hrabosky, 2003; McMillan, Stice & Rohde, 2011), and is perhaps the
most frequently explored research question. This research question has also been
investigated in other forms of cognitive therapy, such as mindfulness-based cognitive
therapy as a relapse prevention strategy for depression (Murphy & Lahtinen, 2011).
Surprisingly, three quantitative reviews have shown that the association between
compliance and symptom change is small, in the vicinity of r = .22 (Beutler, Malik,
Talebi, Fleming, & Moleiro, 2004; Kazantzis et al., 2000; Mausbach, Moore, Roesch,
Cardenas, & Patterson, 2010). This finding makes little sense in the context of a
medium effect size resulting from studies that compare therapy with and without
homework. It makes little sense unless we consider one thing—that compliance is not
always the most important construct of interest.
If we can dispense with the word “compliance,” perhaps the term “engage-
ment” would be a less pejorative term that more obviously incorporates a notion of
continuum. Engagement can happen to a lesser or greater extent, whereas one is
either “compliant” or “not.” This all-or-nothing polarized view of patient homework
behavior is a likely culprit for the therapist’s negative emotions identified above.
Engagement also allows for the possibility that the activity itself may pose some
challenge. This is certainly the case with therapeutic homework assignments, as they
are often emotionally charged and are technically/skillfully challenging tasks that
require some amount of deliberate effort. Engagement also allows for the reality that
change happens constantly, and that environments/situations are therefore difficult
to predict. In the example below, Janine and her therapist discuss the experience of
carrying out her behavioral experiment of initiating social interaction, and some of
the concerns and barriers for the task:
THERAPIST: What got in the way?

PATIENT: For one thing, I realized I didn’t have their phone numbers any more.
THERAPIST: As you were checking, how were you feeling—emotionally?
PATIENT: I felt a little relieved, because I wouldn’t have to call them.
THERAPIST: Anything else?
PATIENT: Well, I was thinking that even if I did call them they wouldn’t want to go to
the movies with me. So, I felt relieved initially that I wouldn’t have to do it … but,
then I felt anxious because I thought you would be angry with me.
THERAPIST: I am pleased you told me about that—it sounds like there were two
concerns there: What would actually happen with making social contact and how our
discussion would turn out—is that right?
PATIENT: Yes.
THERAPIST: Well … please allow me to convey that I do not feel angry or disappointed
in any way. In fact, my perspective of these things is that they are a way to generate and
explore new ideas. Sometimes practical things get in the way, or maybe the activity itself
was too difficult. Knowing this is helpful because we get a better window into your
experience … and in learning what works, we often need to find what doesn’t work.
PATIENT: OK—that’s reassuring to know.
THERAPIST: What did you get from the beginning steps of the experiment?
PATIENT: I guess that I adopted my usual avoidance strategy. I could have looked their
numbers up or emailed them instead.
THERAPIST: Great! That is something we’ve learnt from doing this. What else?
PATIENT: That you weren’t angry that I didn’t do it—that surprised me.
As illustrated, Janine and her therapist attended to the useful learning from the
homework, and the discussion also led to feedback from the patient about the likely
response from the therapist. Clearly, if Janine’s therapist had not allowed time for
this discussion, then important information for the case conceptualization would
have been missed. With this information, Janine’s therapist is better equipped to
encourage engagement, to maintain a positive alliance, and to help Janine work
with her pervasive beliefs about other people (including her therapist) and the
world.
A Focus on Self-Monitoring
As a specific between-session therapeutic activity, self-monitoring has received focused

attention in research and practice for at least four decades (e.g., Mahoney, Moura, &
Wade, 1973). There has been considerable discussion and evaluation regarding the
reliability and validity of the information provided by patients through self-monitoring
(Ajzen, Timko, & White, 1982; Kazdin, 1974), as well as comparisons of different
self-monitoring targets in treatment for depression (e.g., activity vs. mood; see
Harmon, Nelson, & Hayes, 1980) and utility in the treatment of anxiety disorders
(e.g., Craske & Tsao, 1999) and eating disorders (e.g., Wilson & Vitousek, 1999).
There is supportive evidence for the contribution of self-monitoring in psychotherapy
for various mental health conditions (e.g., Burke, Wang, & Sevick, 2011), yet where
monitoring is used to measure adherence with therapeutic homework, comparisons
to objective assessments have led to questions regarding the reliability and validity of
resultant “compliance” self-monitoring by patients (e.g., Neimeyer & Feixas, 1990;
Taylor, Agras, Schneider, & Allen, 1983).
From this point forward, we shift our attention to the role of the therapist and
specific therapist behaviors involved in the effective selection, planning, and review
of homework assignments. Research suggests that therapist competence in assigning
and dealing with homework within the session is essential to patients’ engagement
with homework and treatment outcome (Bryant, Simons, & Thase, 1999; Detweiler-
Bedell & Whisman, 2005; Shaw et al., 1999; Weck, Hilling, Schermelleh-Engel,
Rudari, & Stangier, 2011).
Understanding Why Patients Engage with Homework
If you were asked to take the book you are reading, close it, and attempt to spin the
entire volume on a single index finger, similar to the way in which a basketball player
spins a ball, you would likely ask the question, Why? It seems that having a reason for
a behavior, especially those that require effort, is critical to understanding sustained
engagement in that behavior.
Theories exist that are predicated upon decades of sound empirical research that
attest to the role of beliefs in determining human behavior, and engagement in health
behaviors. Attempting to spin a book on your index finger may appeal to those more
practiced at spinning objects on their fingers—basketball players, jugglers—but will
immediately conflict with others who hold value in the paper versions of practice
resources. For example, many colleagues refrain from writing on the pages of their
textbooks. They prefer to make their notes elsewhere in order to keep the book
in pristine shape, whereas others highlight and write all over the pages, and some
fold or tear out pages. Thus, one layer of cognition we need to attend to relates
to task-specific cognitions. What does the patient think of the task? Before deciding
on the next homework task, the patient should have the opportunity to gain some
experiential learning from in-session practice of the task, and to express his or her
task-specific thoughts, especially with regard to its relevance, difficulty, and some
feedback about how ready and able he or she is to try it. This information can be used
in collaboratively designing homework.
A further consideration is whether the task seems relevant to the patient’s thera-
peutic goals and personal values. The patient needs both a short-term and a long-term
benefit to the investment of time and energy in therapeutic homework. Behavior the-
ories suggest that situational antecedents are important for triggering the realization
that the application of a therapeutic skill is needed. At the same time, intrinsic and
environmental reinforcement is needed to generalize and maintain the practice of
therapeutic skills. However, what is reinforcing for one person may be punitive for
another. Consequently, therapists need to be guided by feedback from the patient
about the homework task. This is a fundamental principle of motivational interview-
ing: There needs to be (from the patient’s perspective) a clear and immediate benefit
to the therapeutic “action” that contributes to a long-term goal (Arkowitz, Westra,
Miller, & Rollnick, 2008; Dozois, 2010; Rosengren, 2009).
A therapeutic activity might only be evaluated as conflicting with a personal value
once a patient has tried it and had the opportunity for an in-session experience of the
task. Thus, it is important to consider what engaging in the task means to the patient.
Many patients will see their performance with therapeutic homework as a marker or
gauge of their personal value, or the likely outcome of their therapy. Others will find
themselves feeling “controlled” or “told what to do” simply because a plan represents
a limited number of options for the extension of therapeutic work through the week
(J. S. Beck, 2005; Kazantzis, 2011). Once the patient has articulated the personal
meaning of the task, patient and therapist can work together to address any conflicts
with personal values, by, for instance, enlisting greater patient input in the design
of the task, or by exploring and perhaps modifying the patient’s perception of the
conflict.
Patients’ coping strategies can also influence their engagement with tasks. A patient
with an extreme avoidance pattern is likely to struggle with a homework task that
involves experiencing uncomfortable emotions, just as a patient with chronic anger
may resent the idea of a task that involves having him or her practicing new ways of
responding to triggering situations (C. F. Newman, 2011). Thus, it is important to
consider patients’ existing coping strategies when designing tasks.
Elizabeth was certain that she “wouldn’t be able to cope” when first introduced to
the thought record, and so, together with her therapist, she decided to start with
the initial columns of specifying a situation, recording her emotions, and associated
unhelpful automatic thoughts, images, dreams, and fantasies. Elizabeth also found
it validating to complete a second form that acknowledged her doubts about the
task, and her concern about her emotions “spiraling out of control ” because she was
focusing on them. The goal in using homework assignments is to empower patients
to engage with their emotional experience and to motivate them to try out alternative
or refined ways of coping. Without attending to the patient’s personal meaning in
this work, there is a risk of triggering and reinforcing his or her negative beliefs.
Sigmund felt surprised when he recalled his work as a project manager when
attempting an intervention of “evaluating worries.” The activity of focusing on his
worries, scrutinizing their likelihood, and identifying them as helpful or unhelpful
reminded him of ineffectively addressing the concerns of his team members—he said,
“I’m relating this to my team!” Without attending to this memory flashing through
his mind, his therapist may have missed an important opportunity to talk about his
associated feelings of “tenseness” and being “on edge” when engaging with the
cognitive restructuring task.
Anna and her therapist discussed a behavioral experiment after some in-session
practice with a task. Her therapist initiated some Socratic dialogue to explore Anna’s
beliefs about the task, its connection to her personal values, and perceived relevance
to therapy goals within the dialogue:
THERAPIST: So we are talking about opening the door for five people at work this week.
How does this fit with your understanding of how to strengthen relationships?
PATIENT: I think it’s a simple gesture and it’s definitely a step in the right direction.
THERAPIST: What do you think about the task itself—in relation to your personal
values?
PATIENT: I think I’m generally a courteous and helpful person. Maybe this small
gesture will convey that to others too.
THERAPIST: What do you predict will happen?
PATIENT: People will probably look right through me.
THERAPIST: How much do you believe that will happen—on a 0–100% scale?
PATIENT: People are not considerate—I am 100% confident that no one will even
notice; they’ll just walk on by.
THERAPIST: OK, so we have a useful activity on our hands. It is something that reflects
your personal value of being courteous and helpful, but it’s also going to help us gauge
how others respond to this act of consideration. If we view people in just one way or
another, there’s a chance that we miss some exceptions to the rule, or variations among
people—so this experiment is useful in supporting the collection of “data.” We might

find “data” that support your prediction, and some data that don’t.
PATIENT: We’re going to see how people respond.
THERAPIST: Yes, that’s right! And let’s record how they respond. And how do you feel
about proceeding with this task?
PATIENT: Interested actually …
THERAPIST: I’m interested too; let’s figure out how we are going to record these
experiences.
As this example illustrates, we advocate for the use of Socratic dialogue to explore
the patient’s associations with the task, how the task connects with his or her
assumptions, rules, and personal values regarding (a) self, (b) others and the world
including the therapist, (c) the likely outcome of the task (and therapy), (d) distressing
emotions, and (e) compatibility and conflict with existing ways of coping.
Because imagery is the next best thing to being in situations, it serves as a
useful technique for facilitating in-session practice when the immediate environ-
ment is not conducive to such exposure (J. S. Beck, 2011; Kazantzis, Arntz,
Borkovec, Holmes, & Wade, 2010). After having practiced sensation induction
for the treatment of panic through the previous week, Daniel communicated to
his therapist that the hyperventilation exercise failed to trigger any fear response as
planned. Daniel and his therapist used imagery in the following session to enable
him to move into a busy supermarket, cinema theatre, and crowded street to
practice his alternative interpretations of any heightened physiology that he may
experience, such as, “this is my anxiety—and anxiety is normal. It will take me
some time to feel entirely comfortable, but if I stay in the situation long enough,
I know I will start to enjoy being here. It’s an opportunity to practice my therapy
skills!”
One way to select homework assignments is to take an existing therapeutic inter-
vention and incorporate it into work with a patient (e.g., monitoring physiology
[Clark & A. T. Beck, 2010], panic, and worry [Wells, 2009]). Reliance on exist-
ing forms for homework may be more useful at the early stages of therapy or
when the patient is markedly distressed. For example, Jenny likened having too
much choice in therapy to visiting a supermarket with 30 types of mustard while
she was rushing to gather the other dinner party items before picking up her
children from school. Too much choice can be distressing. In fact, a useful rule
of thumb is to consider an inverse relationship between the extent of collabora-
tion, or shared work, in designing homework assignments and the level of patient
distress.
At the other end of the continuum there is the opportunity to design an intervention
from the ground up (to be extended in homework). Behavioral experiments are an
excellent example of this form of homework, as therapists and patients have identified
thoughts to evaluate and have a process of designing a tailored “empirical test” of the
belief through data gathering and/or experimentation with new or adjusted behavior
(Bennett-Levy et al., 2004).
In summary, consideration should be given to the extent of collaboration in “co-
authoring” or designing a therapeutic homework task in the context of each patient’s
distress in-session. The therapist should revert to “off-the-shelf” homework when

patients are more distressed, and encourage patients to design totally new homework
tasks when they are less distressed.
Helping Patients to Plan Their Homework
The majority of the therapeutic activities that patients are asked to engage in
between sessions involve some amount of self-monitoring. Beyond recording subjec-
tive emotions, thoughts, physiology, behaviors, and interactions, there is generally
an implicit need to self-monitor in order to know when to use a therapeutic tech-
nique. Put simply, most homework assignments demand that patients use their
executive functioning abilities. Research on prospective memory and implementa-
tion intentions overlap in pointing to the value in having a clear plan in order
to reduce the demands (or cognitive load) of the task (Gollwitzer & Sheeran,
2006; McDaniel, Howard, & Butler, 2008). CBT homework assignments often
require some prioritization, problem solving of unexpected obstacles, inhibition of
other learned responses (or ways of coping), initiating new responses, and shifting,
focusing, and dividing attention. Thus, the very least therapists can do is support
their patients to arrive at a specific plan that helps them start with the homework
activity.
Consider environmental prompts such as smartphone reminders, alarms, colorful
notes, wearing a watch on a different arm, leaving something unusual out of place,
or putting colorful stickers in prominent places. It is then useful to ask the patient to
summarize the task and present his or her understanding of how the task contributes
to therapy goals. Through collaborative discussion, the therapist takes a questioning
approach to decide on when, where, how often, and for how long the homework
task should be done. Practitioner surveys have shown that only a small proportion of
therapists (25% or less) work with their patients to devise a plan that comprises these
components (Kazantzis & Deane, 1999; Kazantzis & Ronan, 2006). This process is
initially led by the therapist, but requires patients to provide the information, as they
are the expert on their lives. After a few sessions, patients can usually take the lead and
initiate a specific plan with little contribution from the therapist. Initially, however,
arriving at a specific plan may require about 10 minutes of the concluding part of the
therapy session.
We advocate engaging patients to decide on when, where, how often, and for how
long the homework assignment will be done. The same homework can be made more
manageable by reducing its frequency. A more structured and therapist-led process is
needed when the patient is distressed. However, the goal is to create the conditions
under which the patient can put together his or her own plan, especially as the patient
takes more of the lead (and as the patient guides more of the collaborative work in
CBT; see Kazantzis, Arntz, et al., 2010).
Devising a clear plan for the homework with patients often raises likely obstacles
and potential environmental barriers, so it is helpful to ask about these specifically.
Additionally, therapists are wise to summarize the homework and ask patients to
provide feedback about the plan through ratings of their perceived confidence,
readiness, and importance (e.g., using subjective visual analogue scales ranging from
0 = none, to 50 = moderate, to 100 = high). Many therapists are surprised that
their patients are less than 70% confident about the homework, even though there
has been in-session practice, and the patient has decided on the specific plan for
the task. It is vital for therapists to be able to detect and effectively manage early
patient reluctance toward tasks, as this has been found to be a strong predictor
of engagement and treatment outcome (Westra, 2011). The whole is greater than
the sum of its parts, and so it is usually helpful to reconsider some aspect of the
homework, such as prioritizing one part by reducing it into manageable chunks.
When patients rate very low levels of confidence, questions that may be helpful
include:
• “What would make you more confident about the task?”

• “What would need to happen in order for the score to increase from X to 100?”
• “How could the task be changed to increase your confidence? Could we draw on
the help of others to aid you?”
• “What have you learned from previous tasks?”
• “What are the steps you need to take to feel confident to start?”
A written summary of the homework that patients can take home with them has
been demonstrated to increase rates of engagement significantly (Cox, Tisdelle, &
Culbert, 1988), and a variety of summary forms have been recommended in the
professional literature to aid with therapeutic homework (e.g., Kazantzis, Dattilio, &
MacEwan, 2005).
Building Hope and Resilience through Reviewing Homework
If patients are asked to engage in homework assignments, then it follows suit to ask
them about their level of engagement and how they felt about the assignment at
the next session. Some therapists think, “I should only ask patients about homework
if they have done it,” and miss opportunities to gain feedback from patients who
have not engaged with the assignment. Therapists want to acknowledge the work the
patient has done, as well as what may have inhibited him or her from completing
the assignment. The review of homework during each session also conveys to
patients that the ultimate benefit of therapy will be dependent on their degree of
practice between sessions. If therapy is truly about learning, then the homework
review can be focused on what was gained, no matter how small the steps in going
forward.
Structuring sessions and pacing them appropriately depends on an effective review
of therapeutic homework assignments. It is useful to review the practical obstacles
to the task, as distinct from thoughts and emotions generated in completing the task.
For example, Sasha found substantial relief from practicing strategic withdrawal and
arousal reduction in interpersonal interactions where she was arguing and shouting,
yet this new strategy was associated with significant guilt and was accompanied by
the thought: “All these years that I have argued with people, and been aggressive … I’ve
hurt so many because of my selfishness … How could I have given myself permission to
treat people with such disrespect?” Without asking about her emotions and thoughts
when engaging in this task, Sasha’s therapist may have missed vital information for
the session agenda and case conceptualization. Patients also often minimize their
accomplishments, or perceive progress as evidence that their overall functioning is
substandard, so cognitions activated in the homework are critical to be assessed as
part of the review.
The input offered to patients about their homework represents important feedback
about their progress in therapy. For this reason, it is useful to titrate verbal praise
and encouragement carefully so that it is clearly connected to the work done
(i.e., concrete evidence to the patient that the praise is accurate), and that it is
honest, sincere, and appropriate to what the patient has achieved. It is important to
communicate to patients that the skill being learned may be developed or adapted
further, which builds hope and optimism. Sharing stories of other patients who have
been at a similar stage of skill acquisition may also serve as a means of encouraging
patients.
Understanding the patient’s worldview through accurate empathy and understand-
ing is central to effective homework review. Acknowledging the difficulties in the task
(both emotional and achievement-related) and the importance of persisting despite
these challenges communicates to the patient that the therapist believes in his or
her abilities to bolster resilience. Therapists should attend to whether their patients
expect them to be disappointed for work not done, or not completed “properly” or
“adequately,” and take time to discuss their feelings of guilt and shame. Given that
homework is therapeutic work, then it makes sense that the process of engagement
in homework is therapeutic on multiple levels (i.e., through the direct benefits of
the therapeutic task, the patient’s increased appreciation and awareness of his or her
potential, and his or her discussion with a therapist who is accepting and encourag-
ing). It should be borne in mind that the conclusions patients reach from their work
in engaging with homework directly supports their belief about the likely outcome of
their therapy.
Conclusion
No guidance on the use of therapeutic homework in CBT would be complete without

a homework assignment. Take a few moments to reflect on the ideas shared in this
chapter, and ask yourself the following questions: What ideas can I take with me from
this chapter, and how can I implement them effectively in my future work with patients?
Consider what steps you would need to take to implement this plan effectively,
and think about how what you have selected links to your goals as a developing
professional. If you were talking to a colleague, what advice would you give him or
her about incorporating therapeutic homework into his or her sessions after reading this
chapter? Imagine yourself a year from now, if you were sitting down and reflecting on
your therapeutic practice; what aspects regarding the use of homework would you like to
have developed?
Acknowledgements
The authors wish to acknowledge the cognitive therapy teachings, guidance, and
mentorship of Aaron T. Beck (FD and NK), as well as Christine Padesky, Judith
Beck, Kathleen Mooney, and Cory Newman (NK). Special appreciation is extended
to our colleague and valued collaborator Keith Dobson. The authors wish to extend
gratitude to the current trainees and alumni of the Cognitive Behavior Therapy
Research Unit at La Trobe University for their ideas and collaboration, and to those
colleagues from the international CBT community who have shared in discussions
and assisted in developing the ideas represented in this chapter (in alphabetical order):
Tom Borkovec, David A. Clark, Frank Deane, Art Freeman, Stefan Hofmann, Ken
Laidlaw, Robert Neimeyer, Nancy Pachana, Ron Rapee, Kevin Ronan, Gregoris
Simos, Mehmet Sungur, Eleanor Wertheim, and Wong Chee-wing. We also extend
sincere thanks to Judith Stern for feedback on a previous draft of this chapter, and to
all those patients who have worked with us in therapy, since they are our best teachers
about what is ultimately useful when enhancing the use of homework in therapy.
References
Addis, M. E., & Jacobson, N. S. (2000). A closer look at the treatment rationale
and homework compliance in cognitive-behavioral therapy for depression. Cognitive
Therapy and Research, 24, 313–326. doi:10.1023/A:1005563304265
Ajzen, I., Timko, C., & White, J. B. (1982). Self-monitoring and the attitude-behavior
relation. Journal of Personality & Social Psychology, 42, 426–435.
Arkowitz, H., Westra, H. A., Miller, W. R., & Rollnick, S. (2008). Motivational inter-
viewing in the treatment of psychological problems. New York, NY: Guilford Press.
Barlow, D. H., Esler, J. L., & Vitali, A. E. (1998). Psychosocial treatments for panic
disorders, phobias and generalized anxiety disorder. In P. E. Nathan & J. M.
Gorman (Eds.), A guide to treatments that work (pp. 288–318). New York, NY:
Beck, A. T. (1976). Cognitive therapy and the emotional disorders. New York, NY: New
American Library/Meridian.
Beck, A. T., & Dozois, D. J. A. (2011). Cognitive therapy: Current status and future
directions. Annual Review of Medicine, 62, 397–409. doi:10.1146/annurev-med-
05220-100032
Beck, J. S. (2005). Cognitive therapy for challenging problems: What to do when the basics
don’t work. New York, NY: Guilford Press.
Beck, J. S. (2011). Cognitive behavior therapy: Basics and beyond. New York, NY: Guilford
Press.
Beck, J. S., & Tompkins, M. (2007). Cognitive therapy. In N. Kazantzis & L. L’Abate
(Eds.), Handbook of homework assignments in psychotherapy: Research, practice, and
prevention (pp. 51–63). New York, NY: Springer.
Bennett-Levy, J., Butler, G., Fenell, M., Hackmann, A., Mueller, M., & Westbrook, D.
(2004). Oxford guide to behavioural experiments in cognitive therapy. Oxford, Eng-
land: Oxford University Press.
Beutler, L. E., Malik, M., Talebi, H., Fleming, J., & Moleiro, C. (2004). Use of
psychological tests/instruments for treatment planning. In M. E. Maruish (Ed.),
The use of psychological testing for treatment planning and outcomes assessment
(pp. 101–132). Mahwah, NJ: Erlbaum.
Brothers, B. M., Yang, H. C., Strunk, D. R., & Anderson B. L. (2011). Cancer
patients with major depressive disorder: Testing a biobehavioral/cognitive behav-
ior intervention. Journal of Consulting and Clinical Psychology, 79, 253–260.
doi:10.1037/a0022566
Burke, L. E., Wang, J., & Sevick, M. A. (2011). Self-monitoring in weight loss: A
systematic review of the literature. Journal of the American Dietetic Association, 111,
92–102. doi:10.1016/j.jada.2010.10.008
Burns, D. D., & Spangler, D. L. (2000). Does psychotherapy homework lead to improve-
ments in depression in cognitive-behavioral therapy or does improvement lead to
increased homework compliance? Journal of Consulting and Clinical Psychology, 68,
46–56. doi:10.1037//0022-006X.68.1.46
Bryant, M. J., Simons, A. D., & Thase, M. E. (1999). Therapist skill and patient variables
in homework compliance: Controlling an uncontrolled variable in cognitive therapy
outcome research. Cognitive Therapy and Research, 23, 381–399.
Carroll, K. M., Nich, C., & Ball, A. (2005). Practice makes progress? Homework
assignments and outcome in treatment of cocaine dependence. Journal of Consulting
and Clinical Psychology, 73, 749–755. doi:10.1037/0022-006X.73.4.749.
Cash, T. F., & Hrabosky, J. I. (2003). The effects of psychoeducation and self-monitoring
in a cognitive-behavioral program for body-image improvement. Eating Disorders,
11, 255–270. doi:10.1080/10640260390218657
Clark, D. A., & Beck, A. T. (2010). Cognitive therapy of anxiety disorders: Science and
practice. New York, NY: Guilford Press.
Coon, D. W., & Thompson, L. W. (2003). The relationship between homework
compliance and treatment outcomes among older adult outpatients with mild-
to-moderate depression. American Journal of Geriatric Psychiatry, 11, 53–61.
doi:10.1176/appi.ajgp.11.1.53
Cowan, M. J., Freedland, K. E., Burg, M. M., Saab, P. G., Youngblood, M. E.,
Cornell, C. E., … Czajkowski, S. M. (2008). Predictors of treatment response for
depression and inadequate social support: The ENRICHD randomized clinical trial.
Psychotherapy and Psychosomatics, 77 , 27–37. doi:10.1159/000110057
Cox, D. J., Tisdelle, D. A., & Culbert, J. P. (1988). Increasing adherence to behavioral
homework assignments. Journal of Behavioral Therapy, 11, 519–522.
Craske, M. G., & Tsao, J. C. (1999). Self-monitoring with panic and anxiety disorders.
Psychological Assessment, 11, 466–479.
Dattilio, F. M., & Hanna, M. A. (2012). Collaboration in cognitive-behavioral therapy.
Journal of Clinical Psychology, 68, 146–158. doi:10.1002/jclp.21831
Deane, F. P., Glaser, N. M., Oades, L. G., & Kazantzis, N. (2005). Psychologists’ use of
homework assignments with clients who have schizophrenia. Clinical Psychologist, 9,
24–30. doi:10.1080/13284200500048141
Detweiler-Bedell, J. B., & Whisman, M. A. (2005). A lesson in assigning homework: Ther-
apist, client, and task characteristics in cognitive therapy for depression. Professional
Psychology: Research and Practice, 36, 219–223.
Dimeff, L. A., & Marlatt, G. A. (1995). Relapse prevention. In R. K. Hester &
W. R. Miller (Eds.), Handbook of alcoholism treatment approaches: Effective alternatives
(pp. 176–794). Boston, MA: Allyn & Bacon.
Dobson, K. S. (2010). Handbook of cognitive behavioural therapies (3rd ed.). New York,
NY: Guilford Press.
Dozois, D. J. A. (2010). Understanding and enhancing the effects of homework in
cognitive behavioral therapy. Clinical Psychology: Science and Practice, 17 , 157–161.
doi:10.1111/j.1468-2850.2010.01205.x
Dunn, H., Morrison, A. P., & Bentall, R. P. (2002). Patients’ experiences of homework
tasks in cognitive behavioural therapy for psychosis: A qualitative analysis. Clinical
Psychology and Psychotherapy, 9, 361–369. doi:10.1002/cpp.344
Ellison, J., & Greenberg, L. (2007). Emotion-focused experiential therapy. In
N. Kazantzis & L. L’Abate (Eds.), Handbook of homework assignments in psychotherapy:
Research, practice, and prevention (pp. 65–83). New York, NY: Springer.
Fehm, L., & Kazantzis, N. (2004). Attitudes and use of homework assignments in
therapy: A survey of German psychotherapists. Clinical Psychology and Psychotherapy,
11, 332–343. doi:10.1002/cpp.419
Fehm, L., & Mrose, J. (2008). Patients’ perspective on homework assignments in
cognitive-behavioural therapy. Clinical Psychology and Psychotherapy, 15, 320–328.
doi:10.1022/cpp.592
Felmingham, K. L., & Bryant, R. A. (2012). Gender differences in the maintenance of
response to cognitive behavior therapy for posttraumatic stress disorder. Journal of
Consulting and Clinical Psychology, 80, 196–200. doi:10.1037/a0027156
Garland, A. F., Brookman-Frazee, L., & Chavira, D. A. (2010). Are we doing our home-
work? Clinical Psychology: Science and Practice, 17 , 162–165. doi:10.1111/j.1468-
2850.2010.01206.x
Gloster, A. T., Wittchen, H. U., Einsle, F., Lang, T., Helbig-Lang, S., Fydrich, T.,
… Arolt, V. (2011). Psychological treatment for panic disorder with agoraphobia:
A randomized controlled trial to examine the role of therapist-guided exposure
in situ in CBT. Journal of Consulting and Clinical Psychology, 79, 406–420.
doi:10.1037/a0023584
Gollwitzer, P. M., & Sheeran, P. (2006). Implementation intentions and goal achieve-
ment: A meta-analysis of effects. Advances in Experimental Social Psychology, 38,
69–119. doi:10.1016/S0065-2601(06)38002-1
Gonzalez, V. M., Schmitz, J. M., & DeLaune, K. A. (2006). The role of homework
in cognitive-behavioral therapy for cocaine dependence. Journal of Consulting and
Harmon, T. M., Nelson, R. O., & Hayes, S. C. (1980). Self-monitoring of mood
versus activity by depressed clients. Journal of Consulting and Clinical Psychology, 48,
30–38.
Helbig, S., & Fehm, L. (2004). Problems with homework in CBT: Rare excep-
tion or rather frequent? Behavioural and Cognitive Psychotherapy, 32, 291–301.
doi:10.1017/S1352465804001365
Hughes, A. A., & Kendall, P. C. (2007). Prediction of cognitive behaviour treat-
ment outcome for children with anxiety disorders: Therapeutic relationship and
homework compliance. Behavioural and Cognitive Psychotherapy, 35, 487–494.
doi:10.1017/S1352465807003761
Kaplan, R. M., & Saccuzzo, D. P. (2008). Psychological testing: Principles, applications,
and issues (7th ed.). Belmont, CA: Wadsworth.
Kazantzis, N. (2000). Power to detect homework effects in psychotherapy out-
come research. Journal of Consulting and Clinical Psychology, 68, 166–170.
doi:10.1037//0022-006X.68.1.166
Kazantzis, N. (2011). On becoming a therapist: Helping clients try “My own therapy.”
In H. G. Rosenthal (Ed.), Favorite counselling and therapy homework assignments
(pp. 205–208). New York, NY: Routledge.
Kazantzis, N., Arntz, A. R., Borkovec, T., Holmes, E. A., & Wade, T. (2010).
Unresolved issues regarding homework assignments in cognitive and behavioural
therapies: An expert panel discussion at AACBT. Behaviour Change, 27 , 119–129.
doi:10.1375/bech.27.3.119
Kazantzis, N., Beck, J. S., Dattilio, F. M., Dobson, K. S., & Rapee, R. (in press).
Collaborative empiricism as the central therapeutic relationship element in cognitive
behavior therapy: An expert panel discussion at the 7th International Congress of
Cognitive Psychotherapy. International Journal of Cognitive Therapy.
Kazantzis, N., Busch, R., Ronan, K. R., & Merrick, P. L. (2007). Using home-
work assignments in psychotherapy: Differences by theoretical orientation and
professional training? Behavioural and Cognitive Psychotherapy, 35, 121–128.
doi:10.1017/S1352465806003328
Kazantzis, N., & Daniel, J. (2009). Homework assignments. In G. Simos (Ed.), Cognitive
behaviour therapy: A guide for the practicing clinician (2nd ed., Vol. 2, pp. 165–186).
New York, NY: Routledge.
Kazantzis, N., Dattilio, F. M., & MacEwan, J. (2005). In pursuit of homework adherence
in behaviour and cognitive behaviour therapy: Comment on Malouff and Schutte
(2004). Behavior Therapist, 28, 179–183.
Kazantzis, N., & Deane, F. P. (1999). Psychologists’ use of homework assignments
in clinical practice. Professional Psychology: Research and Practice, 30, 581–585.
doi:10.1037/0735-7028.30.6.581
Kazantzis, N., Deane, F. P., & Ronan, K. R. (2000). Homework assignments in cognitive
and behavioral therapy: A meta-analysis. Clinical Psychology: Science and Practice, 7 ,
189–202. doi:10.1093/clipsy.7.2.189
Kazantzis, N., Lampropoulos, G. L., & Deane, F. P. (2005b). A national survey of
practicing psychologists’ use and attitudes towards homework in psychotherapy.
Journal of Consulting and Clinical Psychology, 73, 742–748. doi:10.1037/0022-
006X.73.4.742
Kazantzis, N., Petrik, A. M., & Cummins, A. (2012). Homework assign-
ments. Accepted entry in Common Language for Psychotherapy Procedures.
www.commonlanguagepsychotherapy.org
Kazantzis, N., & Ronan, K. R. (2006). Can between-session (homework) activities be
considered a common factor in psychotherapy? Journal of Psychotherapy Integration,
16, 115–127. doi:10.1037/1053-0479.16.2.115
Kazantzis, N., Ronan, K. R., & Deane, F. P. (2001). Concluding causation from
correlation: Comment on Burns and Spangler (2000). Journal of Consulting and
Clinical Psychology, 69, 1079–1083. doi:10.1037//0022-006X.69.6.1079
Kazantzis, N., Whittington, C., & Dattilio, F. (2010b). Meta-analysis of homework effects
in cognitive and behavioural therapy: A replication and extension. Clinical Psychology:
Science and Practice, 17 , 144–156. doi:10.1111/j.1468-2850.2010.01204.x
Kazdin, A. E. (1974). Reactive self-monitoring: The effects of response desirability, goal
setting, and feedback. Journal of Consulting and Clinical Psychology, 42, 704–716.
Lambert, M., Harmon, S., & Slade, K. (2007). Directions for research on homework. In
Leahy, R. L. (2001). Overcoming resistance in cognitive therapy. New York, NY: Guilford
Press.
Ledley, D., & Huppert, J. (2007). Behavior therapy. In N. Kazantzis & L. L’Abate
(Eds.), Handbook of homework assignments in psychotherapy: Research, practice, and
prevention (pp. 19–34). New York, NY: Springer.
Linehan, M. (1993). Cognitive-behavioral treatment of borderline personality disorder.
Mahoney, M. J., Moura, N. G., & Wade, T. C. (1973). Relative efficacy of self-reward, self-
punishment, and self-monitoring techniques for weight loss. Journal of Consulting
Mausbach, B. T., Moore, R., Roesch, S., Cardenas, V., & Patterson, T. L. (2010).
The relationship between homework compliance and therapy outcomes: An updated
meta-analysis. Cognitive Therapy Research, 34, 429–438. doi:10.1007/s10608-010-
9297-z
McDaniel, M. A., Howard, D. C., & Butler, K. M. (2008). Implementation intentions
facilitate prospective memory under high attention demands. Memory & Cognition,
36, 716–724. doi:10.3758/MC.36.4.716
McGraw, K. O. (1991). Problems with the BESD: A comment on Rosenthal’s “How are
we doing in soft psychology?” American Psychologist, 46, 1084–1086.
McMillan, W., Stice, E., & Rohde, P. (2011). High and low-level dissonance-based
eating disorder prevention programs with young women with body image concerns:
An experimental trial. Journal of Consulting and Clinical Psychology, 79, 129–134.
doi:10.1037/a0022143
Murphy, H., & Lahtinen, M. (2011). Understanding the impact of meditative
homework on depression in the context of mindfulness based cognitive therapy
(MBCT): An interpretative phenomenological analysis. European Psychologist, 26,
659. doi:10.1016/S0924-9338(11)72365-3
Neimeyer, R. A., & Feixas, G. (1990). The role of homework and skill acquisition in the
outcome of group cognitive therapy for depression. Behavior Therapy, 21, 281–292.
Neimeyer, R. A., Kazantzis, N., Kassler, D. M., Baker, K. D., & Fletcher, R.
(2008). Group cognitive behavioral therapy for depression outcomes predicted
by willingness to engage in homework, compliance with homework, and cog-
nitive restructuring skill acquisition. Cognitive Behaviour Therapy, 37 , 199–215.
doi:10.1080/16506070801981240
Neimeyer, R. A., & Winter, D. (2007). Personal construct therapy. In N. Kazantzis &
L. L’Abate (Eds.), Handbook of homework assignments in psychotherapy: Research,
practice, and prevention (pp. 151–171). New York, NY: Springer.
Newman, C. F. (2011). When clients’ morbid avoidance and chronic anger impede their
response to cognitive-behavioral therapy for depression. Cognitive and Behavioral
Newman, M. G., Castonguay, L. G., Borkovec, T. D., Fisher, A. J., Boswell, J. F.,
Szkodny, L. E., & Nordberg, S. S. (2011). A randomized controlled trial of cognitive-
behavioral therapy for generalized anxiety disorder with integrated techniques from
emotion-focused and interpersonal therapies. Journal of Consulting and Clinical
Psychology, 79, 171–181. doi:10.1037/a0022489
Persons, J. B., Davidson, J., & Tompkins, M. A. (2000). Essential components of cognitive-
behavior therapy for depression. Washington, DC: American Psychological Association.
Resick, P. A., Williams, L. F., Suvak, M. K., Monson, C. M., & Gradus, J. L. (2012).
Long-term outcomes of cognitive-behavioral treatments for posttraumatic stress
disorder among female rape survivors. Journal of Consulting and Clinical Psychology,
80, 201–210. doi:10.1037/a0026602
Robbins, M., Szapocznik, J., & Pe’rez, G. (2007). Brief strategic family therapy. In
Rosengren, D. B. (2009). Building motivational interviewing skills: A practitioner work-
book. New York, NY: Guilford Press.
Rosenthal, R. (1991). Meta-analysis: A review. Psychosomatic Medicine, 53, 247–271.
Schmidt, N. B., & Woolaway-Bickel, K. (2000). The effect of treatment compliance
on outcome in cognitive-behavioral therapy for panic disorder: Quantity versus
quality. Journal of Consulting and Clinical Psychology, 68, 1–18. doi:10.1037/0022-
006X.68.1.13
Shaw, B. F., Elkin, I., Yamaguchi, J., Olmsted, M., Vallis, T. M., Dobson, K. S., …
Imber, S. D. (1999). Therapist competence ratings in relation to clinical outcome in
cognitive therapy of depression. Journal of Consulting and Clinical Psychology, 67 ,
837–846.
Simpson, H. B., Maher, M. J., Page, J. R., Gibbons, C. J., Franklin, M. E., & Foa, E. B.
(2010). Development of a patient adherence scale for exposure and response preven-
tion therapy. Behavior Therapy, 41, 30–37. doi:10.1016/j.beth.2008.12.002
Simpson, H. B., Maher, M. J., Wang, Y., Bao, Y., Foa, E. B., & Franklin, M. (2011).
Patient adherence predicts outcome from cognitive behavioral therapy in obsessive-
compulsive disorder. Journal of Consulting and Clinical Psychology, 79, 247–252.
doi:10.1037/a0022659
Startup, M., & Edmonds, J. (1994). Compliance with homework assignments in
cognitive-behavioral psychotherapy for depression: Relation to outcome and
methods of enhancement. Cognitive Therapy and Research, 18, 567–579.
doi:10.1007BF02355669
Stricker, G. (2007). Psychodynamic therapy. In N. Kazantzis & L. L’Abate (Eds.),
Handbook of homework assignments in psychotherapy: Research, practice, and prevention
(pp. 101–111). New York, NY: Springer.
Taylor, L. B., Agras, W. S., Schneider, J. A., & Allen, R. A. (1983). Adherence to
instructions to practice relaxation exercises. Journal of Consulting and Clinical
Thase, M. E., & Callan, J. A. (2006). The role of homework in cognitive behav-
ior therapy of depression. Journal of Psychotherapy Integration, 16, 162–177.
doi:10.1037/1053-0479.16.2.162
Tolin, D. F., Frost, R. O., & Steketee, G. (2007). An open trial of cognitive-behavioral
therapy for compulsive hoarding. Behaviour Research and Therapy, 45, 1461–1470.
doi:10.1016/j.brat.2007.01.001
Twohig, M., Pierson, H., & Hayes, S. (2007). Acceptance and commitment therapy. In
Urbina, S. (2004). Essentials of psychological testing. Hoboken, NJ: John Wiley & Sons,
Inc.
Vincelli, F., Anolli, L., Bouchard, S., Wiederhold, B. K., Zurloni, V., & Riva, G.
(2003). Experiential cognitive therapy in the treatment of panic disorders with
agoraphobia: A controlled study. CyberPsychology & Behavior, 6, 321–328.
doi:10.1089/109493103322011632
Weck, F., Hilling, C., Schermelleh-Engel, K., Rudari, V., & Stangier, U. (2011).
Reliability of adherence and competence assessment in cognitive behavioral ther-
apy: Influence of clinical experience. Journal of Nervous and Mental Disease, 199,
276–279. doi:10.1097/NMD.0b013e3182124617
Press.
Westra, H. A. (2011). Comparing the predictive capacity of observed in-session resistance
to self-reported motivation in cognitive behavioral therapy. Behaviour Research and
Therapy, 49, 106–113. doi:10.1016/j.brat.2010.11.007
Westra, H. A., & Dozois, D. J. A. (2006). Preparing clients for cognitive behavioral
therapy: A randomized pilot study of motivational interviewing for anxiety. Cognitive
Therapy and Research, 30, 481–498. doi:10.1007/s10608-006-9016-y
Westra, H. A., Dozois, D. J. A., & Marcus, M. (2007). Expectancy, homework com-
pliance, and initial change in cognitive-behavioral therapy for anxiety. Journal of
Consulting and Clinical Psychology, 75, 363–373. doi:10.1037/0022-006X.75.3.363
Wetherell, J. L., Gatz, M., & Craske, M. G. (2003). Treatment of generalized anxiety
disorder in older adults. Journal of Consulting and Clinical Psychology, 71, 31–40.
doi:10.1037/0022-006X.71.1.31
Wilson, G. T., & Vitousek, K. M. (1999). Self-monitoring in the assessment of eating
disorders. Psychological Assessment, 11, 480–489.
Witkiewitz, K., & Bowen, S. (2010). Depression, craving and substance use following a
randomized trial of mindfulness-based relapse prevention. Journal of Consulting and
Witty, M. C. (2007). Client-centered therapy. In N. Kazantzis & L. L’Abate (Eds.),
Handbook of homework assignments in psychotherapy: Research, practice, and prevention
(pp. 35–50). New York, NY: Springer.
Woods, C. M., Chambless, D. L., & Steketee, G. (2002). Homework compliance and
behavior therapy outcome for panic with agoraphobia and obsessive compulsive dis-
order. Cognitive Behaviour Therapy, 31, 88–95. doi:10.1080/16506070252959526
Young, J., & Mufson, L. (2007). Interpersonal psychotherapy. In N. Kazantzis &
L. L’Abate (Eds.), Handbook of homework assignments in psychotherapy: Research,
practice, and prevention (pp. 85–100). New York, NY: Springer.
Zettle, R. D., & Hayes, S. C. (1987). Component and process analysis of cognitive
therapy. Psychological Reports, 61, 939–953.
15
Using Motivational Interviewing
to Manage Resistance
Henny A. Westra
York University, Canada
Limited client engagement and compliance remain major factors limiting the efficacy
of existing treatments for many major mental health problems. For example, in a
recent survey of practitioner-identified obstacles to the implementation of empirically
supported treatments for panic disorder, client unwillingness to engage in treatment
was reported by 61% of therapists, and minimal client motivation at the outset of
therapy was identified as a problem by 67% of the therapists surveyed (American
Psychological Association [APA], 2010). Moreover, homework noncompliance is a
common problem with surveys of practicing therapists indicating that the majority of
clients in cognitive behavioral therapy (CBT) exhibit noncompliance or only partial
compliance with homework (Helbig & Fehm, 2004).
Motivational interviewing (MI) is a brief, client-centered, directive method for
enhancing intrinsic motivation for change (Miller & Rollnick, 2002). Although
MI is an empirically supported treatment for substance abuse, extending it to the
treatment of other major mental health problems is clearly appealing to clinicians
and researchers, and conceptual and empirical work in these areas is advancing
quickly (e.g., Arkowitz, Westra, Miller, & Rollnick, 2008; Westra, 2012). MI is
likely appealing since it addresses important clinical problems (i.e., resistance, ambiva-
lence, lack of engagement in treatment), and can complement rather than replace
existing treatments. For example, MI is rapidly gaining momentum as an adjunct
to, or integrated with, other treatments for major mental health problems, such as
CBT.
This chapter starts by reviewing the importance of resistance in various forms, and
then argues that a major contribution of MI is the provision of a framework for
viewing and responding effectively to resistance. An overview of the basic philosophy
and principles of MI is then provided, followed by a consideration of how MI can
inform responses to various forms of resistance. Finally, existing support for MI is

DOI: 10.1002/9781118528563.wbcbt15
outlined, and some future directions are considered for the integration of MI into
existing treatment approaches.
Resistance
Change is typically a very turbulent process that is fraught with competing and oppos-
ing feelings. Although clients come to treatment because they desire change, they may
simultaneously fear and oppose it. Research suggests that many individuals with major
mental health problems enter therapy with significant reservations, fears, or concerns
about treatment and change (e.g., Kushner & Sher, 1989). In certain populations,
such as among individuals with eating disorders, for example, noncompliance with
treatment and resistance to change are the norm (e.g., Vitousek, Watson, & Wilson,
1998). However, it is a misnomer to consider resistance solely as a client variable. In
MI, resistance is considered a product of the client’s ambivalence about change and
how a therapist responds to that ambivalence (Moyers & Rollnick, 2002). That is,
sustained client resistance in MI is considered a clinician skill error.
Despite being used interchangeably in the literature, it is useful to consider two
types of resistance: (a) resistance to change or intrapsychic resistance, and (b) resistance
to the therapist or treatment. The first type of resistance occurs within the client and
reflects competing motivational forces, that is, “There is a part of me that knows I
need (and want) to change and, yet, another part of me that stops me from changing.”
This type of resistance is best characterized as ambivalence about change and reflects
a client variable or characteristic. Clients vary considerably in terms of their degree of
ambivalence or “stuckness” regarding change.
The second type of resistance in therapy is interpersonal and reflects opposition to
the therapist or the treatment. In this type of resistance, there must be someone or
something to resist (i.e., the client resisting the therapist or application of the treatment
methods). For example, Newman (1994) outlines various forms that resistance can
take in CBT including refusal to follow through with homework, taking actions that
run counter to what was agreed upon in session, high levels of expressed emotion
toward the therapist, in-session avoidance such as silence or frequent use of “I don’t
know,” gratuitous debates with the therapist, and misinterpretation of the therapist’s
comments, among others.
While it is tempting to consider opposition to the therapist or treatment (i.e.,
interpersonal resistance) as an aspect of the client, it is more typically a reflection
of interpersonal process gone awry. Often, such resistance arises from the therapists’
directive (rather than supportive or exploratory) management of ambivalence. For
example, the therapist may indicate a preferred or healthier way of viewing a stressful
situation and the client disagrees (e.g., “I wish I could see it that way but I
don’t”) or the therapist suggests a homework assignment and the client objects
(e.g., “That sounds too hard”). The presence of such interpersonal resistance reflects
lack of collaboration and represents strains or ruptures in the therapeutic alliance.
Thus, this type of resistance is best considered an interpersonal process variable,
rather than a client characteristic. Such client disengagement is a signal of alliance
strain, which the therapist then needs to take corrective action to resolve in order
Motivational Interviewing 333
to reengage the client (typically by the judicious use of empathy). For example,
Aspland, Llewelyn, Hardy, Barkham, and Stiles (2008) found that such alliance
strains often arise in CBT in the context of therapist demand (e.g., convincing or
persuading) and are corrected only when the therapist realigns to understand the
client’s viewpoint.
The presence of interpersonal resistance (client disengagement from the therapist)
has been consistently found to be toxic to therapeutic outcomes. In their review of the
literature on (interpersonal) resistance, Beutler and colleagues concluded that there
is strong and consistent evidence that the effectiveness of psychotherapy is associated
with the relative absence of resistance (Beutler, Harwood, Michelson, Song, &
Holman, 2011). Even though it is relatively rare compared to client cooperation,
interpersonal resistance as early as the first session of therapy is a very strong
predictor of reduced subsequent engagement in CBT (in-session task involvement,
Jungbluth & Shirk, 2009; homework compliance, Aviram & Westra, 2011) and
poorer treatment outcome (Aviram & Westra, 2011; Westra, 2011). For example,
using observational coding of the first session of CBT, Aviram, Westra, and Eastwood
(2011) found that clients’ clear and unqualified opposition to the therapist (e.g.,
ignoring, interrupting, disagreeing, challenging) accounted for 30% of the variance
in outcomes for generalized anxiety disorder. Moreover, client hostility (direct or
indirect criticism of the therapist) accounted for an additional 10% of the variance
in treatment outcome over and above clear resistance. Hostility was even rarer than
interpersonal resistance, but the presence of even one instance of client hostility
toward the therapist in the first session of therapy was ultimately capable of predicting
treatment outcome. Such findings are consistent with other work suggesting that
even a small amount of hostility and negative interpersonal process can negatively
impact therapy outcomes (e.g., Binder & Strupp, 1997).
Given the strong capacity of interpersonal resistance to predict outcomes, the
presence of such resistance should then serve as a critical process marker in therapy.
Stated differently, not all moments may be equally important in the therapy process
and the identification of key moments (even if relatively rare) of tension in the therapy
alliance and client disengagement seem to be very important. In fact, observed
in-session resistance has been found to be a far better predictor of outcomes than
client self-reported motivation (Westra, 2011). In their review, Orlinsky, Grawe, and
Parks (1994) identified clients’ active involvement with the process of treatment as
among the most critical contributors to treatment outcomes. This result is consistent
with other studies finding that alliance ruptures are associated with poorer treatment
outcomes across a range of therapies, including CBT (Safran, Muran, & Eubanks-
Carter, 2011; Westra, Constantino, & Aviram, 2011).
Thus, it becomes incumbent on the therapist continually to monitor client engage-
ment with the process of therapy, and gauge the level of harmony and collaboration
in the process. Therapists also need to become adept at identifying the signs of
in-session client disengagement from the process of therapy (disagreeing, ignoring,
interrupting, withdrawal, passivity, criticizing, etc.). Moreover, since such process
markers (i.e., higher levels of interpersonal resistance) are strong predictors of sub-
sequent engagement (e.g., later homework compliance), therapists do not have to
wait until the client fails to complete homework to realize that there is a problem
with client engagement. Once identified, the manner in which therapists respond to
resistance plays a major role in perpetuating or diminishing it. In particular, therapist
directiveness has been found to reliably increase resistance (Beutler et al., 2011;
Beutler, Moleiro, & Talebi, 2002) whereas supportive approaches decrease resistance
(e.g., Patterson & Forgatch, 1985). For example, Miller, Benefield, and Tonigan
(1993) randomly assigned clients with problem drinking to therapists who used
either a client-centered or directive-confrontational counseling style. The directive
counseling style was associated with significantly higher levels of resistance which, in
turn, predicted poorer outcomes 1-year posttreatment. Aviram and Westra (2011)
found that the use of MI prior to CBT for anxiety (relative to no MI before CBT) was
associated with large reductions in observed interpersonal resistance. This reduction
in interpersonal resistance, in turn, mediated treatment outcomes. In other words,
clients who received MI in this study were visibly more engaged with the therapy
process in CBT than were individuals who had not received MI. Moreover, postther-
apy interviews revealed that clients who received MI prior to CBT reported that they
were more actively engaged in CBT and experienced their CBT therapists as more
collaborative than did participants who did not receive prior MI (Kertes, Westra,
Angus, & Marcus, 2011).
Finally, there is now evidence suggesting that the effective (supportive and
empathic) management of interpersonal resistance may also have implications for
the important common factor of client belief in the possibility that therapy will be
useful (i.e., outcome expectations; Constantino, Arnkoff, Glass, Ametrano, & Smith,
2011). Ahmed, Westra, and Constantino (2010) compared the interpersonal process
in session one of CBT for generalized anxiety disorder between clients who went on,
immediately after that session, to have high versus low outcome expectations (i.e.,
optimistic or pessimistic that treatment could help). Although groups were equiv-
alent overall in outcome expectations prior to the session, marked between-group
differences were found in interpersonal process during segments of the session when
interpersonal resistance was present. In essence, therapists of clients who went on to
have high outcome expectations managed to stay in friendly, affiliative harmony with
clients when their clients expressed doubts or disagreements. In contrast, clients who
went on to have low outcome expectations had therapists who had a much more
difficult time maintaining a harmonious encounter in the presence of client opposi-
tion. Nearly half the time in the low expectations group (versus less than 20% of the
time in the high expectations group), interactions during resistance episodes were
noncomplementary or nonreciprocal (i.e., client not following therapist, therapist not
following client) which is indicative of less satisfying, conflictual, anxiety-ridden, and
less stable interactions. In other words, therapists who managed to stay friendly and
warm, and were able to hear and respond to the client’s messages, even during times
of client doubt and opposition, or when clients presented challenges to the therapy or
therapist, had clients who went on to be more hopeful about the value of treatment.
This study further underscores not only the importance of navigating resistance well,
but also of relational skills and process sensitivity in contributing to client belief in
therapy.
However, responding to client opposition supportively, rather than directively,
is easier said than done. In a CBT context, reactions to resistance can often take
the form of “convincing or persuading” the client of the merits of change or of

the therapist’s offerings. Thus, therapists can sometimes feel like they are debating
with clients or working harder than their clients. Leahy (2001) notes that cognitive
behavioral therapists faced with resistance are typically encouraged to continue to
apply standard cognitive behavioral techniques. Raue and Goldfried (1994) suggest
that when reluctance to participate is expressed, the therapist’s role is to convince a
client that complying is in his or her best interests, fostering an attitude of friendly
submission. Indeed, cognitive behavioral therapists have been observed responding
to resistance and noncompliance by increasing their adherence to CBT techniques
(Aspland et al., 2008; Castonguay, Goldfried, Wiser, Raue, & Hayes, 1996).
To complicate matters further, resistance itself can be a trigger for therapist control.
Francis et al. (2005), for example, randomly assigned practitioners to interview an
individual (an actor) who portrayed a smoker either high or low in resistance to
change. Under conditions of high versus low client resistance, practitioners exhibited
significantly higher levels of confrontation, asked more closed and fewer open-ended
questions, and offered less praise and encouragement. Similarly, in a series of analogue
studies, Strupp and colleagues (as cited in Binder & Strupp, 1997) observed that
therapists often reacted negatively to patients who acted passively, pressed the therapist
for advice, or complained about the therapy or the therapist. These reactions were
often subtle and attributed to the motivational or interpersonal deficiencies of the
patients.
Thus, a major contribution of MI to clinical practice is the provision of an alterna-
tive, nonpejorative framework (with accompanying clinical strategies) for effectively
managing resistance. That is, regardless of whether the client articulates resistance to
change (i.e., arguments against change) or interpersonal opposition to the therapist
(disagreement, challenging, ignoring, etc.), MI provides a valuable way of thinking
about and responding effectively in these moments in order to maintain client engage-
ment. This may be particularly useful given that resistance represents a significant
threat to the therapeutic alliance and can often derail the therapeutic process. That
is, resistance is a critical “fork in the road” (i.e., process marker) for therapists, and
minimizing resistance is an important therapeutic task. Moreover, the data are very
clear that resistance is quite malleable and highly responsive to clinician style (Aviram
& Westra, 2011; Beutler et al., 2011; Miller et al., 1993). Below, an overview of MI
is provided, followed by a discussion of how MI, specifically, can be used to guide
therapist responses to both types of resistance, whether ambivalence about change or
interpersonal opposition to the therapist.
What Is Motivational Interviewing?
Any discussion of MI should begin with the “MI spirit” or client-centered nature of
the approach, since this is considered essential to the effective use of the method.
MI without the underlying spirit is like words without music and is not considered
MI (Rollnick & Miller, 1995). MI is an evolution of the client-centered therapy
explicated by Carl Rogers (1951, 1965) who emphasized empathic understanding of
the client’s internal frame of reference, and therapist communication and provision of
core facilitative relational conditions for client growth and change including accurate
empathy, unconditional positive regard, and therapist genuineness or congruence
(Rogers, 1957).
Like client-centered therapy, MI stresses the essential importance of the devel-
opment of a safe, collaborative atmosphere in which the client can sort out his or
her conflicting and often contradictory views of change. In this sense, MI converges
with the client-centered tradition of prioritizing the therapeutic relationship as an
essential vehicle in which greater self-awareness can be developed and new mean-
ings generated. Rogers’s emphasis on the importance of the therapeutic relationship
has since been supported by decades of research on the importance of relatedness
including research on the therapeutic alliance (Constantino, Castonguay, & Schut,
2002; Horvath & Symonds, 1991), attachment (Cassidy & Shaver, 1999), and the
necessity of caring, affection, and interpersonal safety for facilitating exploration and
new learning (Gilbert, 1993, 2010). In client accounts of their experiences of MI,
therapist empathy, and the provision of safety and freedom to explore, emerge as
prominent aspects of the approach (Marcus, Westra, Angus, & Kertes, 2011).
Consistent with its client-centered roots, Miller and Rollnick have emphasized
that MI is fundamentally a way of being with clients. This emphasis is consistent
with Rogers’s view of empathy as an attitude or way of being rather than a specific
technique per se (Rogers, 1980). The attitude one holds toward the client (prizing,
unconditional regard, warmth, genuineness, viewing the client as expert, etc.) is
more pivotal in MI than are the specific techniques. Stated differently, MI is not a
set of techniques. MI cannot be distilled into a set of questions or techniques one
can memorize and regurgitate in the absence of this fundamental spirit or attitude.
In other words, techniques can never be disembedded from their relational context
which is of paramount importance in MI. In fact, MI without a manual tends to
be more effective than structured MI with a manual (Hettema, Steele, & Miller,
2005). Similarly, MI cannot be equated with any particular method; it is not the
sum of its constituent parts. Rather, any technique (decisional balance, importance
and confidence ratings, forward looking, etc.) is merely an expression or instantiation
of the underlying spirit and objectives of MI. Even decisional balance, a technique
with which MI is often (incorrectly) equated, for example, is not an exercise that one
completes and is not even mandatory; rather it is merely a convenient and potentially
useful heuristic for advancing therapists’ (and therefore clients’) understanding and
exploration of ambivalence about change.
Defining the Spirit of Motivational Interviewing

Miller and Rollnick (2002) define the spirit of MI as consisting of three major dimen-
sions: collaboration, evocation, and preservation of client autonomy. In addition to
the expression of empathy, these constitute the major dimensions on which adherence
to MI is measured (Moyers, Martin, Manuel, & Miller, 2003). Collaboration refers to
working together in partnership or harmony with the client. Whereas all therapeutic
approaches strive to create a collaborative environment, in MI these efforts flow from a
particular view of the client and the change process. Namely, the client is not viewed as
deficient or lacking knowledge or expertise that the therapist then supplies, but rather
he or she is seen as already possessing all that is needed. Accordingly, motivation for
change and client resources in bringing about change are presumed to exist already
and are explored, elaborated, and supported. Thus, in MI the therapist considers the
client, and not him- or herself, as the authority or expert. Accordingly, MI therapists
avoid the use of persuasion and confronting clients with their point of view.
Evocation is the process of drawing out or calling forth the client’s ideas, rather
than seeking to emphasize or impose one’s own ideas. Evocative clinicians show a
high level of curiosity and a particular interest in supporting and helping clients to
articulate their own ideas regarding change. In MI, it is the client and not the therapist
who articulates the reasons for change and resolves ambivalence about change. This
is often a bottom-up or emergent process that requires patience: watching, waiting,
listening for, seeking, and creating opportunities to elicit client ideas regarding change
and the process of change. MI therapists actively avoid imposing their own views of
reasons for change, they do not educate or give opinions without being invited, and
they hold their own ideas lightly and are prepared to relinquish them, recognizing
the client’s authority as the arbiter of all decisions regarding change.
Again, the assumption underlying this evocative stance is that clients already
inherently possess the motivation and resources needed to accomplish behavior
change. The clinician who practices MI trusts this and thus seeks to identify, call
forth, elaborate, and mobilize these intrinsic resources, goals, desires, and values
in order to stimulate behavioral change. The therapist consistently communicates
the message: “I don’t have what you need, but you do.” This approach is at times
surprising for clients who often readily defer to others due to lack of confidence in their
own abilities to make decisions, take effective action, or pursue meaningful, satisfying
directions in their lives. Thus, this therapist belief in and approach to the client is a
very important antidote to the typical lack of self-regard and self-efficacy often seen
in clients with anxiety. The therapist’s belief in the client’s ability competently to
navigate the way forward itself translates into greater client self-belief, self-trust, and
agency.
Preserving and supporting client autonomy involves accepting that clients may
choose not to change, may avoid or delay change, or may proceed with change in an
unconventional manner. There is a need actively to recognize that the client is the
only authority on decisions regarding change and that this can never be appropriated
or usurped by another—no matter how well intentioned. The autonomy-supportive
clinician conveys an understanding that the critical variables for change are within the
client and can never be imposed by others. That is, motivation arises from personal
goals and values and not from external sources (including therapists).
Thus, MI is not coercive or “strategic.” MI is not a clever way of getting the
client to do what the therapist wants him or her to do. In fact, such controlling and
coercive attitudes are antithetical to the spirit of MI. The MI therapist recognizes,
sometimes explicitly, that choices always reside with the individual and can never be
appropriated by another. Pressuring and persuading clients (explicitly or implicitly)
to act in accordance with the therapist’s aspirations, desires, and needs introduces
contingencies in the relationship (i.e., conditional positive regard—“I will like and
accept you if you do this or think that … but not if you don’t”). Even if one “gains
compliance” (i.e., the client submits or relents), this “choice” is now confounded by
the client’s need to maintain harmony in the therapeutic relationship and may not
reflect consistency with his or her own intrinsic direction. The clinician practicing
MI actively becomes aware of, brackets, or “lets go” of any personal motivations or
aspirations for the client in order to be open to exploring the client’s goals, desires,
motives, and aspirations.
Another way in which the client’s autonomy and authority is communicated is
through the use of tentativeness (e.g., “I’m not sure about this … ,” “This may or
may not fit for you … ,” “If I hear you right, you are saying … ”), and encouraging
the client to check therapist inputs (e.g., reflections, feedback) against his or her own
experience. Essentially, the attitude is one of: “See what you think of this and check it
against your own experience, ideas, and preferences because what you think, not what
I think, is the most important thing here.” The implicit message is that the therapist
can never possess the truth about the client and can only ever guess about his or
her experience and offer thoughts (in the form of reflections, questions, feedback,
suggestions, ideas, etc.) for possible consideration if the client chooses to do so. It
is the client who is the ultimate arbiter of his or her choices and decisions regarding
if, when, and how to change. Accordingly, MI is not something one does to a client,
but rather with a client.
In short, in MI, clients are regarded as the best experts on themselves, with the
freedom to make their own choices, and as having an inherent and intrinsic knowledge
of what is best for them. The therapist operates as an evocative consultant or guide in
the client’s journey. In essence, through being collaborative, evocative, and preserving
and supporting autonomy, MI seeks to help clients recognize themselves as an authority.
MI promotes and supports the clients’ active use of that authority to make choices,
informed by a heightened awareness of their own best interests, values, and valued
directions.
Using Motivational Interviewing to Work with Resistance
Earlier, a distinction was drawn between two types of resistance: resistance to change
or ambivalence and resistance or opposition to the therapist or treatment. The first is
an intrapsychic or client variable whereas the second is an interpersonal phenomenon
and represents lack of collaboration between therapist and client. A major contribution
of MI is in the management of resistance—regardless of which type.
In general, MI strategies for navigating resistance reflect a spirit or attitude of
“dancing rather than wrestling” with resistance. This involves reframing or shifting
one’s view of resistance. In MI, resistance is not viewed as an obstacle to be defeated
but rather as important information to be understood, validated, and integrated. In
essence, at these times the client is sending critical signals that he or she has important
concerns that need to be heard and processed. Navigating resistance in this manner
can be among the most difficult of clinical skills to master (but highly worthwhile
in safeguarding the therapeutic alliance and allowing the client to process and work
toward resolving conflicting feelings that typically accompany change and treatment).
We now turn to how MI can be used to address both major types of resistance and
provide clinical illustrations.
Working with Resistance to Change (Ambivalence)
MI works from the assumption that many clients who seek therapy are ambivalent
about change and/or engaging in treatment, and that motivation may ebb and flow
during the course of therapy. That is, clients are not viewed pejoratively as “unmoti-
vated” or “resistant,” but rather, as “stuck” due to their internal experience of ambiva-
lence, which consists of forces for and against change. The MI therapist works with
fluctuations in motivation by adopting a position of equipoise with respect to change
and preserving client volition regarding change, rather than advocating for change.
Resistance to change (arguments against change or in favor of the status quo)
simply reflects important information to be understood and integrated. Here, clients
are merely articulating that there is an important part of them that is afraid of change
or resists change (typically for very good reasons). In exploring this part of the person,
the therapist consistently uses empathic listening to genuinely hear and validate the
“good things” the client is attempting to express and achieve through the “problem”
(and the bad things he or she is trying to avoid by not changing). In other words, the
therapist needs to be able to hear and help the client understand these objections to
change in order to allow the client to process them.
In exploring the status quo (the not-changing position), the therapist seeks the
answers to the following questions:
• “What is good about being the way you are (e.g., the problem/anxiety/
depression/bulimia, etc.)?”
• “What is helpful about the current behaviors or coping strategies (e.g., avoid-
ing, checking, ritualizing, getting reassurance, being overprotective, worrying,
isolating, planning, ruminating)?”
• “What important needs are being met by the problem?”
• “For what problem does this represent a solution?”
• “What positive motives and intentions are being expressed by the problem?”
• “What are the downsides to changing this problem? What would be bad about
change?”
• “How would change create its own set of problems or challenges?”
That is, what appears maladaptive on the surface is often driven by core needs such as
the desire for comfort, safety, connection, control, familiarity, success, freedom from
aversive experiences or consequences, and so on. The status quo often offers familiarity,
predictability, a sense of control (i.e., “the devil you know”), whereas change and the
steps to produce change are fraught with risk, uncertainty, unfamiliarity, discomfort,
and ambiguity (e.g., “Can I do it? Who will I be? What if I fail? How will others
regard me?”). Thus, when people act in ways that do not make sense to them (or
to others such as family members or helpers), there are “good reasons” (positive
intentions) underlying these actions and beliefs.
A rule of thumb for the MI therapist is to assume that if a client is thinking or doing
something, and persisting with it despite all of his or her efforts not to, there are
important reasons. Clients have been “led astray” by learning history (e.g., necessary
rules for survival and getting affection or support from important others) and previous
experience (e.g., avoidance is reinforcing in that it creates a positive feeling of safety
and may also reinforce the validity of the negative assumption), and have not learned
more adaptive ways of meeting these core needs. Thus, the job of the therapist is
to know that clients are after good things, to help them discover the motivations,
needs, and desires that are being expressed through the “problem,” and to increase
awareness of these so they can evaluate for themselves the need for and utility of the
assumptions/behavior in light of underlying values and needs.
Consider the following example of a 25-year-old client who articulated ambivalence
about his style of managing conflict. He indicated significant dissatisfaction at his
tendency to be withholding and punitive to others who have hurt or angered him.
In particular, this client characterized his approach as “immature” and noted that he
often sulks for a protracted period of time and is passive-aggressive (e.g., indirectly
indicating displeasure such as slamming doors, stomping around, giving people
“the silent treatment,” etc.), rather than more directly and assertively expressing his
feelings and navigating conflict openly. The client noted that although he knew what
a better strategy would be, he was consistently unable to navigate these situations in a
more “mature” manner. Having identified this ambivalence and internal resistance to
change, the therapist sought to explore the existing behavior and work to understand
the “good things” or positive motives which were being expressed by it.
THERAPIST: I hear that you are displeased with yourself for acting in an “immature”
manner. Often when we find ourselves doing things that we don’t like, it can serve us
somehow to get something important. If you are willing, can you say what are you
attempting to get or hoping to get by dragging out your displeasure at the other
person?
CLIENT: (pause) I think I want them to notice me—and to know that they hurt me.
THERAPIST: So this is a way of communicating very important feelings; things you don’t
want people to overlook or just pass over. And that sounds important given that you’ve
said that you often feel invisible or unimportant to others—it’s hard to get their
attention. (garnered from previous sessions with client; the therapist is attempting to
reframe “negative” behavior during conflict)
CLIENT: Right. Like I try and try to get my parents to take me seriously but usually, I
feel like I might as well just talk to the wall.
THERAPIST: So it goes nowhere and that’s what you’re used to. And you’ve had to
develop creative ways to get noticed—to be taken seriously. If I hear you right, you
have tried the “more mature” approach, probably quite a few times, and it hasn’t
worked.
CLIENT: Absolutely. Being rational and reasonable never accomplishes anything with
them.
THERAPIST: So it may not be ideal, and there are some things you don’t like about how
you’re acting—but it works! And it certainly sounds better than the alternative of just
giving up. (the therapist is seeking not only to understand what perpetuates the existing
behavior but also to validate that the behavior makes sense)
CLIENT: That’s true. But why can’t they just listen to reason? Why do I have to resort
to this?
THERAPIST: You sound frustrated with the situation and with yourself, for having to act
in ways that another part of you—the mature part—really dislikes. I’m curious. What
happens when you act this way with your parents? (i.e., the therapist, believing that there
are positive motives underlying seemingly negative and self-defeating behaviors, is trying to
identify these by exploring the genesis of this pattern)
CLIENT: Well, my dad, who just ignores me most of the time, comes around. Like when
I’m mad I usually say, “I don’t want to eat supper”—which is a big deal because of my
diabetes. Then he actually goes out of his way to come up to my room. And then he is
very sweet and kind and asks me to calm down. And then I usually draw it out—my
anger—some more.
THERAPIST: And what is it like when he comes to you and is kind?
CLIENT: It feels really good. Like he talks with me and notices me … (pause) and I feel
powerful.
THERAPIST: So quite a nice change from feeling helpless and powerless with him! And it
sounds like those are the rare moments where you feel connected with him—feel like
he cares (Client: Yes, absolutely). So it makes a lot of sense then that you would act this
way. If I’m hearing it right, it sounds like a brilliant and necessary strategy to get some
control and feel close to others. (the therapist is prizing and validating)
CLIENT: I never thought about it that way. But it actually does feel really good. Even
though I know I’m being stubborn and difficult, I like it in some ways.
THERAPIST: And you learned that people are like that—that they can only hear you
when you are stubborn and withdraw. So naturally, you would keep acting that way.
(here the therapist is guessing at an underlying assumption in order to deepen empathic
understanding and help the client examine the assumption for himself, if he chooses to)
CLIENT: But I don’t think that everyone is like that though.
THERAPIST: So there’s another part of you that thinks that the world, or others, may
operate with different rules or ways of conducting themselves. What makes you say
that? (the client, having further uncovered and heard what he thinks, then begins to
challenge the assumption; the therapist hears this protesting voice and invites the client to
expand further, inviting change talk. Importantly, the protest has arisen from the client
and not the therapist)
CLIENT: Well, my girlfriend. She really cares about me and how I’m feeling. She often
asks me how I’m doing, even when I’m not angry with her but I seem upset about
something or seem like I’ve had a bad day.
THERAPIST: So if I hear you right, you are saying, “I don’t have to be this way in order
for her to take an interest. I learned to be this way; it’s well-practiced—and it
works—at least with some people. But I may not have to be this way with everyone in
order to be taken seriously or to get others interested in me.” Is that right?
CLIENT: Yes. I hate it when I act all stubborn and immature with her because she
doesn’t deserve it and I just feel silly.
When the therapist reframes problematic views and reactions in this way, it not only
assists in helping clients become more aware of and deconstruct them, but also reduces
clients’ pejorative perceptions of resistance to change. Such pejorative perceptions of
ambivalence and resistance to change are very common and clients frequently express
frustration with themselves, or become overtly self-critical, because of their continued
thinking or acting in ways that they are painfully and acutely aware are self-defeating.
Therefore, the therapist holding and reflecting a more compassionate and accepting
view of resistance to change as understandable, normal, and informative can be a
powerful antidote to the client’s pejorative, self-critical attitudes and provide potent
modeling for enhancing positive client self-regard.
Therapists learning MI can sometimes articulate anxiety about reflecting, res-

onating, or siding with the reasons for not changing. This can indeed feel like an
unfamiliar position, particularly for therapists who are used to being more directive
and are adept at, and more familiar with, advocating for change. There can be a fear
that supporting clients’ understanding of the good reasons for not changing might
facilitate a decision not to change or is giving them “permission” to not change.
Here, it is important to remember that decisions about change can only rest with the
client and can never be usurped by another. Moreover, in exploring the advantages
to staying the same, therapists are not in fact reinforcing maladaptive behavior (e.g.,
avoidance, isolation, drinking), but rather, accepting and validating the motivations
underlying the behavior. One can support the client’s inherent desire for safety
and connection with others, for example, while facilitating his or her own deter-
mination of whether the current means for accomplishing these ends are sufficient,
useful, and congruent with values. Finally, empathic understanding is not the same
as agreement; the latter is a judgment that comes from the therapist’s own frame of
reference, whereas the former is merely an attempt to understand the client’s frame
of reference.
Therapists may also be tempted to view such methods as a clever way of overcoming
resistance to change so that one can move more productively to helping the client
take action to achieve change. While this is of course ultimately true, it can represent a
subtle, but very important, deviation from MI spirit. Any therapist agenda for change,
no matter how well intentioned, can interfere with communicating and embodying
the sincerity, genuineness, and congruence that underlies the spirit of MI.
Rolling with Interpersonal Resistance

In MI, interpersonal resistance or opposition to the direction of the therapist (or
treatment) is simply a signal of client disengagement—of momentary disharmony
in the relationship. This form of resistance can commonly occur when the therapist
advises, directs, or makes suggestions in the context of client ambivalence. As discussed
previously, identifying and minimizing such interactions is vital to successful therapy
since interpersonal resistance, even in small doses, can adversely impact therapy process
and outcomes.
Miller and Rollnick (2002) discuss such resistance as reflecting a “stop” signal by the
client that indicates that the therapist is moving too quickly or is ahead of the client’s
current level of readiness. This resistance communicates vitally important information
about engagement and collaboration; namely, that the therapist is not on the same
page as the client—the therapist is not appreciating something important that the
client is attempting to communicate or bring into the conversation. Identifying and
effectively navigating (rolling with) resistance is a key skill in MI, and as such may
hold promise in helping therapists develop confidence and competence in responding
to key and commonly occurring clinical events in CBT such as client resistance
(disagreement, challenging, side-tracking and ignoring, etc.) and noncompliance.
Specific strategies for rolling with resistance are outlined in MI (Miller & Roll-
nick, 2002) and include various forms of reflection (e.g., double-sided, amplified),
reframing resistance (seeing the wisdom in it), getting alongside of resistance, and
emphasizing person choice and autonomy, among others (several of these strategies
are illustrated in the example below). The therapist must continually monitor the
interaction for evidence of client disengagement (interpersonal resistance); rather than
persisting with his or her own agenda, the therapist needs to shift to effectively hear
the message that the client is communicating.
We now turn to an example of client opposition to the therapist (i.e., interpersonal
resistance) for a client seeking therapy to reduce chronic tendencies toward excessive
organization and orderliness that she would exhibit as well as impose on others.
Within the example, the signals of client disengagement are noted. Following this is
an outline of how the same interaction might proceed if it were conducted in MI
style, using MI strategies for rolling with resistance.
THERAPIST: So if you were to begin changing this problem, where would you start?
CLIENT: (quickly) I don’t know. I have no idea. (resistance: passivity reflecting
disengagement)
THERAPIST: Is there anything from your previous experience of getting over the fear of
driving that could be useful here?
CLIENT: I don’t think that’s the same at all. (resistance: client disagreeing, objecting to
therapist’s suggestion)
THERAPIST: Well, actually strategies for overcoming anxiety can have a lot in common,
even though the situation is different. It sounds like in the past, when you overcame
your fear of driving, you let go of some of the specific behaviors that the anxiety told
you were necessary to stay safe—like not driving fast, not venturing too far … You
changed things up. For being overly organized, a similar strategy might involve letting
go of some of the organizing and not having everything in its place all the time. This
might be a kind of experiment to see if you need to do those things. It will make you
more anxious in the short term—just like the driving did—but you might find out
whether or not the anxiety eventually goes down as you change things up. How does
that …
CLIENT: (interrupts) I don’t want people to think I’m lazy though if I don’t clean up
right away. (resistance: interrupting, disagreeing, articulating arguments for not
changing)
THERAPIST: Would people think that though? Is there a chance they wouldn’t think
that?
CLIENT: (passively) Well, maybe not but it’s important to me to be impressive to others.
Like when we get together with other parents, and my kids will talk about all the fun
things we do, people say, “Gosh, you do a lot of stuff with your kids.” And that makes
me feel good. It makes me feel like I’m a great mom. (resistance: passivity in initial
agreement with the therapist, that feels like “throw away” agreement, and then elaboration
of disagreement)
THERAPIST: I could be wrong about this, but I also seem to recall that one of the
reasons you wanted to work on the problem is because you’re concerned about how
being overly organized might affect your kids. Is that right?
CLIENT: Yes, I do worry that I might be pushing them too hard but I worry too about
letting things go. (resistance: “Yes, but …”)
THERAPIST: I wonder if the best thing for your kids would be for you to be less
perfect—less organized.
CLIENT: I do want them to have a terrific childhood though. (resistance: ignoring and
disagreeing)
THERAPIST: And it sounds like your anxiety says that a perfect childhood is one that is
completely stimulating. I wonder if another version of a terrific childhood is one in
which you do things with your kids but it’s more balanced, where you let go of some
stuff—where you don’t have to be on the go all the time and everything doesn’t have
to be super organized.
CLIENT: I’d like my kids to have more freedom but I have a hard time letting go of
some things. (resistance: “Yes, but …”)
THERAPIST: Well, we can work on that together.
Here, by repeatedly placing demands on the ambivalent client, the therapist creates
a tense, conflictual interpersonal climate. By continuing with his or her agenda for
the client to change and see/do things differently, and failing to hear the client’s
objections (and more broadly, the client’s signals of resistance and disengagement
with the proposed task), the client is placed in the position of further articulating
objections to change in order to oppose the therapist. However, the client is simply
articulating that there is an important part of her that resists or fears change, and is
seeking to have this heard and understood. If this important information is not heard,
the client can persist (and often turn up the volume or make repeated attempts to
communicate her objections to change). In essence this results in client and therapist
acting out the client’s ambivalence (each taking a side), rather than helping the client
to process her ambivalence and work through it. In order to work more harmoniously
and reestablish collaboration, the therapist integrating MI would be alert for such
signals of disharmony and shift from a directive to a more supportive, exploratory,
and empathic stance, as in the following example:
THERAPIST: So if you were to begin changing this problem, where would you start?
CLIENT: (quickly) I don’t know. I have no idea. (resistance: passivity reflecting
disengagement)
THERAPIST: It’s hard to know even where to begin. And only you can know whether it
makes sense right now to start changing this. It might not. What are your thoughts?
(noticing resistance and explicitly emphasizing client choice and control)
CLIENT: Well, I do worry that I’m setting a bad example for my kids. I feel like I push
them too hard and I need to let go of some of that. But at the same time, I worry
about letting go too. (note here that the therapist’s support of the client’s autonomy allows
the client to articulate her ambivalence—but not have to disagree or oppose the therapist
in order to do so)
THERAPIST: It sounds like you feel conflicted about changing this. And I’m also hearing
that you might be afraid of what would happen if you do let up more. Is that right? (the
therapist reflects and aims to help the client further understand her ambivalence, getting
alongside of resistance by doing so the therapist is showing the client that he or she is willing
and able to hear objections to change and/or concerns about treatment)
CLIENT: Yes. Like I worry a lot about what other people think of me. It’s important to
me that people look up to me. Like when people say, “Gosh, you do a lot of fun stuff
with your kids,” I feel really proud as a mom. (the therapist’s continued empathic
responding eliminates interpersonal resistance; it enables the client to feel safe to explore
further)
THERAPIST: Naturally, who wouldn’t? So, this is an important way of feeling good
about yourself. (validating underlying positive intentions of the existing behavior)
CLIENT: Right. Like right now, other parents look up to me. They ask me for advice.
They admire me.
THERAPIST: And that feels good. And it sounds like it’s important not to risk losing that
… because you’re thinking, “If I weren’t the perfect mom, people might not respect
me … and I might damage my kids too. I would feel worse and they would feel worse.”
(amplified reflection of resistance to change; further guessing at underlying assumptions)
CLIENT: That sounds a bit extreme actually. (emergence of change position in response to
rolling with resistance; note here that the therapist’s task is to continually hear which side of
the ambivalence the client is articulating and seek to elaborate it in order to understand it
more fully; here, since the change position emerges, the therapist seeks to elaborate this)
THERAPIST: Maybe that’s not really true. Can you say more?
CLIENT: Well, I know that I overdo it with my kids and I need to let up sometimes.
And as much as I like working hard to be a great parent, I think going overboard also
sets a bad example for them too. Like, I already see my son getting flustered when his
things are out of order. He gets really upset about it and he’s five! (notice here as well
that the therapist’s rolling with resistance allows the client—and not the therapist—to
articulate the arguments for change)
THERAPIST: So while being a perfect mom is really gratifying in many ways, there’s a
sense that there is a significant cost to this—this could hurt my kids. And when you
think about that, you feel … (encouraging further elaboration of emergent change voice)
CLIENT: (sullen) Sad … that he might turn out to have anxiety like me … (pause) and
angry at myself for setting him up for that.
THERAPIST: I can see from how you say that that this really troubles you (Client: Yes).
And you also feel like this is something you might have some control over (pause). This
might be going too far, but I’m also hearing “If the perfectionism hurts my kids, it may
not be worth it.” (the therapist is explicitly attuned to how the client talks; also bringing
the two sides of ambivalence together to help the client work toward further resolving it)
CLIENT: Yeah. They are just too important. (pause) But I think it’s going to be hard
too. (ambivalence and resistance reemerge as the client more fully articulates or aligns
with the change position; this is very common and the therapist then hears this and
continues to roll with resistance as needed)
THERAPIST: Absolutely. There is a powerful part of you that tells you to back off from
being less perfectionistic and at the same time, it’s something you want. (reflection of
ambivalence)
Sometimes only momentary efforts to roll with resistance are needed, whereas at
other times more extended use of this empathic, exploratory style is required to
reestablish engagement. Notice that the MI strategies for navigating interpersonal
resistance (rolling with resistance, as outlined by Miller & Rollnick, 2002) illustrated
in the latter part of this brief vignette are identical in spirit to those used in working
with resistance to change. In essence, regardless of whether resistance appears in the
clinical encounter between client and therapist (disagreeing, ignoring, passivity, etc.)
or involves a client-articulated internal reticence to change, the general directive is to
resist defeating the resistance (as this will only either amplify interpersonal resistance
or fail to help the client resolve ambivalence). Rather, from an MI perspective, one
seeks to understand, validate, elaborate, and more generally roll with resistance and
get alongside of it. Note that when used to respond to alliance tensions (passivity,
arguing, etc.) these strategies can often have a rather immediate impact of diminishing
resistance, reengaging the client, and reestablishing client–therapist collaboration.
Note that in both illustrations above, the client articulated important reservations
about or objections to change. However, in the first (MI-inconsistent) illustration
these were associated with a feeling of disharmony, tension, or client and therapist
being at cross-purposes. In the second (MI-consistent) illustration, such disharmony
was not present. Stated differently, in the MI-consistent illustration, the client is safe
or free to articulate objections to change or treatment without fear of alienating the
therapist or threatening the therapeutic alliance.
Evidence for Extending Motivational Interviewing
The diversity in the ways that MI (and/or related procedures that include elements
of MI, often known as motivational enhancement therapy [MET]) has been utilized
across major mental health populations is striking (for a review, see Westra, Aviram, &
Doell, 2011). Most commonly, MI has been used as a prelude or pretreatment to other
therapies, or as an approach that is integrated into standard assessment and intake
procedures designed to increase motivation and engagement in treatment. MI has also
been added or integrated throughout treatment as one part of a larger multicomponent
treatment package. It has also been used to increase treatment-seeking among those
who are either not seeking or refuse treatment, and to increase antidepressant and
antipsychotic medication compliance. Other recommended possibilities for the use of
MI have included early prevention among those deemed at risk for developing mental
health problems, training significant others in MI to facilitate client recovery, and the
use of MI as a foundational framework into which other treatments can be integrated.
MI is a well-supported treatment in the substance abuse domain (e.g., Hettema
et al., 2005; Lundahl, Kunz, Brownell, Tollefson, & Burke, 2010) and it seems to
make good clinical sense to integrate it into the treatment of other major mental health
problems. However, apart from research in the area of dual diagnosis (psychosis and
substance abuse), research has only recently begun to test the value of adding MI to
existing treatments for common mental health problems (Westra, 2011). Consistent
with the early stage of this work, this research includes uncontrolled case studies and
controlled pilot studies.
Although most research on the application of MI to the treatment of major mental
health problems is in the early stages and has a number of important methodological
limitations, existing findings strongly support the continued evaluation of the potential
of MI to enhance outcomes. In general, positive findings for enhancing engagement
with, and response to, treatment have been reported for MI as a prelude to other
therapies in areas such as anxiety disorders (e.g., obsessive-compulsive disorder:
McCabe, Rowa, Antony, Young, & Swinson, 2008; generalized anxiety disorder:
Westra, Arkowitz, & Dozois, 2009), depression (e.g., Swartz et al., 2006; Van
Vorrhees et al., 2009), and eating disorders (e.g., Cassin, von Ranson, Heng, Brar,
& Wojtowicz, 2008; Wade, Frayne, Edwards, Robertson, & Gilchrist, 2009). In
the area of dual diagnosis (psychosis with comorbid substance abuse), randomized
controlled trials (RCTs) comparing adapted MI interventions have been found to be
superior to education controls in reducing substance abuse and improving psychiatric
symptoms (e.g., Bellack, Bennett, Gearon, Brown, & Yang, 2006; Kavanagh et al.,
2004). Here, RCTs have also supported the use of integrated MI interventions
in enhancing adherence to antipsychotic medication (e.g., Gray, Wykes, Edmonds,
Leese, & Gournay, 2004; Kemp, Kirov, Everitt, Hayward, & David, 1998).
Interestingly, although MI has not been consistently associated with higher self-
reported motivation in some domains (e.g., anxiety, depression) relative to controls,
it is consistently associated with a specific behavior change (e.g., entry into treatment,
attendance, decreased symptoms). It may be the case that in these domains, clients
are understandably reluctant to report themselves as less than optimally interested in
reducing highly aversive affective states such as anxiety or depression. As such, self-
report measures tend to exhibit ceiling effects, thereby limiting their utility. Despite
this, advantages in favor of MI are importantly observed on behavioral targets and
actual symptom change.
Moreover, the findings from existing studies on extending MI to other major
mental health problems are impressive given that many of the populations included
in these studies have quite severe symptoms and are difficult to engage (e.g., those
refusing treatment or typically unwilling to seek therapy, those with severe eating
disorders, severe anxiety disorders, comorbid psychosis, and substance abuse). Even
modest success in improving engagement and outcomes with treatment among these
individuals represents a significant accomplishment, and merits further exploration.
While promising, most of these studies have a number of important limitations, and
additional research, using rigorous controlled designs, is needed to determine the
value of adding and/or integrating MI with other treatments for common mental
health problems.
Training and Future Directions
MI is deceptively simple. As Miller and Rollnick (2009) note, MI involves a complex

set of skills that are used flexibly, responding to moment-to-moment changes in
the client. Remaining in harmony with another requires a continual and high level
of attunement and responsivity to one’s partner—noticing moment-to-moment
fluctuations in order to know what to do next. Moreover, complex skills such as
empathy, providing unconditional regard, and prizing clients (especially when it
might be tempting to feel frustrated with them) are seemingly straightforward but
very difficult to instantiate in practice. Particularly if therapists come from a more
directive therapy orientation, skillfully blending supportive and directive approaches
can be very challenging. More information on useful sources to develop MI skills is
presented in the “Further Reading” section.
Some trainees take to MI more easily than others and this is an interesting question
in its own right regarding the facilitative preconditions for effective MI practice
and competence. Miller and colleagues’ work on training in MI suggests that direct
coaching and feedback are essential to competent MI practice. Clinicians should resist
the temptation to assume they already do MI, because self-perceived competence
in MI and in reflective listening more generally is unrelated to actual observed
proficiency (Miller & Mount, 2001). Clinicians should also avoid assuming that
adequate MI proficiency can be attained by attending a workshop (Miller, Yahne,
Moyers, Martinez, & Pirritano, 2004)—in much the same way as one cannot learn
to play the violin in a day (Miller & Rollnick, 2009).
In considering future directions for research on MI for major mental health
problems beyond addictions, there is a very clear need for controlled, rigorous
clinical trials of MI for most major mental problems. This is especially important
given that MI is being widely recommended by clinical researchers for inclusion
in existing treatments for many major mental health problems, but very few well-
controlled studies (randomly assigning clients to MI or an equivalent therapist
contact or therapy control) have been conducted to date. Moreover, process research
on mechanisms of MI is largely absent in the existing literature. While MI is associated
with increased attendance and engagement with treatment, more research from well-
controlled studies is required to identify whether such effects (or others) account for
or mediate the impact of adding MI on clinical outcomes. Additionally, quantitative
and qualitative research methods are needed to identify the major active ingredients
within MI. For example, Marcus et al. (2011) reported that client accounts of their
experiences of MI as a pretreatment for generalized anxiety disorder reflected increased
motivation, the importance of therapist empathy, and the creation of a safe climate
to explore feelings about change. The delineation of these mechanisms has important
implications both for understanding how MI works, and for effective training in MI.
Commensurate with this, the development of adequate measures (both self-report
and therapy process measures such as resistance or client active engagement in actual
therapy sessions) will help facilitate a clearer delineation of the impact and mechanisms
of MI.
Relatedly, more research is needed to identify those for whom MI is particularly
indicated (i.e., moderators of treatment effects). MI may not be necessary or useful
for all clients. Similarly, not all clients may need the same dose of MI. For example,
Westra et al. (2009) found that only those with high worry severity exhibited
augmented treatment response when MI was added to existing treatment, compared
to those with moderate worry severity. Identifying the characteristics of individuals
who are particularly likely to require and respond to MI (e.g., individual differences
in motivation, resistance, interpersonal problems, expectations, etc.) will assist in
tailoring treatment and identifying markers of the need to shift between MI and
more action-oriented treatments during therapy. Relatedly, given the heavy reliance
on empathy and relationship development in MI, it will be useful to evaluate whether
MI can be effectively delivered for these populations in group formats. As research
on MI evolves in these mental health domains, identifying individual differences in
treatment response, and critically evaluating the formats of MI delivery, will represent
important research goals.
In summary, interest in and research on MI for major mental health problems
beyond addictions is evolving rapidly. Such extensions of MI make good clinical
sense given the increasing recognition of the importance of client engagement
and disengagement with therapy, and the need to explicitly integrate approaches
for helping clients navigate ambivalence about change. Moreover, MI is a flexible
approach that can be added to or integrated with existing empirically supported
approaches to treatment for a wide range of mental health problems. Given the
significance of resistance (both resistance to change, and resistance to therapy or
the therapist) to therapy process and outcomes, MI occupies an important place in

clinical practice. In particular, the emphasis in MI on understanding and rolling with
resistance provides the therapist with important and effective ways of responding
in the presence of process markers of resistance to maintain collaboration, reduce
therapist frustration, and facilitate high levels of client engagement.
References
Ahmed, M., Westra, H. A., & Constantino, M. J. (2010). Interpersonal process during resistance
in CBT associated with high vs low client outcome expectations: A micro-process analysis. Paper
presented at the annual meeting of the Society for Psychotherapy Research, Asilomar, CA.
American Psychological Association. (2010). Division 12 Committee on building a two-way
bridge between research and practice: Clinicians’ experiences in using an empirically
supported treatment for panic disorder. Clinical Psychologist, 64, 10–20.
Arkowitz, H., Westra H. A., Miller, W. R., & Rollnick, S. (2008). Motivational interviewing
in the treatment of psychological problems. New York, NY: Guilford Press.
Aspland, H., Llewelyn, S., Hardy, G. E., Barkham, M., & Stiles, W. (2008). Alliance rup-
tures and rupture resolution in cognitive-behavior therapy: A preliminary task analysis.
Psychotherapy Research, 18, 699–710.
Aviram, A., & Westra, H. A. (2011). The impact of motivational interviewing on resistance
in cognitive behavioural therapy for generalized anxiety disorder. Psychotherapy Research,
21, 698–708.
Aviram, A., Westra, H. A., & Eastwood, J. (2011, June). Patterns of early resistance and client
outcome in cognitive behavioural therapy. Paper presented at the Meeting of the North
American Society for Psychotherapy Research, Banff, Canada.
Bellack, A. S., Bennett, M. E., Gearon, J. S., Brown, C. H., & Yang, Y. (2006). A randomized
clinical trial of a new behavioral treatment for drug abuse in people with severe and
persistent mental illness. Archives of General Psychiatry, 63, 426–432.
Beutler, L. E., Harwood, T. M., Michelson, A., Song, X., & Holman, J. (2011). Resis-
tance/reactance level. Journal of Clinical Psychology, 67 , 133–142.
Beutler, L. E., Moleiro, C. M., & Talebi, H. (2002). Resistance in psychotherapy: What con-
clusions are supported by research. Journal of Clinical Psychology In Session: Psychotherapy
in Practice, 58, 207–217.
Binder, J. L., & Strupp, H. H. (1997). “Negative process”: A recurrently discovered and
underestimated facet of therapeutic process and outcome in the individual psychotherapy
of adults. Clinical Psychology: Science and Practice, 4, 121–139.
Cassidy, J., & Shaver, P. R. (Eds.) (1999). Handbook of attachment: Theory, research, and
clinical applications. New York, NY: Guilford Press.
Cassin, S. E., von Ranson, K. M., Heng, K., Brar, J., & Wojtowicz, A. E. (2008). Adapted
motivational interviewing for women with binge eating disorder: A randomized controlled
trial. Psychology of Addictive Behaviors, 22, 417–425.
Castonguay, L. G., Goldfried, M. R., Wiser, S., Raue, P. J., & Hayes, A. M. (1996). Predicting
the effect of cognitive therapy for depression: A study of unique and common factors.
Constantino, M. J., Arnkoff, D. B., Glass, C. R., Ametrano, R. M., & Smith, J. Z. (2011).
Expectations. Journal of Clinical Psychology, 67 , 184–192.
Constantino, M. J., Castonguay, L. G., & Schut, A. J. (2002). The working alliance: A flagship
for the “scientist-practitioner” model in psychotherapy. In G. S. Tryon (Ed.), Counseling
based on process research: Applying what we know (pp. 81–131). Boston, MA: Allyn &
Bacon.
Francis, N., Rollnick, S., McCambridge, J., Butler, C., Lane, C., & Hood, K. (2005). When
smokers are resistant to change: Experimental analysis of the effect of patient resistance
on practitioner behaviour. Addiction, 100, 1175–1182.
Gilbert, P. (1993). Defence and safety: Their function in social behaviour and psychopathology.
British Journal of Clinical Psychology, 32, 131–153.
Gilbert, P. (2010). Attachment and the importance of affection. In P. Gilbert (Ed.), Compassion
focused therapy (pp. 39–42). New York, NY: Routledge.
Gray, R., Wykes, T., Edmonds, M., Leese, M., & Gournay, K. (2004). Effect of a medi-
cation management training package for nurses on clinical outcomes for patients with
schizophrenia: Cluster randomised controlled trial. British Journal of Psychiatry, 185,
157–162.
Helbig, S., & Fehm, L. (2004). Problems with homework in CBT: Rare exception or rather
frequent? Behavioral and Cognitive Psychotherapy, 32, 291–301.
Hettema, J., Steele, J., & Miller, W. R. (2005). Motivational interviewing. Annual Review of
Horvath, A. O., & Symonds, B. D. (1991). Relation between working alliance and outcome
in psychotherapy: A meta-analysis. Journal of Counseling Psychology, 38, 139–149.
Jungbluth, N. J., & Shirk, S. R. (2009). Therapist strategies for building involvement in
cognitive-behavioral therapy for adolescent depression. Journal of Consulting & Clinical
Psychology, 77 , 1179–1184.
Kavanagh, D. J., Young, R., White, A., Saunders, J. B., Wallis, J., Shockley, N., … Clair, A.
(2004). A brief motivational intervention for substance misuse in recent-onset psychosis.
Drug and Alcohol Review, 23, 151–155.
Kemp, R., Kirov, G., Everitt, B., Hayward, P., & David, A. (1998). Randomised controlled trial
of compliance therapy: 18-month follow-up. British Journal of Psychiatry, 172, 416–419.
Kertes, A., Westra, H. A., Angus, L., & Marcus, M. (2011). Client experiences of cognitive
behavioral therapy for generalized anxiety disorder: The impact of adding motivational
interviewing. Cognitive & Behavioural Practice, 18, 55–69.
Kushner, M. G., & Sher, K. J. (1989). Fear of psychological treatment and its relation to mental
health service avoidance. Professional Psychology: Research and Practice, 20, 251–257.
Leahy, R. L. (2001). Overcoming resistance in cognitive therapy. New York, NY: Guilford Press.
Lundahl, B. W., Kunz, C., Brownell, C., Tollefson, D., & Burke, B. (2010). A meta-analysis of
motivational interviewing: Twenty-five years of empirical studies. Research on Social Work
Practice, 20, 137–160.
Marcus, M., Westra, H. A., Angus, L., & Kertes, A. (2011). Client experiences of motivational
interviewing for generalized anxiety disorder. Psychotherapy Research, 21, 447–461.
McCabe, R. E., Rowa, K., Antony, M. M., Young, L., & Swinson, R. P. (2008, November).
Using motivational enhancement to augment treatment outcome following exposure and
response prevention for obsessive compulsive disorder: Preliminary findings. Paper presented at
the Annual Meeting of the Association for Behavioral and Cognitive Therapies, Orlando,
FL.
Miller, W. R., Benefield, R. G., & Tonigan, J. S. (1993). Enhancing motivation for change in
problem drinking: A controlled comparison of two therapist styles. Journal of Consulting
Miller, W. R., & Mount, K. A. (2001). A small study of training in motivational interviewing:
Does one workshop change clinician and client behavior? Behavioural & Cognitive
Miller, W. R., & Rollnick, S. (2009). Ten things that motivational interviewing is not.
Behavioural and Cognitive Psychotherapy, 37 , 129–140.
Miller, W. R., Yahne, C. E., Moyers, T. B., Martinez, J., & Pirritano, M. (2004). A randomized
trial of methods to help clinicians learn motivational interviewing. Journal of Consulting
& Clinical Psychology, 71, 754–763.
Moyers, T. B., Martin, T., Manuel, J. K., & Miller, W. R. (2003). The motivational interviewing
treatment integrity (MITI) code (coding manual). Albuquerque, NM: University of New
Mexico, Center on Alcoholism, Substance Abuse and Addictions (CASAA).
Moyers, T. B., & Rollnick, S. (2002). A motivational interviewing perspective on resistance in
psychotherapy. Journal of Clinical Psychology, 58, 185–193.
Newman, C. F. (1994). Understanding client resistance: Methods for enhancing motivation
for change. Cognitive and Behavioral Practice, 1, 47–69.
Orlinsky, D. E., Grawe, K., & Parks, B. K. (1994). Process and outcome in psychotherapy:
Noch einmal. In A. E. Bergin & S. L. Garfield (Eds.), Handbook of psychotherapy and
behavior change (4th ed., pp. 270–376). Chichester, England: John Wiley & Sons, Ltd.
Patterson, G. R., & Forgatch, M. S. (1985). Therapist behavior as a determinant for client
noncompliance: A paradox for the behavior modifier. Journal of Consulting and Clinical
Raue, P. J., & Goldfried, M. R. (1994). The therapeutic alliance in cognitive behavioral
therapy. In A. O. Horvath (Ed.), The working alliance: Theory, research, and practice (pp.
131–152). New York, NY: John Wiley & Sons, Inc.
Rogers, C. R. (1951). Client-centered therapy. Boston, MA: Houghton Mifflin.
Rogers, C. R. (1957). The necessary and sufficient conditions of therapeutic personality
change. Journal of Consulting Psychology, 21, 95–103.
Rogers, C. R. (1965). Client-centered therapy: Its current practice, implications, and theory.
Boston, MA: Houghton Mifflin.
Rogers, C. R. (1980). A way of being. Boston, MA: Houghton Mifflin.
Rollnick, S., & Miller, W. R. (1995). What is motivational interviewing? Behavioral & Cognitive
Safran, J. D., Muran, J. C., & Eubanks-Carter, C. (2011). Repairing alliance ruptures. In J. C.
Norcross (Ed.), Psychotherapy relationships that work: Evidence-based responsiveness (2nd
ed., pp. 224–238). New York, NY: Oxford University Press.
Swartz, H. A., Zuckoff, A., Frank, E., Spielvogle, H. N., Shear, M. K., Fleming M. A. D.,
& Scott, J. (2006). An open-label trial of enhanced brief interpersonal psychotherapy
in depressed mothers whose children are receiving psychiatric treatment. Depression and
Anxiety, 23, 398–404.
Van Vorrhees, B. W., Fogel, J., Pomper, B. E., Marko, M., Reid, N., Watson, N., …
Domanico, R. (2009). Adolescent dose and ratings of an internet-based depression
prevention program: A randomized trial of primary care physician brief advice versus a
motivational interview. Journal of Cognitive and Behavioral Psychotherapies, 9, 1–19.
Vitousek, K., Watson, S., & Wilson, G. T. (1998). Enhancing motivation for change in
treatment-resistant eating disorders. Clinical Psychology Review, 18, 391–420.
Wade, T. D., Frayne, A., Edwards, S. A., Robertson, T., & Gilchrist, P. (2009). Motivational
change in an inpatient anorexia nervosa population and implications for treatment.
Australian and New Zealand Journal of Psychiatry, 43, 235–243.
Westra, H. A. (2011). Comparing the predictive capacity of observed in-session resistance to
self-reported motivation in cognitive behavioral therapy. Behavior Research and Therapy,
49, 106–113.
Westra, H. A. (2012). Motivational interviewing in the treatment of anxiety. New York, NY:
Guilford Press.
Westra, H. A., Arkowitz, H., & Dozois, D. J. A. (2009). Adding a motivational interview-
ing pretreatment to cognitive behavioral therapy for generalized anxiety disorder: A
preliminary randomized controlled trial. Journal of Anxiety Disorders, 23, 1106–1117.
Westra, H. A., Aviram, A., & Doell, F. (2011). Extending motivational interviewing to the
treatment of major mental health problems: Current directions and evidence. Canadian
Journal of Psychiatry, 56, 643–650.
Westra, H. A., Constantino, M. J., & Aviram, A. (2011). The impact of alliance ruptures on
client outcome expectations in cognitive behavioral therapy. Psychotherapy Research, 21,
472–481.
16
Dealing with Difficult Cases
Leslie Sokol and Marci G. Fox
Academy of Cognitive Therapy, United States
Emily Becker-Weidman
Center for Family Development and New York University,
Child Study Center, United States
Roadblocks to the therapeutic process can significantly interfere with effective treat-
ment. These obstacles can be categorized into three main areas: (a) the therapist’s
ability to conceptualize the case and apply effective interventions, (b) the therapist’s
application of session structure, conducted collaboratively with the patient, and (c)
patient variables, such as level of commitment and complexity of diagnosis. Cognitive
behavioral therapy (CBT) emphasizes the importance of individually tailoring treat-
ment to each patient, based on the case conceptualization, problem areas, and overall
goals. At the same time it is important for the therapist to be flexible and creative in
his or her design of treatment by collaborating with the patient and applying empirical
evidence supporting each intervention.
Difficulty Conceptualizing the Patient and the Problem
Case conceptualization is a key element of effective treatment; an incorrect or

misapplied conceptualization can be a significant roadblock to effective therapy.
A fine-tuned case conceptualization is critical to developing an understanding of a
patient and how he or she makes sense of self, others, and the world (A. T. Beck, Rush,
Shaw, & Emery, 1979). Without a comprehensive case formulation, the therapist
tends to operate less effectively, applying interventions randomly and hoping that they
work. The case conceptualization is the therapist’s working model of a patient and
fosters a clear understanding of the patient’s perspective and view of self (Kuyken,
Padesky, & Dudley, 2009). The more multifaceted the patient, the more complex
and essential the conceptualization becomes.
The case conceptualization is the individually tailored road map of each patient.
According to Persons (2006), case conceptualization-driven psychotherapy is based on

DOI: 10.1002/9781118528563.wbcbt16
individualized case formulation in order to guide treatment planning and intervention

selection, utilizing a hypothesis-testing empirical approach. It is important for the
clinician to develop the conceptualization based on the patient’s clinical presentation
as early as the intake evaluation and to modify it throughout the course of treatment
as the therapist learns more about the patient. The case conceptualization consists
of the patient’s diagnosis, current problems including how they developed and how
they are maintained, associated dysfunctional thoughts, and the beliefs that trigger
the emotional, physiological, and behavioral reactions (J. S. Beck, 1995). Case
conceptualization includes a focus on events and automatic thoughts, as well as early
experiences and core and intermediate beliefs related to automatic thoughts (Wenzel,
Brown, & Beck, 2009). A solid case formulation also involves an emphasis on a
patient’s typical behavioral and coping strategies.
Brian, for example, lashes out at others when he believes he is being criticized. In the
past he has been treated for anger management but finds that he experiences continued
distress and resorts to storming out of the room or yelling at colleagues. A careful
evaluation of Brian’s behaviors might lead to a conceptualization that posits that
Brian’s self-doubt about being capable gets activated through his negative conditional
assumption. He assumes, “If I’m questioned, given feedback, or criticized, then I’m
not capable,” versus “If people praise me or reinforce the work I’m doing, then they
will think I’m capable.” In this model, his belligerent behavior is a protective reaction
to feeling incompetent. In order to work effectively with Brian, it is important
to identify self-doubt regarding his competence and modify this belief. Whereas
interventions targeting overt aggression and anger failed in the past, interventions
that focus on his specific negative view of himself and replace it with a more positive,
accurate, and realistic belief are likely to be effective. In this way, Brian can also
develop a larger repertoire of effective strategies to use so that he is less likely to fall
back into anger outbursts.
Certain information processing biases can interfere with the ability to formulate
a case accurately. Clinician biases or diagnostic overshadowing may influence the
construction of the case conceptualization. As general guidelines to assist in case
conceptualization and treatment planning, several strategies that have demonstrated
potential for improving the accuracy of a formulation include: (a) needing simulta-
neously to consider several alternative diagnoses, explanations, and treatment plans,
(b) addressing environmental as well as internal factors influencing patient behaviors,
(c) decreasing reliance on memory alone in decision making, and (d) using formal
decision aids such as diagnostic criteria, norms, and base rates to improve accuracy
(Arkes, 1991; Falvey, 2001; Gambrill, 1990; Garb, 1998; Turk & Salovey, 1986). In
addition to these guidelines, bias can be mitigated by a good case conceptualization.
Sperry, Gudeman, Blackwell, and Faulkner (1992) contend that a good conceptual-
ization consists of three components: a diagnostic formulation, a clinical formulation,
and a treatment formulation, which then serve as the blueprint for selecting treatment
interventions.
A solid case conceptualization is critical in identifying dysfunctional negative beliefs
that can often be roadblocks in therapy. For example, a patient with driving phobia
stated that she was fully committed to the goal of driving yet her unwillingness
to do the exposure homework suggested otherwise. A diagnostic formulation of
Dealing with Difficult Cases 355
her phobia indicated that she had an exaggerated view of the danger of driving
and underestimated her abilities to cope with the act of driving. Examining her
exaggerations of danger and underestimation of resources was not enough to help
her face her fears and overcome her avoidance. A clinical formulation identified a
belief that she was fragile at the core. The therapist concluded that her avoidance
was therefore a result of three factors. First, as she was not fully committed to the
goal, she failed to make a scheduled appointment to do the driving and allowed
other tasks to take priority. Second, she avoided the driving to avoid the discomfort
she feared it would produce. Third, and most importantly, she held an underlying
belief that on the days she avoided driving she was too fragile to face the task. These
conclusions provided a clear treatment formulation for how to help her overcome
her avoidance. The patient was helped to recognize that when she commits to a
goal, she does it. Reminding herself of her reasons for facing this task enhanced her
commitment. Making a day, time, and plan to drive was critical in completing the
task. The patient was helped to draw the conclusion that the goal of exposure is not to
be discomfort-free but to face doing what she believes she is unable to do. She learned
that the feared consequences were unfounded. Instead of thinking that she was too
fragile to face the exposure, and listening to automatic thoughts that reinforced that
view, she saw herself as strong and capable.
Summarizing her successful exposure experiences provided the data for a positive
self-view. After reviewing the progress she made resisting the urge to exit the highway,
electing to drive challenging roads, changing lanes, and making left-hand turns, she
was able to conclude that she could do it. The fact that she overcame her fear, stayed
in uncomfortable situations, and completed effective exposure meant that she was not
the fragile person she believed and was in fact a strong, capable woman. Utilizing her
inner strength equipped her to continue with additional exposure assignments, which
helped in other spheres of her life as well. Instead of letting her insecurity of being
fragile get in the way and listening to her automatic thoughts that told her she was
not capable of completing a task on any given day, she was free now to take action
without letting the invalid excuse of being too fragile get in the way.
Difficulty Identifying Key Problems and Defining Clear Goals
During the intake evaluation it is essential to identify the main problem areas for
the patient. The problem list reflects all the difficulties and stressors in the patient’s
life, including mood, interpersonal relationships, financial and other hardships, and
addiction issues. Each problem area can elicit cognitive, emotional, behavioral, and
physiological responses and motivation. Challenging patients tend to have a longer
list of difficulties, which can feel overwhelming to both the therapist and patient.
It can be useful to break complex difficulties into smaller, manageable, concrete
problems. Linking the problem list to overall goals in treatment, while keeping the
case conceptualization firmly in mind, is also important. In this way, both parties
are focused on how to work in the most efficient way and treatment progress is
better monitored. In addition, a positive outcome is facilitated by prioritizing the goal
list collaboratively, and setting up a realistic time frame (longer for more complex
cases). For instance, if a patient with depression tells the therapist that his or her
goal is to be happy, then it is essential to operationalize the abstract into specifics.
For this patient “being happy” may mean decreasing isolation, connecting more
with family and friends, reducing self-criticism, examining thoughts more realistically,
getting to work on time, figuring out pleasant activities, or even asserting oneself.
Especially with complex cases, it is also important for the therapist to use his or her
own clinical judgment to make sure that patients are strengthened with skills before
moving to interventions that may increase their vulnerability. Further, making sure
that the agenda is continually linked to the overall goals and frequently reviewing
overall progress will help both the patient and the clinician evaluate progress more
objectively.
Difficulty Linking the Agenda to Treatment Goals
The treatment goals that are developed during the intake evaluation or the initial
sessions provide essential information for setting the agenda within each session.
The goals can be thought of as the overall framework for treatment, along with
crises occurring during the week, specific difficulties, and homework assignments
collaboratively added into the agenda when indicated. Goals are initially developed
and prioritized early in therapy. These goals are later broken down into specific target
areas that are manageable for the allotted time.
Agenda setting is one of the most important components of a session and differ-
entiates a structured from an unstructured session. An agenda is a short list of clearly
defined topics that the therapist and patient agree will be the focus of the session.
The clinician can collaboratively set the agenda with a direct question to the patient:
“What would you like to put on the agenda for the session today?” The therapist
can also suggest items or limit the patient’s choices by giving options: “Would you
prefer to work on X or Y?” (Persons, Davidson, & Tompkins, 2001). It is also
recommended that the therapist work collaboratively and incorporate the prioritized
goals progressively into the agenda. If the therapist sets the agenda without inviting
input from the patient, the patient may not feel motivated to put energy into the
session. If the patient sets the agenda without input from the therapist, maladaptive
patterns or a focus on less significant issues may prevent effective use of the therapy
session. Thus, it is critical that both the patient and therapist play an active role in
contributing to the agenda. Once items are agreed on, it is helpful to prioritize them
so the most important objectives receive sufficient attention.
When working with difficult patients, who often come in with a “crisis of the week,”
the therapist may become confused about what issues to tackle first. Linehan (1993)
provides a helpful heuristic for ranking issues: suicidal and life-threatening behavior
first, then therapy-interfering behaviors second (such as homework compliance),
and finally life-interfering problems, which include all other problem behaviors. In
addition, it may be necessary to edit the agenda based on a review of homework.
Given that many patients cannot manage their time effectively, it is important for
the therapist to help set a realistic agenda. Also, in terms of setting an agenda, once
an item is chosen, Socratic questioning can be helpful to turn a vague item (such as
problems with a spouse or partner) into a specific difficulty to be tackled (such as

equitably sharing household responsibilities). Sometimes it is difficult for patients to
offer agenda items because they may have previously attended therapy that was more
passive and might expect the therapist to “fix” them. Individual case formulation of
each patient can yield hypotheses about the origins of agenda-setting difficulty.
CBT strives to help patients adopt problem-solving approaches to agenda items and
also recognizes that, when people are upset, they may need time to vent and receive
validation before they are ready to proceed. To help a patient make the transition to
a problem-solving stance, the therapist can explicitly label this issue for the patient
(e.g., “You sound very upset about X. Is that something you would like help with?”)
(Burns, 1999). Validation strategies developed by Linehan (1993) for working with
borderline personality disorder are also helpful.
A frequent problematic issue that can derail setting an explicit agenda is that the
check-in portion of the session turns into the therapy session. For example, Joe
may come into session and start talking generally about work stress. Using Socratic
questioning to work with Joe to be as specific as possible about how and what he
would like to address regarding work can help to maximize therapeutic efficiency.
By doing this, Joe is able to report that he avoids asserting himself and believes that
he is being taking advantage of by his coworkers. The agenda item is then set to
identify specific areas where Joe believes that this is happening, clarify his role and
responsibilities, and practice communicating in an assertive way.
Difficulty Staying on Task/Topic in the Session and

Maintaining Structure
To help prepare the patient for the structured and goal-oriented nature of therapy,
it is important for the therapist to focus first on psychoeducation. The therapist
should describe the features of CBT and the structure of each session during the
intake evaluation. An effective CBT session includes orientation to the structure of
the session, check-in, agenda setting, homework review, and work on the agenda,
periodic summaries, homework assignment, session summary, and feedback (Persons
et al., 2001). The use of structure facilitates efforts to teach skills and accomplish
goals effectively. Being structured also models for the patient the types of skills the
therapist is trying to teach: goal-oriented, active, problem-solving behaviors focused
on specific difficulties.
Research evidence supports the notion that structured sessions are helpful for
patients with depression (Shaw et al., 1999) and that setting an agenda and
assigning and reviewing homework predicts symptom reduction in these individ-
uals (DeRubeis & Feeley, 1990; Feeley, DeRubeis, & Gelfand, 1999). Structure
promotes goal-directed conversations that maximize the work that takes place in
every session.
The following case illustrates how the therapist can gently impose session guidelines
and the utility of structure. Alexa is used to unstructured sessions because she had
been in treatment with a therapist who utilized a different theoretical approach than
CBT. Her current cognitive behavioral therapist discusses the structure of treatment
with her, and Alexa is better able to see how the overall goals for treatment could
be broken down into workable and manageable units. She is also able to see how her
treatment goals are closely aligned to what is upsetting her. When Alexa experiences
difficulty focusing and tends to go off on tangents, the clinician helps her by gently
getting her back on track. This helps her use the session time more effectively,
organize herself, and self-monitor her progress with the initial goals she set in
treatment.
Difficulty Identifying the Key Cognitions or Behaviors that

Are Important for the Therapeutic Work
One of the central tenets of cognitive theory is its emphasis on the significance of the
patients’ beliefs about themselves, their world, and the future (A. T. Beck et al., 1979).
Aaron T. Beck theorizes that much of the patient’s emotional distress is a result of the
problematic, inflexible ways he or she interprets events (A. T. Beck et al., 1979). Strong
unpleasant affect is often a signal that key cognitions have been elicited. According
to the cognitive model, psychological problems involve problems in thinking. By
modifying key inaccurate situation-specific automatic thoughts, symptomatic distress
can be alleviated. Identifying, evaluating, and modifying more central underlying
beliefs are essential; otherwise situation-specific distressing thoughts will continue to
occur.
Cognitive therapy strives to modify the patient’s core dysfunctional beliefs that are
accepted by the patient as fundamental truths. This treatment focuses on helping
patients to identify and change maladaptive self-schemas and replace them with real-
istic and accurate beliefs about themselves (A. T. Beck & Dozois, 2011; Newman,
2008). Identifying and targeting these cognitions and beliefs is not always easy; how-
ever, it is vitally important. Dysfunctional attitudes not only contribute to the patient’s
symptoms and current complaints, they also have the potential to derail therapy and
impede progress. For example, individuals with high levels of perfectionism may have
unrealistic coping goals and inflated standards that may undermine therapy progress or
the maintenance of gains (Hewitt & Flett, 1996). Further, results from the National
Institute of Mental Health Treatment of Depression Collaborative Research Program
indicate that therapeutic outcome in adults (as indicated by severity of depression,
general clinical functioning, and social adjustment) was significantly related to pre-
treatment dysfunctional attitudes, specifically perfectionism (Blatt, Quinlan, Pilkonis,
& Shea, 1995). There is also evidence that changing dysfunctional beliefs is an
important mechanism of change in individual and group psychotherapy (Jónsson,
Hougaard, & Bennedsen, 2011).
A universal goal of therapy is to reduce distress. When symptoms are acute and
troublesome or significantly interfere with functioning, the patient tends to be
highly motivated to do whatever is necessary to reduce distress. In these cases,
the triggers of distress, whether external stressors (work, relationship, hardship) or
internal experiences (bodily sensations, pain, unpleasant emotions, images) are readily
identified and access to the key cognition or ineffective behavior ascertained. Targeting
the key cognition or behavior and formulating how to evaluate and modify it are
often among the more difficult challenges.
Joan is an example of a patient without a significant psychiatric history. After dating
someone who seemed wonderful, she found herself married to a controlling, verbally
abusive man who was caught engaging in several extramarital affairs during their
marriage. Although a new mother, she divorced her husband. Three years later, she
was once again dating a boyfriend from the past who appeared to be a stable, loving
soul mate for her future. Now engaged to be married, she was acutely anxious, crying
all the time, and wondering if she really wanted this. She could not imagine facing
her impending engagement party. Therapy focused on the immediate problem at
hand, the upcoming party, and her uncertainty about the relationship. However, the
question was whether it was negative biases associated with depression that influenced
her perception of the relationship or whether this upcoming marriage was a mistake.
The primary goal of therapy was to figure out what she wanted. Looking at the option
of postponing the party, it became clear that the negative consequences of canceling
the party were less than going through with it. This realization allowed Joan to take
action, which immediately reduced her anxiety. The marriage decision was the priority
goal in therapy, and the key cognitions were defined as those associated with the
distress around this decision: “I will disappoint my mother. I could be walking away
from something really good. My daughter will be hurt. I don’t want to hurt him.”
These thoughts resulted in her feeling anxious, guilty, and sad. Identifying the key
cognitions makes the therapist’s road map clear. Guided Socratic questions led her to
conclude that she was a formidable woman who did not need a partner but would
want one if it made sense. Joan recognized that the qualities she wanted in a partner
were significantly lacking in this person and in this relationship. The pain she would
cause from the breakup would ultimately be less than the pain of a mistake. Helping
Joan to evaluate the situation objectively enabled her to take courageous action and
break off the engagement.
Harry is an example of a patient with chronic depression. Harry had been depressed
for over a year, was on disability leave from work, and lived alone, separated from
his wife and family. His problem list was extensive, including hopelessness, inactivity,
social isolation, inability to work, financial difficulties, tiredness, and overeating.
When an acute stressor—his daughter’s upcoming wedding—presented itself, his
depression convinced him he would never be able to participate and would disappoint
both himself and his daughter. The goal of attending his daughter’s wedding would
be a way to work on his goals of reconnecting to his family, becoming more active
and involved, returning to work, and finding his way back to hope. When thinking
about going to the wedding, thoughts associated with the hopelessness erupted: “It
will be too much for me. I won’t be able to do it. I’ll be too tired. I’m too fat.
They don’t want me there; what’s the point in going?” In this case pinpointing the
key cognitions was easy but modifying them was the challenge. Accepting that one
conversation is not going to change an embedded negative perspective and providing
some behavioral proof of progress helps move patients along. It is helpful to provide
patients with the possibility, not the certainty, that they can face what they believe
they cannot.
Identifying and evaluating the key cognitions can be challenging in chronic cases
where there is longstanding mood dysregulation and dysfunctional behavior. Difficulty
in identifying the key cognition may result when the situation-specific cognition is
not the real culprit for distress. Instead, the underlying belief is more important to
address, as it is that belief that leads the person to see the specific situation through a
distorted perspective or have negative automatic thoughts.
Take the case of Jo, who has been significantly impacted by bipolar disorder for
her entire adult life. Life’s stressors tend to unravel her on a regular basis. Whether
it is a sick cat, a pending social security disability review, food stamps running out,
or a postponed psychiatric appointment, the automatic thoughts are similar: “I can’t
handle this. Something bad is going to happen. It’s all on me. It’s too much. I’m
not safe. I won’t survive.” Rather than systematically evaluating each thought in
every situation, it would be more fruitful to recognize the underlying beliefs that fuel
these cognitions. When Jo is unable to cope, she believes that she is helpless and
lazy. By actively restructuring these thoughts she is better able to appraise situations
realistically rather than automatically assuming that they mean that she is helpless
and lazy. Accepting that depression makes it harder for her to do things and that
her disorganized thought makes every task more challenging for her will help her to
disengage from the inference that she is lazy. Similarly, by restructuring the belief that
she is lazy she is able to use external resources more effectively. Instead of needing to
prove she is not lazy by demanding she do every task alone, she is more able to ask
for help when warranted. Helping her see that asking for and getting assistance makes
her less helpless and more capable is critical. Collaboratively helping her recognize
that she has faced similar problems before, that solutions have been found in these
circumstances, and that she can seek the help of others, if necessary, allows her to
modify her view of self as helpless and lazy toward one of being competent and
determined. This new realistic, positive view leads her to more effective behaviors.
Sometimes the problem in more challenging cases is focusing on the appropriate
behavior. This is often the case when the behavioral problem is avoidance. The patient
with panic disorder whose fear of bodily sensations remains is typically unwilling to
face the interoceptive exposure to disconfirm his or her fears. Individuals with
phobias are avoidant of facing their feared situations, thus never disproving their
fearful predictions. Patients with obsessional problems are unable to learn that they
are exaggerating the importance of their thoughts when they try to avoid through
thought suppression or by engaging in compulsions and ritualistic behaviors. When
they avoid tasks and people, individuals with depression are unable to see how capable
or cared about they are. A similar situation occurs when patients avoid assertive action
and avoid addressing problems. Facing the avoidance head on can open the door
to therapeutic progress. It is important to acknowledge that avoidance is serving
a protective purpose for these patients. It allows them to feel safe by minimizing
exposure to what patients believe are intolerable experiences. The therapist can
validate the patient, acknowledging that the strategy is effective at minimizing distress
and works in the short term. At the same time, the therapist can point out the negative
long-term consequences of the patient’s behavior and the need to come up with an
alternative behavior that works and is not destructive. Providing a clear rationale for
actively addressing the avoidance is a critical first step. The second step is to arm
patients with tools that equip them to face the discomfort of not avoiding, which
often means helping them to see that the danger is imagined or exaggerated. Last,
the ineffective avoidance is replaced with action.
Complex Cases
In complex cases, there are often multiple diagnoses and possible rule-outs. Problems
arise when one intervention strategy conflicts with another or when there is a
dilemma about which problem to address first. The difficulties that result from
multiple diagnoses can be mitigated by having a clear cognitive conceptualization of
each diagnostic disorder. By identifying the problem in thinking associated with each
issue, it becomes possible to address any number of determined difficulties in any
given session.
Choosing which problem to address first is often a quandary. Good collaboration
with the patient by directly asking him or her which problem is causing the most
distress in his or her life can help with this predicament. Often this is the case
when both anxiety and depression are present. Anxiety may be important to address
first if it limits one’s functioning or if the fear that it will never improve leads to
depression. Although the optimal path may not be obvious, having a clear cognitive
conceptualization of the problems allows for multiple problems to be addressed in a
systematic fashion.
Difficulty Summarizing Work and Making Learning Explicit
Summaries are helpful during the session to provide a review of what has been learned,
clarify what will be covered next, and improve collaboration and time management.
Therapy material is often highly emotionally charged. Capsule summaries are used
throughout the session to fortify learning, check-in on understanding, help the patient
draw accurate conclusions, and make sure that the focus in the session remains on the
collaboratively agreed-upon area of focus. The final summary of the session is typically
done by the patient with the therapist serving as a guide. The final summary pulls
together the main points of the session, makes sure that the therapist and the patient
collaboratively draw the same conclusions, actively addresses the patient’s thoughts
and feelings about the session, and reviews the newly assigned homework.
Capsule summaries help patients focus and remember what has been learned at
the conclusion of each agenda item or intervention. These summaries also strengthen
collaboration between the therapist and the patient by acknowledging accomplishment
of the agenda item. Capsule summaries are used to check in with the patient and deter-
mine if therapy is having a beneficial effect. This strategy is also used to offer patients
options for how to spend the remainder of the session. The final summary and asking
for feedback are an important part of the session because there are often discrepancies
in the therapist’s and the patient’s perception of the therapy session. Takeaways
from the session can also be fleshed out. End-of-session summaries and feedback are
particularly important when working with patients who are prone to interpersonal
difficulties and misunderstandings. Feedback allows any miscommunications to be

aired and addressed.
Capsule summaries throughout therapy sessions and final summaries at the end of
the session are mechanisms to make sure the therapeutic learning is explicit. Rather
than assume that the patient understands and embraces the therapeutic insight and
learning, it is important to stop and ascertain whether that is indeed the case. Providing
a good summary means asking the patient what the data mean. Ideally, a therapist
guides the patient to develop his or her own conclusions, but the burden of making
sure a conclusion is drawn is the responsibility of the therapist. Summarizing also
allows for greater collaboration and active involvement on the part of the patient, as
well as a means to pinpoint those key cognitions and, more important, the maladaptive
and restructured beliefs that are essential to patient recovery.
Obtaining feedback is another way to improve positive outcomes in therapy. In
fact, paraphrasing has a significant effect on immediate outcomes in therapy. Research
suggests that how a therapist responds is associated with feeling supported and reduces
negative reactions in patients (Hill et al., 2001). This finding is consistent with skills
training programs (e.g., Egan, 2010) that suggest that paraphrasing requires that
the counselor listen to what the patient is saying and then demonstrate a sense of
understanding the patient. The American Psychological Association Division 29 Task
Force for Empirically Supported Relationships has made several recommendations to
help patients achieve positive outcomes in psychotherapy. Based on these recommen-
dations, Ackerman, Bowen, Beier, and Kanfer (2001) suggest that it is important to
monitor patients’ reactions continually throughout treatment to help both the therapy
relationship and the overall outcome. Checking in with patients throughout treatment
creates opportunities to build a solid working relationship, repair misunderstandings,
revise applied interventions, and avoid premature termination.
A growing body of research investigating the effects of patient feedback in psy-
chotherapy has yielded encouraging results (e.g., Lambert et al., 2001, 2002; Reese,
Norsworthy, & Rowlands, 2009; Whipple et al., 2003). Patient feedback has consis-
tently been found to benefit patients identified as at risk for terminating treatment
prematurely. Feedback can become a natural part of the therapy process by regularly
asking the patient what he or she thinks about the work that is taking place. The
therapist may ask if the work is helpful, clear, and understandable, or unhelpful and
vague. Feedback can be conducted verbally throughout treatment or more formally in
written form after each session. Clinicians should be careful not to make the mistake
of asking for feedback that has already been provided. When a patient says the session
was helpful and he or she has a clear plan for the week, the therapist has already
received feedback and asking for more is redundant and a sign of inattention to the
patient.
Missing the clues that patients are dissatisfied with the treatment, along with
poor summaries and not making the learning explicit, likely plays a significant role
in negative therapy consequences (Lambert & Shimokawa, 2011). Although the
degree to which psychotherapy can have negative rather than positive consequences
for patients is often ignored, estimates are that 5–10% of adults participating in
clinical trials leave treatment worse off than when they began (Lambert & Ogles,
2004).
Missed Appointments, Real Life Stressors,

Lateness, and Resistance
Missed appointments, real life stressors, lateness, and resistance can be significant
stumbling blocks that get in the way of effective treatment. It is important to address
these interfering factors on the part of the patient immediately and effectively. The
way to do this is through utilizing the case conceptualization as well as therapist dis-
cernment. By understanding the patient and collaboratively addressing the interfering
issue, the therapist can immediately place the problem on the agenda, objectively
examine its impact, and develop a direct plan of action.
Missed appointments can hinder therapeutic outcome. Patients who frequently
miss appointments may not be receiving the ideal treatment, leading to premature
termination (Berrigan & Garfield, 1981) or decreased efficacy (LaGanga & Lawrence,
2007; Leichsenring & Rabung, 2008). Similarly, outcome may be affected when a
patient is late and the appointment time is compromised. Explanations for missed
appointments can be grouped into four broad categories: clinical problems (illness),
practical matters (schedule conflicts, family emergency, weather, transportation),
motivational issues (the patient forgot, low motivation for treatment, difficulty
prioritizing self-care), and negative treatment reactions (Defife, Conklin, Smith, &
Poole, 2010).
Helping the patient understand his or her psychopathology and how it impacts
functioning can facilitate outcome. This involves psychoeducation about the nature
of the patient’s disorder, sharing the case conceptualization with the patient, and
providing the appropriate rationale and intervention strategy. For example, explaining
to a patient that he or she has a depressive disorder and how this has negatively
affected his or her judgment of self, the future, and the world (A. T. Beck et al.,
1979) helps develop a more accurate understanding of the impact of the depression.
The therapist also explains how a negative viewpoint leads the patient to avoid work
and others, imagine a more hopeless future, and discount the help that is available.
Letting patients know that therapy can ameliorate this bias in thinking and help
them draw more accurate conclusions that free them to participate actively once
again, see a more hopeful future, and gain a more positive view of others, facilitates
recovery. Therapy can then be tailored individually to remove negative biases in
thinking so that patients can draw more accurate conclusions, reduce avoidance and
hopelessness, and more accurately appraise external resources and social support. This
can serve to enhance motivation to continue in treatment because the difficulties
are collaboratively transformed into goals. Patients who believe that the cognitive
rationale resonates with their own view of depression improve faster and have less
resistance than do individuals who perceive a discrepancy between the cognitive
formulation and their own conceptualization of their problems (Fennell & Teasdale,
1987).
Identifying problems, brainstorming solutions, formulating plans, and guiding
the patient toward action help to eliminate practical obstacles to treatment (e.g.,
issues with transportation, last-minute work or personal requests, childcare issues, or
finances). It is important to identify such issues with the patient so that the costs and
benefits of various solutions can be discussed collaboratively. Together, reasonable

management strategies can be then worked out. For example, instead of agreeing
to a personal errand or a work-related request, the patient may be better prepared
to assertively say, “No.” Helping patients make the therapy appointment a priority,
only to be changed in an emergency, helps eliminate treatment being put aside. For
disorganized patients, helping them create schedules with the therapy appointment
in place may generalize to other areas of their lives and aid them globally. Specifying
a time to call for transportation requests or examining different childcare options are
also considerations in looking for solutions.
Real life stressors may have a significant impact on treatment compliance. In one
study, almost 20% of participants reported termination due to difficulties unrelated
to treatment. Reasons for termination included relocation, job constraints, financial
hardship, schedule conflicts, relationship difficulties, and transportation and health
issues (Roe, Dekel, Harel, & Fennig, 2006). Even in middle-class and college-age
populations, external factors are among the leading causes of treatment termination
(McNeill, May, & Lee, 1987; Renk & Dinger, 2002).
Stressors that may impact on ongoing treatment include finances, housing, medical
problems in the patient or a family member, chronic pain, addiction, childcare
difficulties, aging and ailing parents, and employment-related issues. The goal of
therapy is not necessarily to fix these problems but to help the patient cope.
Unfortunately, real life stressors are often out of the control of the patient. In
such cases, the therapist should focus on acceptance strategies. To minimize its
impact on treatment, it is important to gain a clear understanding of the stressor and
acknowledge it, work toward accepting those things over which the patient has no
control, make a point to help the patient refrain from making unwarranted judgments
about him- or herself or the future, and help the patient take the most appropriate
effective action possible, recognizing that sometimes the best action is no action.
Formulating a plan means helping the patient make specific arrangements actively
to address the problem at hand. For example, when a therapy session falls on a
Tuesday following a Monday holiday, the patient who uses subsidized government
transit can set a time on the preceding Friday to call and arrange for his or her Tuesday
transit. Letting employers and people in their personal lives know ahead of time that
they are unavailable at a time when therapy is scheduled can minimize last-minute
requests. Missed appointments can be reduced by requesting childcare help ahead of
time, even if it is only as back-up.
Identifying the problem and having a plan sometimes is not enough, and it may
be critical to help the patient take the appropriate action so these practical matters
do not interfere with therapy. Helping the patient take effective action can mean:
initiating the action right in session or immediately following the session, having the
patient check in with a text or phone message that he took action (no conversation
necessary), validating that operating in new ways can be difficult or uncomfortable at
first but will become second nature with time, and always reminding the patient that
action can happen even if the patient lacks complete faith in the solution or believes
that he or she does not have the effort, energy, or motivation to do it.
Motivational issues are important to address head on. Making a commitment
to therapy and having a patient do his or her part is essential. Often a forgotten
appointment may represent a lack of commitment. Ask your patient, “Are you
committed to therapy and the work necessary for your recovery? How committed are
you … 10%, 50%, or 90%? Are you committed enough to make therapy a priority?
Are you committed enough to tolerate the discomfort that change may produce?”
Commitment can be enhanced by reiterating and regularly reminding the patient of
the rationale for his or her participation in treatment. The therapist can accomplish
this by (a) spelling out the link between the immediate work that is important to do
and overall goals, (b) identifying a goal the patient highly values, such as achievement,
mobility, freedom, independence, or friendship, and (c) reminding the patient how
that goal is directly linked to taking the necessary action required of therapy. For
example, an individual with a driving phobia who has been canceling sessions because
he or she is not doing the agreed-upon exposure can benefit from being reminded
that driving over those bridges is an accomplishment and that each step moves him
or her closer to achieving the overall goals. Reminding patients of some of the
reasons that compel them to work toward their goals (e.g., providing opportunities
to earn more money, job advancement, being a healthy role model for their children,
greater freedom, increased confidence, alleviation of unnecessary problems) may also
be helpful.
Additionally, the failure to prioritize self-care may be linked to faulty cogni-
tive assumptions that demand that patients make others’ needs and/or work a
priority in order for them to be liked, accepted, worthy, or a success. Helping
patients learn that self-worth, desirability, or success is independent of these arbi-
trary rules allows these unreasonable demands to be broken. For example, helping
patients understand that they can say no, take care of themselves, and put their
own needs first does not globally negate the good, likeable people they are. Simi-
larly, walking away from the office before nonessential work is completed does not
negate the fact that they may be hardworking, competent/capable, or responsible
employees.
Perhaps the greatest obstacle in getting patients to focus fully on the in-session
work is avoidance of discomfort. The paradox is that in their desire to avoid
emotional pain they actually create more pain by avoiding the necessary work.
Negative treatment reactions are magnified when this avoided distress is faced in
session (e.g., when a patient is asked to face material or participate in interoceptive
experiences). Exposure to discomfort is essential as it proves to the patient that
he or she can face it and tolerate it without the feared imagined consequences.
Talking about unpleasant things is linked to unpleasant feelings, but helping patients
see these situations through more accurate and reasonable perspectives will aid in
reducing those dreaded feelings. That is why at the very onset of therapy, it is not
enough to identify inaccurate thinking. One must skillfully evaluate and modify those
thoughts into a more reasonable viewpoint so that emotional relief is obtained. For
example, the therapist might begin interoceptive exposure by asking the patient,
“What do you fear most about the experience of anxiety?” Using a number of
interoceptive exposures, such as overbreathing for a minute, spinning around in a
chair, or breathing through a small straw with the nose pinched, and then exposing
the patient to his feared symptoms is all it usually takes to begin to modify inaccurate
views.
Resistance
Several studies indicate that successful therapy is highly related to increases in

resistance and that low resistance corresponds with negative outcomes (Bischoff &
Tracey, 1995). However, too much or too little resistance may be counterproductive.
Managing resistance in therapy can be aided by changing one’s interactional style to
combat the patient’s efforts to repress anxiety-provoking memories and insights or
efforts to fight the therapist’s influence (Bischoff & Tracey, 1995).
One of the key principles of CBT is guided discovery. The technique of Socratic
questioning guides patients to participate actively in evaluating evidence and to
consider alternative viewpoints, thereby helping them to draw their own conclusions.
Guided discovery allows patients to feel in control of making decisions and take
effective action. J. S. Beck (1995) sees the techniques of Socratic dialogue and guided
discovery as a way for patients to gain the insights they have formulated themselves.
Instead of telling a patient that he or she is unlikely to fail a board exam, the therapist
might ask the following questions: “What have you done to prepare for the exam?
Have you taken a board review course? Have you taken any practice exams? Will
the test be asking you questions in which you have expertise or experience? What
percentages of people pass the exam? Have you taken any exams of this nature before
and how have you done?” Instead of telling a patient it would not be the end of
the world if he or she failed, the therapist could ask the following questions: “Can
you take the exam more than once? How many times? Would you lose your job or
have a pay cut if you fail? Would your life change in any way if you fail? Have others
failed and if so what happened?” This guided discovery method is a direct way to
combat the resistance that may develop if the therapist’s style is too directive (Beutler,
Moleiro, & Talebi, 2002; Karno & Longabaugh, 2005). These cognitive techniques
give the patient more options and more responsibility and encourage the patient to
be the one to present goals (Newman, 1994, 2002; Safran & Segal, 1990).
It is often emphasized that if a patient exhibits signs of noncompliance, the therapist
should make certain that the patient has understood and accepted the goal, process,
and reasoning of therapy (Beutler et al., 2002; Newman, 2002). Making sure that
the patient and the therapist share similar goals can help in this area. Examining the
goals through a cost–benefit analysis can provide the rationale to actively engage the
patient and to make sure that goals are agreed upon collaboratively. A willingness to
modify, renegotiate, and empathize with the challenges can help overcome resistance
(Haugaard & Sandberg, 2008).
Reevaluations or renegotiations of goals are connected to the fact that the therapist’s
approach may significantly contribute to lack of progress. Young, Weinberger, and
Beck (1996), for instance, point out that the lack of progress may be due to the
therapist inaccurately assessing the situation, which may be viewed from multiple
levels. At the situation-specific level, it is crucial that the key cognition or behavior be
identified in order for distress to be reduced. It is also important to make sure that
the automatic thought or maladaptive behavior being examined is associated with
distress and produces a positive effect, if modified. At a deeper level, reducing the
distress in any given situation does not necessarily prepare the patient for ongoing
or future stressors. Identification of the global, more pervasive negative self-beliefs is

critical in producing enduring change (Segal et al., 2006). For example, a recently
divorced woman who learns to accept that she can have a good time at a party
without a husband or a date will not necessarily be able to generalize that view and
know that pleasure and a sense of accomplishment can be experienced even if she
never has a significant other in her life. This reinforces the need for a clear cognitive
conceptualization of the patient in order to overcome resistance.
Even if the therapist has identified the problem and has a clear strategy for
intervention, difficulties arise when the patient has a different view. The patient may
deny he or she has a problem, believe the problem is solely biological and needs only a
pharmacological intervention, and/or fail to embrace the cognitive model. According
to Leahy (2001), failure to establish a mutually agreed-upon objective is one of the
primary therapist errors. Mitchell (2006) warns therapists to avoid being too much
of an expert which can be defined as being too knowledgeable or obvious, as this can
result in “Yes, but … ” answers. “The patient cannot be resistant if there is nothing
to resist,” quips Mitchell (2006), who advocates for the use of Socratic questions
and an empathic style to display uncertainty. A suggested way to engage a patient
is to make examples personal. Use personal examples to socialize the patient to the
model and do this socialization from the very onset of therapy. If a therapist knows,
based on information gleaned in the interview, that a patient’s automatic thought is
inaccurate, the therapist can help to test the validity of the thought. Consider, for
example, a patient who has had a successful business for many years and is now in
jeopardy of having to sell out or shut down. He or she may conclude that he or
she is a failure. This situation can be used to socialize him or her to the cognitive
model. The therapist can emphasize that this patient ran a successful business for over
20 years, employed many people, negotiated endless contracts, provided benefits for
employees, bought him- or herself a home, car, and possessions, and was able to save.
Pointing out that the patient is only now struggling with a business that is crumbling
in this economy allows the therapist to provide guidance to the more reasonable
conclusion that this current hardship is not the only measure of the patient’s success
and clearly not a determination of failure. If this conversation changes the patient’s
view and subsequently his or her affect and behavior, it is a golden opportunity to
both socialize him or her to the model and overcome resistance.
It is possible that resistance also may be a result of either real or imagined danger
of change. The resistance to change for fear of losing something is often referred to
as secondary gain. Patients may fear that they will lose something, such as money,
support, love, or the relationship with their therapist, or have to do something they
have been avoiding, such as returning to work, facing a troubled relationship, or being
alone, or they may fear failing at therapy itself. Identifying the imagined dangers,
helping patients see that the danger is not as probable or the consequences are not as
significant as they think, and helping them develop skills or appreciate the resources
they have equips them to face these threats. This strategy also helps to alleviate
much fear and resistance. Even when there really are potential dangers, therapy can
help the person be prepared to face them. A common example is when a disability
gains the individual government money, subsidies, or housing. Helping the patient
see that gaining mobility, a reduction in suffering, and a higher level of functioning
does not necessarily eliminate the need for the resources he or she currently accesses.
Disability income does not stop even if one gets a job. It only stops if the income
exceeds a specific amount, and only if that income has been in place for a significant
period of time. In some cases, therapeutic gain might result in the loss of those
government resources but reap a much greater gain of resources that the patient can
now obtain for him- or herself. Another example is the case of a woman who had been
struggling with severe depression for most of her adult life. Her husband had taken
full responsibility for both the financial and the majority of the home responsibilities,
including child care. As long as his wife was disabled by her depression, he took care
of her too. However, once therapy helped this woman overcome her depression and
improved her level of functioning, her husband, then believing she could survive on
her own, asked for a divorce. In this case, getting better did come at a price, but in
the long run helping the patient see the benefits of recovery (the ability to attend her
children’s sporting events, join them for dinner, interact with other adults, rediscover
her former passion for visiting museums, and be able to visit her children in college
next year) outweighed the price of the loss of her marriage.
Timing can play an important role in resistance. According to Leahy (2001),
slowing the pace of therapy, rather than offering explanations before the patient is
ready to accept them or confronting the patient too soon, can minimize resistance.
If exhaustion plays a role in resistance, taking smaller steps and inquiring as to what
the therapist can say or do that might move the patient to make at least some
progress toward treatment goals can be helpful (Leahy, 2001). The patient may be
psychologically drained or overwhelmed and not have the energy to take on the tasks
that will lead to change. In these circumstances, it may be important to allow the
patient to replenish his or her energy. Leahy (2001) also highlights the importance
of not personalizing the resistance but rather accepting it as a fact in therapy.
Effective strategies for overcoming resistance are often specific to the particular
patient and dependent on the underlying cause of the resistance to change. For
example, one patient resisted any movement toward the goal of engaging in more
social interactions and allowing people back into her life. She feared her ability to
judge accurately who could be trusted, became overly concerned about the anxiety
and stress that this action would take, and feared her inability to cope should a
negative result happen. Having been abused and battered for years and betrayed by
a community of people she thought she could trust, she felt too worn down for the
challenge. Before any action toward these goals could be taken, therapy had to help
her learn how to recognize real signs of danger, see that she could assertively set
limits and say no, engage in social activities with short notice and thus not have to
make a long-term commitment, rely on others including her therapist to help evaluate
situations, and find tiny ways she could start to make inroads toward her goals. Once
armed with new resources, short phone contact became an entry point.
Another patient was intensely distressed and suffering from chronic pain, depression,
and insecurity. The load of her problems seemed unbearable. Acknowledging and
empathizing with her pain and her struggles allowed the therapist to help the patient
set short-term goals that would not overly tax her. She learned that she could engage
in therapy by giving herself permission to care for herself, improve balance, and move
forward slowly. She also learned that she could set one small goal each day and take
credit for doing it no matter how hard it was or how long it took. Additionally, the
patient learned to ask for help from family members rather than setting Herculean
tasks that were beyond her limitations. With the help of others and these interventions,
she eventually gained the strength to cope with her situation.
Getting Challenging Patients Unstuck
Often when patients are significantly impacted by psychological problems, life stressors
feel overwhelming and the therapeutic progress comes to a halt or regresses. Both the
therapist and the patient can feel stuck when therapeutic progress is at a standstill.
Hopelessness, unwillingness to do homework or exposure work, embedded negative
beliefs, relationship problems in the therapy, and real life stressors frequently impact
this dilemma. Without adequately addressing any or all of these obstacles, therapy will
remain compromised.
Hopelessness is implicated in the course of depression and treatment outcome in
adults (Kuyken, 2004; Whisman, Miller, Norman, & Keitner, 1995) and adolescents
(Barbe, Bridge, Birhamer, Kolko, & Brent, 2004; Brent et al., 1998; Curry et al.,
2006). There is also an association between hopelessness and suicidal ideation and
behavior in a variety of adult (A. T. Beck, Steer, Kovacs, & Garrison, 1985; Cole,
1989; Smith, Alloy, & Abramson, 2006) and adolescent populations (Goldston et al.,
2001; Orbach et al., 2007; Reinecke, DuBois, & Schultz, 2001).
Hopelessness may be a significant obstacle to treatment (TADS Team, 2005). In
adults, studies suggest that there is a greater likelihood that patients with higher
levels of pretreatment hopelessness will drop out of therapy (Papakostas et al.,
2003; Rifai et al., 1994) and report more residual depression scores at termination
(Dahlsgaard, Beck, & Brown, 1998; Whisman et al., 1995). Hopelessness also has
been associated with poor medication compliance (Naidoo, Dick, & Cooper, 2009)
and nonadherence in CBT (Detweiler & Whisman, 1999). In adolescents, change in
hopelessness over the course of treatment has been shown to predict adherence and
drop-out (Becker-Weidman, 2010).
Hopelessness is one of the greatest obstacles to treatment. Believing that there is
no hope increases fatigue, reduces motivation, and negatively biases one’s perspective.
When therapists are hopeless about a case, it may lead them to discontinue strategies
that need more time or begin to embrace the negatively biased views of the patients.
Medeiros and Prochaska (1988) found that the greater degree to which therapists
relied on optimistic perseverance, the better they saw themselves coping with stressful
patients.
Combating hopelessness often involves operating at two levels—situation-specific
hopelessness and more global hopelessness beliefs. On the surface identifying, evaluat-
ing, and modifying the patient’s automatic thoughts that drive the hopelessness in any
specific situation is critical in reducing acute distress. For example, a patient who looks
around at unfinished renovations in his home, a broken appliance, windows without
curtains, and a bed in the middle of his living room may think, “Things will never get
done around here. I will have to live in this unfinished disarray forever.” Reducing
hopelessness in this case means validating the patient’s distress by acknowledging the
reality of the unfinished situation. However, instead of inaccurately concluding the

situation will never improve, it is essential to help the patient see the facts that support
an alternative view—although progress is slow and ultimate change will take a long
time, things have begun to improve and plans are in place for that to continue. In this
case, although the patient may accept that his living situation may eventually improve,
it does not address the deeper level of hopelessness. Overcoming embedded hopeless
is addressed by learning to see small gains, comparing the situation with the worst
of times and not the best, and acknowledging the experience, outside help, skills, or
new knowledge that better equip the patient to face difficulties. For a patient who
previously spent four hours a day in a shower and could not leave his home, taking
care of his aging mother, driving her to doctors and adult care, food shopping and
preparing meals, running errands, and walking the family dog became fuel to beat the
entrenched hopelessness.
Unwillingness to Do Homework or Exposure
A central tenet of CBT is that in order for patients to learn to cope more effectively,
they must practice their therapy tools between sessions. Research has shown that the
better the quality of one’s homework, the better the prognosis (Kazantzis, Deane, &
Ronan, 2000; Mausbach, Moore, Roesch, Cardenas, & Patterson, 2010). Further,
Persons, Burns, and Perloff (1988) found that adherence to CBT was associated with
better treatment response and that patients who did homework outside of session
improved three times more than did patients who failed to complete therapeutic
assignments. In challenging patients, often the lack of therapeutic gain is attributable
to their unwillingness to engage in homework. Homework compliance is increased
when patients have a clear rationale for the assignment, collaboratively play a role
in its design, accept the cognitive model and thus believe the assignment will help
them achieve their goals, believe they have the resources to tolerate the discomfort
the assignment may produce, are committed to the goals to which the assignment
is linked, and have discussed and problem solved any practical obstacles that could
hinder their participation in the task. Reviewing the homework during each session
is also important (Scheel, Hanson, & Razzhavaikina, 2004). Assigning homework
throughout the therapy session as significant subject matter arises emphasizes the
homework’s relevance to the session.
Difficulty Addressing the Underlying Beliefs:

Schema, Doubt, Insecurity
An individual’s insecurity is often the biggest obstacle to therapeutic progress.

Labeling one’s doubt (often referred to as a negative core belief or the most
fundamental understanding of the self), evaluating that doubt, and modifying it into
a more realistic, accurate, and positive view of the self is critical in moving stuck cases.
Cognitive behavioral approaches to improve self-esteem may decrease depressive
symptoms and move therapy forward (Overholser, 1996). In fact, at least with regard
to depression, self-esteem has been found to be a significant predictor of short-term
outcome (Harris & French, 2009).
When a patient says, “No one wants to spend time with me,” the therapist can
elicit the core belief associated with that thought. The therapist might ask, “What
does that mean about you that no one wants to spend time with you?” Often
the response reflects a deeper belief, such as, “I am undesirable, unlikable, and
unworthy.” When a patient is unwilling to comply with homework, an exposure
task, or talking about distressing information in session, he or she often says, “It’s
too hard. It’s too much. I can’t handle this.” Digging deeper, the therapist can
ask, “What does it mean about you that it’s so hard, it’s too much for you, or
you can’t handle it?” A response may be, “I’m weak, I’m a failure, I’m helpless.”
It is important that patients learn that just because they have given themselves this
label does not make it true. There may, in fact, be many life experiences they have
used to confirm this view of themselves, but no unpleasant label is globally true
and often those life experiences could be interpreted in ways that undermine their
negative conclusions. For example, a patient may believe he or she is bad because
of past abuse rather than recognizing that the abuse had nothing to do with his
or her character. Once the doubt is thoroughly evaluated, a new more realistic and
positive view is formulated and strengthened (Fox & Sokol, 2011; Sokol & Fox,
2009).
Imagine a patient with panic disorder who is unwilling to do interoceptive exposure
in and out of session. No matter how much the therapist talks about the importance
and reasons to do the work, the patient resists. Identifying the patient’s doubt label,
“I’m weak,” may be the critical factor in obtaining his or her cooperation. Helping the
patient to modify his or her self-view to see that he or she is stronger than previously
thought may provide the fortification needed to face the exposure. Actually facing
the exposure now, in fact, provides the data for the new positive view of self to be
reinforced.
Another example of the importance of addressing underlying beliefs is patients who
believe they are helpless and are therefore unlikely to participate actively in their own
treatment. These individuals tend to sit back patiently waiting for medication to work
or for the therapist to “fix” them. Helping these patients see they are not as helpless
as they think and that they actually have the intelligence, skills, and experience to
face the work will enhance their cooperation. Once they begin taking action on their
own behalf, new information compiles which starts to change the faulty viewpoints
originally held. For example, a patient who was positive for HIV believed that he
was too frail and helpless to live independently, which resulted in him living in an
unhealthy codependent relationship. Curling up in bed and avoiding responsibility
convinced him that he was unable to care for himself. By collaboratively helping him
take on daily chores, venture out alone, pursue outside interests, cook for himself,
and most importantly begin to consider the viewpoint that, just because he spent his
life believing he was helpless did not make it true, allowed him eventually to move
out of that unhealthy environment. Living independently, cooking, and taking care
of himself allowed him to be surrounded by friendly neighbors and bolstered his view
that he is capable.
Relationship Problems in Therapy
The relationship between the therapist and the patient can play a significant role in
working with challenging cases (Watson & Kalogerakos, 2010). The existence of a
working alliance between the therapist and patient is viewed as a critical component
of the therapeutic process (Bachelor, 1995). Two decades of empirical research have
consistently linked the quality of the alliance between therapist and patient with
therapy outcome (Horvath, 2001).
In cases in which the patient’s difficulties are chronic and the patient is exhausted
from the battle, the therapist can provide the energy, determination, coaching, and
even the cheerleading that the patient may need. It is important to validate the patient’s
suffering and struggle but not buy into distorted views. The therapist might say, “I
recognize how hard it has been for you. I understand how much pain you’ve had to
carry. But, that doesn’t mean you have to give up or that together we can’t figure out
how to get through this.” In fact, when working with patients for long periods of time,
there are often occasions where they have faced difficult problems or situations and
overcome them. It is helpful to point out those data and help them understand that, if
solutions have been found in the past, they can likely be found now. When the patient
says, “I can’t do it,” the therapist can be the voice of reason and say, “I know you can do
it because I have seen you …,” and specify all the examples of this happening. A good
relationship can act as a safeguard in suicidal patients, providing data to dispute erro-
neous negative beliefs, such as, “No one cares,” “I don’t matter to anyone,” or “No
one would notice if I died” (Ellis & Newman, 1996). The therapist can point out that
he or she cares and that it would matter. Keep in mind that it is important to support
the patient not only in words but nonverbally as well. The therapist should be aware of
the signals he or she sends out. In this regard, Fridlund (1994) provided evidence that
facial expressions function primarily to manipulate the emotional states of other peo-
ple, so a therapist’s nonverbal cues can be just as important as his or her verbalizations.
When a patient has a difficult time forming any alliance with the therapist, therapy
also can be negatively affected. J. S. Beck (2005) suggested that a patient’s anger
from feeling invalidated, rejected, controlled, misunderstood, or not cared about
and a patient’s skepticism, feelings of coercion, resistance to the structure of ther-
apy, and unwillingness to reveal important information are all common difficulties
that arise as a result of a therapeutic relationship issue. Leahy (2001) noted that
some patients enjoy manipulating other people. By not “moving” or responding
therapeutically, they experience power in recognizing that they can manipulate the
therapist. Defiance can also be a passive-aggressive behavior in therapy that is an
angry reaction toward feeling controlled by an authority figure. Being aware of these
potential barriers can help the therapist recognize them when they arise. Address-
ing them compassionately in an objective and constructive way can help therapy
progress.
Overview: Helping Difficult Patients Engage in the

Therapeutic Process
In summary, there are many ways therapists can maximize therapeutic gain and
minimize factors that interfere with the therapeutic process. Essential to symptom
relief and therapeutic progress is having a cognitive conceptualization of both the
patient and his or her problem. Identifying a detailed and comprehensive problem
list is also essential. Clearly defined, measureable goals facilitate effective treatment.
Linking the agenda to the goals keeps the therapy focused and on task, minimizing
derailment from extraneous topics.
Symptomatic relief is more efficient when the cognitive and behavioral components
driving the distress are identified. The most essential task is to make therapeutic
learning explicit. Summarizing throughout and at the end of every session facilitates
that end. It is important to acknowledge and address real life stressors and face
resistance head on.
Hopelessness is one of the greatest obstacles to therapeutic gain; thus, combating
hopelessness is critical. Similarly, homework noncompliance and avoidance can prevent
change from occurring and must be addressed. In order to help challenging patients
get unstuck, it is often necessary to identify, evaluate, and modify the underlying
negative pervasive beliefs. The quality of the alliance between the therapist and the
patient can play a key role in therapeutic gain. In sum, when the therapist understands
the patient and his or her difficulties, the road to recovery becomes clear.
References
Ackerman, P. L., Bowen, K. R., Beier, M., & Kanfer, R. (2001). Determinants of individual
differences and gender differences in knowledge. Journal of Educational Psychology, 93,
797–825.
Arkes, H. R. (1991). Costs and benefits of judgment errors: Implications for debiasing.
Bachelor, A. (1995). Clients’ perception of the therapeutic alliance: A qualitative analysis.
Journal of Counseling Psychology, 42, 323–337.
Barbe, R., Bridge, J., Birhamer, B., Kolko, D., & Brent, D. (2004). Suicidality and its
relationship to treatment outcome in depressed adolescents. Suicide and Life-Threatening
Behavior, 34, 44–55.
Beck, A. T., & Dozois, D. J. A. (2011). Cognitive therapy: Current status and future directions.
Annual Review of Medicine, 62, 397–409.
Beck, A. T., Rush, A., Shaw, B., & Emery, G. (1979). Cognitive therapy of depression. New
Beck, A. T., Steer, R. A., Kovacs, M., & Garrison, B. (1985). Hopelessness and eventual suicide:
A 10 year prospective study of patients hospitalized with suicidal intention. American
Beck, J. S. (1995). Cognitive therapy basics and beyond. New York, NY: Guilford Press.
Beck, J. S. (2005). Cognitive therapy for challenging problems: What to do when the basics don’t
work. New York, NY: Guilford Press.
Becker-Weidman, E. (2010). Change in hopelessness and acute treatment outcomes among
depressed adolescents (Unpublished doctoral dissertation). Northwestern University, IL.
Berrigan, L. P., & Garfield, S. L. (1981). Relationship of missed psychotherapy appointments
to premature termination and social class. British Journal of Clinical Psychology, 20,
239–242.
Beutler, L. E., Moleiro, C., & Talebi, H. (2002). Resistance in psychotherapy: What conclusions
are supported by research. Journal of Clinical Psychology, 58, 207–217.
Bischoff, M. M., & Tracey, T. J. G. (1995). Client resistance as predicted by therapist behavior:
A study of sequential dependence. Journal of Counseling Psychology, 42, 487–495.
Blatt, S. J., Quinlan, D. M., Pilkonis, P. A., & Shea, M. T. (1995). Impact of perfectionism and
need for approval on the brief treatment of depression: The National Institute of Mental
Health Treatment of Depression Collaborative Research Program revisited. Journal of
Brent, D., Kolko, D., Birmaher, B., Baugher, M., Bridge, J., Roth, C., & Holder, D. (1998).
Predictors of treatment efficacy in a clinical trial of three psychosocial treatments for
adolescent depression. Journal of the American Academy of Child & Adolescent Psychiatry,
37 , 906–914.
Burns, D. D. (1999). The feeling good handbook (rev. ed.). New York, NY: Plume/Penguin
Books.
Cole, D. (1989). Psychopathology of adolescent suicide: Hopelessness, coping beliefs, and
depression. Journal of Abnormal Psychology, 98, 248–255.
Curry, J., Rohde, P., Simons, A., Silva, S., Vitiello, B., Kratochvil, C., … March, J. (2006).
Predictors and moderators of acute outcome in the Treatment for Adolescents with
Depression Study (TADS). Journal of the American Academy of Child & Adolescent
Psychiatry, 45, 1427–1439.
Dahlsgaard, K., Beck, A., & Brown, G. (1998). Inadequate response to therapy as a predictor
to suicide. Suicide and Life-Threatening Behavior, 28, 197–204.
Defife, J. A., Conklin, C. Z., Smith, J. M., & Poole, J. (2010). Psychotherapy appointment
no-shows: Rates and reasons. Psychotherapy: Theory, Research & Practice, 47 , 413–417.
DeRubeis, R. J., & Feeley, M. (1990). Determinants of change in cognitive therapy for
depression. Cognitive Therapy and Research, 14, 469–482.
Detweiler, J. B., & Whisman, M. A. (1999). The role of homework assignments in cognitive
therapy for depression: Potential methods for enhancing adherence. Clinical Psychology:
Science and Practice, 6, 267–282.
Egan, G. (2010). The skilled helper (9th ed.). Monterey, CA: Brooks/Cole.
Ellis, T., & Newman, C. (1996). Choosing to live: How to defeat suicide through cognitive therapy.
Oakland, CA: New Harbinger.
Falvey, J. E. (2001). Clinical judgment in case conceptualization and treatment planning across
mental health disciplines. Journal of Counseling & Development, 79, 292–303.
Feeley, M., DeRubeis, R. J., & Gelfand, L. A. (1999). The temporal relation of adherence and
alliance to symptom change in cognitive therapy for depression. Journal of Consulting
and Clinical Psychology, 67 , 578–582.
Fennell, M. J., & Teasdale, J. D. (1987). Cognitive therapy for depression: Individual differences
and the process of change. Cognitive Therapy and Research, 11, 253–271.
Fox, M. G., & Sokol, L. (2011). Think confident, be confident for teens: A cognitive therapy
guide to overcoming self-doubt and creating unshakable self-esteem. Oakland, CA: New
Harbinger.
Fridlund, A. J. (1994). Human facial expression: An evolutionary view. San Diego, CA:
Academic Press.
Gambrill, E. D. (1990). Critical thinking in clinical practice: Improving the accuracy of
judgments and decisions about clients. San Francisco, CA: Jossey-Bass.
Garb, H. N. (1998). Case formulation. In H. N. Garb (Ed.), Studying the clinician: Judg-
ment research and psychological assessment (pp. 85–101). Washington, DC: American
Goldston, D. B., Daniel, S. S., Reboussin, B. A., Reboussin, D. M., Frazier, P. H., & Harris,
A. E. (2001). Cognitive risk factors and suicide attempts among formerly hospitalized
adolescents: A prospective naturalistic study. Journal of the American Academy of Child
& Adolescent Psychiatry, 40, 91–99.
Harris, G., & French, D. (2009). Treatment outcome in psychiatric inpatients: The dis-
criminative value of self-esteem. International Journal of Psychiatry in Medicine, 39,
227–241.
Haugaard, C., & Sandberg, K. (2008). Resistance in cognitive therapy: An analysis of paradigm
and contemporary practice. Nordic Psychology, 60, 24–42.
Hewitt, P. L., & Flett, G. L. (1996). Personality traits and the coping process. In M. Zeidner &
N. S. Endler (Eds.), Handbook of coping: Theory applications (pp. 410–433). Chichester,
England: John Wiley & Sons, Ltd.
Hill, C., Helms, J., Tichenor, V., Spiegel, S., O’Grady, K., & Perry, E. (2001). Effects of
therapist response modes in brief psychotherapy. In C. E. Hill (Ed.), Helping skills: The
empirical foundation (pp. 61–86). Washington, DC: American Psychological Association.
Horvath, A. (2001). The alliance. Psychotherapy: Theory, Research, Practice, & Training, 38,
365–372.
Jónsson, H., Hougaard, E., & Bennedsen, B. (2011). Dysfunctional beliefs in group and
individual cognitive behavioral therapy for obsessive compulsive disorder. Journal of
Anxiety Disorders, 25, 483–489.
Karno, M. P., & Longabaugh R. (2005). Less directiveness by therapists improves drinking
outcomes of reactant clients in alcoholism treatment. Journal of Consulting and Clinical
Kazantzis, N., Deane, F. P., & Ronan, K. R. (2000). Homework assignments in cognitive and
behavioral therapy: A meta-analysis. Clinical Psychology: Science & Practice, 7 , 189–202.
Kuyken, W. (2004). Cognitive therapy outcome: The effects of hopelessness in a naturalistic
outcome study. Behaviour Research and Therapy, 42, 631–646.
Press.
LaGanga, L. R., & Lawrence, S. R. (2007). Clinic overbooking to improve patient access and
increase provider productivity. Decision Sciences, 38, 251–276.
Lambert, M. J., & Ogles, B. M. (2004). The efficacy and effectiveness of psychotherapy. In
M. J. Lambert (Ed.), Bergin and Garfield’s handbook of psychotherapy and behavior change
(5th ed., pp. 139–193). New York, NY: John Wiley & Sons, Inc.
Lambert, M. J., & Shimokawa, K. (2011). Collecting client feedback. Psychotherapy, 48,
72–79.
Lambert, M. J., Whipple, J. L., Smart, D. W., Vermeersch, D. A., Nielsen, S. L., & Hawkins,
E. J. (2001). The effects of providing therapists with feedback on patient progress during
psychotherapy: Are outcomes enhanced? Psychotherapy Research, 11, 49–68.
Lambert, M. J., Whipple, J. L., Vermeersch, D. A., Smart, D. W., Hawkins, E. J., Nielsen, S.
L., & Goates, M. (2002). Enhancing psychotherapy outcomes via providing feedback on
client progress: A replication. Clinical Psychology & Psychotherapy, 9, 91–103.
Leahy, R. L. (2001). Overcoming resistance in cognitive therapy. New York, NY: Guilford Press.
Leichsenring, F., & Rabung, S. (2008). Effectiveness of long-term psychodynamic psychother-
apy: A meta-analysis. Journal of the American Medical Association, 300, 1551–1565.
Linehan, M. M. (1993). Cognitive-behavioral treatment of borderline personality disorder. New
Mausbach, B. T., Moore, R., Roesch, S., Cardenas, V., & Patterson, T. L. (2010). The
relationship between homework compliance and therapy outcomes: An updated meta-
analysis. Cognitive Therapy and Research, 34, 429–438.
McNeill, B., May, R., & Lee, V. (1987). Perceptions of counselor source characteristics by
premature and successful terminators. Journal of Counseling Psychology, 34, 86–89.
Medeiros, M., & Prochaska, J. (1988). Coping strategies that psychotherapists use in working
with stressful clients. Professional Psychology: Research and Practice, 19, 112–114.
Mitchell, C. (2006). Resistant client: We’ve all had them; Here’s how to help them! Retrieved
from http://www.psychotherapy.net/article/resistant-clients
Naidoo, P., Dick, J., & Cooper, D. (2009). Exploring tuberculosis patients’ adherence to
treatment regimens and prevention programs at a public health site. Qualitative Health
Research, 19, 55–70.
Newman, C. F. (1994). Understanding client resistance: Methods for enhancing motivation to
change. Cognitive and Behavioural Practice, 1, 47–69.
Newman, C. F. (2002). A cognitive perspective on resistance in psychotherapy. Journal of
Newman, C. (2008). Identifying and modifying maladaptive schemas. In W. Donohue &
J. Fisher (Eds.), Cognitive behavior therapy: Applying empirically supported techniques in
your practice (2nd ed., pp. 457–465). Hoboken, NJ: John Wiley & Sons, Inc.
Orbach, I., Blomenson, R., Mikulincer, M., Gilboa-Schechtman, E., Rogolsky, M., &
Retzoni, G. (2007). Perceiving a problem-solving task as a threat and suicidal behavior in
adolescents. Journal of Social and Clinical Psychology, 26, 1010–1034.
Overholser, J. (1996). Cognitive-behavioral treatment of depression, part V: Enhancing
self-esteem and self-control. Journal of Contemporary Psychotherapy, 26, 163–176.
Papakostas, G. I., Petersen, T. J., Farabaugh, A. H., Murakami, J. L., Pava, J. A., Alpert,
J. E., … Nierenberg, A. A. (2003). Psychiatric comorbidity as a predictor of clinical
response to nortriptyline in treatment-resistant major depressive disorder. Journal of
Clinical Psychiatry, 64, 1357–1361.
Persons, J. B. (2006). Case formulation-driven psychotherapy. Clinical Psychology: Science and
Practice, 13, 167–170.
Persons, J. B., Burns, D. D., & Perloff, J. M. (1988). Predictors of dropout and outcome
in cognitive therapy for depression in a private practice setting. Cognitive Therapy and
Research, 12, 557–575.
Persons, J. B., Davidson, J., & Tompkins, M. A. (2001). Essential components of cognitive-
behavior therapy for depression. Washington, DC: American Psychological Association.
Reese, R. J., Norsworthy, L. A., & Rowlands, S. R. (2009). Does a continuous feedback system
improve psychotherapy outcome? Psychotherapy: Theory, Research, Practice, Training, 46,
418–431.
Reinecke, M. A., DuBois, D. L., & Schultz, T. M. (2001). Social problem solving, mood, and
suicidality among inpatient adolescents. Cognitive Therapy and Research, 25, 743–756.
Renk, K., & Dinger, T. (2002). Reasons for therapy termination in a university psychology
clinic. Journal of Clinical Psychology, 58, 1173–1181.
Rifai, A., George, C., Stack, J., Mann, J., & Reynolds, C. F. (1994). Hopelessness in suicide
attempters after acute treatment of major depression in late life. American Journal of
Psychiatry, 151, 1687–1690.
Roe, D., Dekel, R., Harel, G., & Fennig, S. (2006). Clients’ reasons for terminating psy-
chotherapy: A qualitative and qualitative inquiry. Psychology and Psychotherapy: Theory,
Research and Practice, 79, 529–538.
Safran, J. D., & Segal, V. Z. (1990). Interpersonal process in cognitive therapy. New York, NY:
Basic Books.
Scheel, M. J., Hanson, W. E., & Razzhavaikina, T. I. (2004). The process of recommending
homework in psychotherapy: A review of therapist delivery methods, client acceptability,
and factors that affect compliance. Psychotherapy: Theory, Research, Practice, Training, 41,
38–55.
Segal, Z., Kennedy, S., Gemar, M., Hood, K., Pedersen, R., & Buis, T. (2006). Cognitive
reactivity to sad mood provocation and the prediction of depressive relapse. Archives of
Shaw, B. F., Elkin, I., Yamaguchi, J., Olmsted, M., Vallis, T. M., Dobson, K. S., … Imber,
S. D. (1999). Therapist competence ratings in relation to clinical outcome in cognitive
therapy of depression. Journal of Consulting and Clinical Psychology, 67 , 837–846.
Smith, J., Alloy, L., & Abramson, L. (2006). Cognitive vulnerability to depression, rumination,
hopelessness, and suicidal ideation: Multiple pathways to self-injurious thinking. Suicide
and Life-Threatening Behavior, 36, 443–454.
Sokol, L., & Fox, M. G. (2009). Think confident, be confident: A four step program to eliminate
doubt and achieve lifelong self-esteem. New York, NY: Perigee.
Sperry, L., Gudeman, J. E., Blackwell, B., & Faulkner, L. R. (1992). Psychiatric case formula-
tions. Washington, DC: American Psychiatric Association.
TADS Team (2005). The Treatment for Adolescents with Depression Study (TADS): demo-
graphic and clinical characteristics. Journal of the American Academy of Child and
Adolescent Psychiatry, 44, 28–40.
Turk, D. C., & Salovey, P. (1986). Clinical information processing: Bias inoculation. In R. E.
Ingram (Ed.), Information processing approaches to clinical psychology (pp. 305–323). San
Diego, CA: Academic Press.
Watson, J. C., & Kalogerakos, F. (2010). The therapeutic alliance in humanistic psychotherapy.
In J. C. Muran & J. P. Barber (Eds.), The therapeutic alliance: An evidence-based guide to
practice (pp. 191–209). New York, NY: Guilford Press.
Wenzel, A., Brown, G. K., & Beck, A. T. (2009). Cognitive therapy for suicidal patients:
Scientific and clinical applications. Washington, DC: American Psychological Association.
Whipple, J. L., Lambert, M. J., Vermeersch, D. A., Smart, D. W., Nielsen, S. L., & Hawkins,
E. J. (2003). Improving the effects of psychotherapy: The use of early identification
of treatment and problem-solving strategies in routine practice. Journal of Counseling
Whisman, M., Miller, I., Norman, W., & Keitner, G. (1995). Hopelessness depression in
depressed inpatients: Symptomology, patient characteristics, and outcome. Cognitive
Therapy and Research, 19, 377–398.
Young, J. E., Weinberger, A., & Beck, A. T. (1996). Cognitive therapy for depression. In D. H.
Barlow (Ed.), Clinical handbook of psychological disorders (pp. 264–308). New York, NY:
Guilford Press.
17
A Cognitive Behavioral Road
Map for Relapse Prevention in
Depression
Shadi Beshai and Keith S. Dobson
University of Calgary, Canada
Depression is one of the most prevalent, debilitating, and economically costly condi-
tions in the world (Murray & Lopez, 1997). Lifetime prevalence estimates of major
depression among adults in the United States are as high as 16.6% (Kessler et al.,
2005). Unfortunately, depression seldom strikes its sufferers only once, as evidence
suggests that those who are inflicted with the disorder go on to develop a career of
depression, often incurring an average of 4.3 episodes in their lifetime (Perris, 1992).
An even more bleak statistic is that 50–80% of those who seek treatment (in the
form of medication or psychotherapy) for their first episode experience a relapse in
symptomatology (Dobson & Ottenbreit, 2004). As such, although therapeutic efforts
that focus on the treatment of acute depression are critically important, attention must
be given to address the chronic nature of the disorder. Given the pernicious (Joiner,
2000), chronic, and evasive nature of depression, a number of authors (e.g., Dozois
& Dobson, 2004; Muñoz, Cuijpers, Smit, Barrera, & Leykin, 2010) have suggested
that the prevention of depression represents the most ethical, logical, and economical
therapeutic option.
Prevention efforts require the ability to focus efforts on at-risk groups, either prior
to the onset of a disorder (i.e., primary or universal prevention) or with groups who
have known risk indicators (i.e., selective prevention) or are showing early signs of a
disorder (i.e., indicated prevention; Institute of Medicine, 2009). Universal prevention
is often a challenge in the area of mental health, however, as population-wide risk
factors are so ubiquitous that it is difficult to target such factors for prevention.
Selective and indicated prevention, or what has been termed secondary prevention
(Dozois & Dobson, 2004), is challenged by the state of the literature on risk factors,
and the ability to detect depression early and potentially prevent the occurrence of a
first episode. While efforts to prevent onset of depression are worthwhile, especially as
the literature on risk continues to grow (Dobson & Dozois, 2008), one of the most

DOI: 10.1002/9781118528563.wbcbt17
consistent predictors of future depression is a history of the disorder. Furthermore,

the population of people who have had an episode of depression is reasonably easy
to identify, so efforts to prevent recurrence (i.e., tertiary prevention) make eminent
sense from a public health perspective.
The focus of this chapter is on tertiary prevention for recurrent depression. As
such, we explore some of the variables that have been identified as moderators of
risk and vulnerability for recurrent depression, as well as the models that have been
presented to account for the chronic nature of the condition. Furthermore, this
conceptual review we provide is used as a blueprint for cognitive behavioral treatment
for recurrent depression (Bieling & Antony, 2003; Rowa, Bieling, & Segal, 2005).
Our intentions are twofold. First, we provide a review of the literature on relapse
and recurrence, while concurrently forging a bridge between research and clinical
practice. It is our contention that the best clinical practice is one that is informed by
state-of-the-art scientific research, and thus a consolidation of these worlds is both
necessary and natural. Before we delve into these topics, however, we provide some
definitional clarity and describe some of the methodological issues in the field.
Definitions and Methodological Issues
According to the Diagnostic and Statistical Manual of Mental Disorders (5th ed., text
rev.; DSM-5; American Psychiatric Association, 2013), a major depressive episode
(MDE) is defined as a period of 2 weeks or more wherein an individual experiences
sad mood most of the day, on most days, and/or anhedonia (i.e., loss of interest or
pleasure). In addition to the presence of at least one of these fundamental symptoms,
the DSM-5 dictates that individuals display four or more other symptoms (e.g., sleep or
appetite disturbance, psychomotor retardation or agitation, diminished concentration
or energy, feelings of worthlessness or guilt, and suicidal ideation) to meet diagnostic
criteria. Exclusionary criteria include circumstances when the symptoms can be
explained by the direct effects of a substance taken by the individual or the direct
effects of a medical condition or disorder. Although the DSM-IV precluded a diagnosis
of MDE if the symptoms occured within 8 weeks of the death of a loved one and could
best be conceptualized as bereavement, this exclusion was eliminated in the DSM-5.
The DSM-5 further provides a variety of subtype specifications for MDE (e.g., with
anxious distress; with psychotic features, with peripartum onset; with seasonal pattern)
which need to be taken into account when a diagnosis is given. It is also important
to note that the DSM-5 recognizes the possibility of recurrent major depression or
major depressive disorder (MDD), the criteria for which stipulate that the sufferer
experience two (or more) distinct episodes, by a period of at least two months during
which diagnostic criteria are not met.
Definitions of relapse, recurrence, remission, and recovery have relied heavily on
the diagnostic criteria presented in the DSM nosological system. For instance, the
MacArthur Foundation Research Network Task Force (Frank et al., 1991) provided
operational definitions of commonly used terms in depression research. Their system
defines “full remission” as a brief period wherein the individual is “asymptomatic”
(i.e., does not meet diagnostic criteria), and “recovery” as an 8-week or longer period
Relapse Prevention in Depression 381
wherein the individual is in full remission. “Relapse” and “recurrence” were also
defined, as a diagnosable return of depressive symptoms subsequent to remission
and recovery, respectively. As such, the critical temporal period (i.e., 8 weeks) used
to distinguish these constructs was borrowed directly from DSM nosology. These
definitional terms remain useful after the publication of the DSM-5, although the rates
of depression, remission, and relapse can all be expected to rise somewhat as a result
of the removal of the exclusionary criterion related to bereavement, noted above.
Although the Frank et al. (1991) conceptualizations of recovery and recurrence are
pragmatic in nature and commonly used, they have been questioned. For instance, the
threshold for “remission” is somewhat ambiguous. If individuals who no longer meet
diagnostic criteria are defined as remitted, then by definition individuals with four of
the nine potential symptoms of MDE are in “remission.” However, such individuals
are clearly still suffering some of the symptoms of the disorder, and indeed, their level
of functioning may be demonstrably worse than before the onset of the most recent
episode of depression. Second, it is recognized that the temporal benchmark of 8
weeks utilized to distinguish remission and recovery is arbitrary. Given such issues, a
number of researchers in the field of depression relapse have relied on cut-off scores
on self-report questionnaires that yield severity scores, such as the Beck Depression
Inventory–II and the Hamilton Rating Scale for Depression, to define these constructs
(see Dozois & Dobson, 2010). It is recognized, however, that the use of cut-offs is
also somewhat arbitrary, and that research and clinical participants who fall below any
particular cut-off score may still experience considerable “residual symptoms.”
Risk and Vulnerability Factors
A number of risk and vulnerability factors have been implicated in depressive relapse
and recurrence. “Risk” can be defined as any factor that is associated with an increase
in the likelihood of the occurrence of a condition (e.g., depressive relapse). Risk
factors are established from evidentiary data, but they do not necessarily have causal
implications. On the other hand, “vulnerability” can be defined as any factor that
is causally associated with the occurrence of a disorder or condition (Dobson &
Dozois, 2008). For example, female gender is a risk factor for depression onset,
whereas depressogenic cognitive style has been described as a vulnerability factor
(Ingram, Miranda, & Segal, 1998). It should also be noted that “resiliency” factors
are sometimes noted for depression. Resiliency factors are in essence the opposite of
risk factors, in that they consist of variables that can be shown to reduce the risk of
depression. These factors are sometimes referred to as “buffers” against the likelihood
of a given disorder (Burcusa & Iacono, 2007). Some of these factors, such as higher
levels of social support, may also be causally related to a reduced risk of depression,
but to date the literature has not advanced to the point of distinguishing causal
resiliency factors from other factors that are simply associated with reduced risk of
onset, relapse, or recurrence of clinical depression.
Despite advances in the field (Dobson & Dozois, 2008), work that specifically
examines vulnerability to relapse has developed more slowly than the literature on
risk, and thus strong conclusions cannot be drawn regarding the causal mechanisms
for depressive relapse and recurrence. The above being said, a number of risk factors
have been identified for relapse and recurrence in depression. History of depressive
episodes has consistently been linked to recurrence, as the number of previous
depressive episodes is positively correlated with a higher likelihood to recurrence
(Beshai, Dobson, Bockting, & Quigley, 2011; Bockting et al., 2006). Furthermore,
a number of researchers (Conradi, de Jonge, & Ormel, 2008; Judd et al., 2002;
Taylor, Walters, Vittengl, Krebaum, & Jarrett, 2010) have observed that the presence
of residual symptoms after the conclusion of a depressive episode is a risk factor
for relapse and recurrence, although more recent evidence suggests otherwise (see
Bertschy et al., 2010). The results obtained by Conradi et al. (2008) suggest that,
while different clinical variables such as the severity of depressive symptoms and
depression-free time are associated with different outcomes, coping potential (i.e.,
a general construct measuring self-esteem and locus of control) and number of
previous episodes were significant predictors for all the outcome variables used in
their study. Burcusa and Iacono (2007) provided a recent review of the depressive
relapse literature. These researchers concluded that a number of the risk factors
that are associated with the onset of depression are also associated with relapse
of the disorder. Such factors include cognitive variables (e.g., rumination, selective
attention, and depressogenic style; Gotlib & Joormann, 2010; Iacoviello, Alloy,
Abramson, Whitehouse, & Hogan, 2006), neuroticism (Barnhofer & Chittka, 2010;
Duggan, Sham, Lee, Minne, & Murray, 1995; Hodgins & Ellenbogen, 2003),
stressful life events (both major life events and daily hassles; Kendler, Karkowski, &
Prescott, 1999; Monroe & Harkness, 2011; Paykel & Cooper, 1992), and social
support (as a resiliency factor; Kessler & Magee, 1994; Stice, Ragan, & Randall,
2004). There are factors, however, that are uniquely associated with relapse. For
instance, a large body of data supports a link between depression recurrence and
the severity of symptoms present in the index episode of depression, which is
the episode directly prior to relapse or recurrence. Furthermore, certain symptoms
such as suicidality appear to predict relapse and recurrence (Burcusa & Iacono,
2007). In addition, the authors identified familial history of depression (recurrent or
otherwise) and/or other psychiatric disorders as a more distal risk factor for depressive
recurrence, in concert with other risk factors. Moreover, some evidence suggests that
the presence of comorbid conditions, especially dysthymia, is a risk factor for chronic
depression. Finally, some authors suggest that a problem- or task-focused coping style
(confrontation of and drive to resolve stressful events), as opposed to emotion-focused
and avoidant strategies, may serve as a protective or resiliency factor against recurrent
depression (e.g., Kuyken & Brewin, 1994). In contrast, emotion-focused coping and
avoidance may be risk factors for recurrent depression.
A number of hypotheses have been forwarded to account for the chronicity of
depression. Some researchers argue that “scarring” occurs as a byproduct of each suc-
cessive episode of depression. The “kindling” hypothesis of relapse, for example, pro-
poses that, with each episode, less severe and frequent external stressors are required
to initiate the downward spiral into depression (Monroe & Harkness, 2005; Post &
Weiss, 1995). Support for the scarring hypothesis of depression is accruing (Bockting
et al., 2006; Kendler, Thornton, & Gardner, 2000; Lewinsohn, Rohde, Seeley, Klein,
& Gotlib, 2000). Relatedly, Teasdale’s (1988) differential activation hypothesis pro-
poses that, with reoccurring episodes, the association between sad mood and negative
thinking patterns is bolstered, resulting in more readily activated mood-congruent
dysfunctional thinking. Thus, a self-perpetuating cognitive pattern is triggered when
the individual experiences sad mood, and this pattern narrows the scope of the
information processing system toward negative content and rumination, which then
exacerbates the sad mood. Third, the stress generation hypothesis of depression pro-
poses that depressed individuals inadvertently engender a greater number of stressful
situations, and that this process intensifies with increasing number of episodes (Ham-
men, 1991). Unlike the “scarring” proposition, however, the stress generation model
suggests that this proclivity toward more stressful environments represents a premor-
bid vulnerability in depression. Clearly, the “scarring,” differential activation, and
stress generation hypotheses are not mutually exclusive. It is probable that one or
more of these various processes are implicated within individual cases of depression.
Burcusa and Iacono (2007) concluded their review by indicating that there is
likely some genetic vulnerability that is specific to depression recurrence. This genetic
vulnerability may be neither necessary nor sufficient to cause relapse and recurrence,
but is rather probably contributory, in that its presence increases the possibility that
recurrence will take place. There is likely a network of causation that is both parallel
and sequential in nature. For instance, genetic vulnerabilities may initiate a chain of
causal factors and these causal factors operate simultaneously but also ignite their
own causal chains. For example, genetic vulnerability may predispose one toward
neurotic personality style, and thereby to subsequent dysfunctional attitudes which,
in concert with stressful life events, may lead to suicidal ideation and/or comorbid
psychiatric conditions. This causal chain is most likely nonlinear in nature and, as such,
the occurrence of a risk factor may retroactively reinforce and strengthen prior risk
factors in the chain. To add to this already complex etiological picture, it is likely that
causal and risk factors interact with one another, and therefore different degrees of
the same variable produce different clinical outcomes. As such, the risk, vulnerability,
and protective factors for recurrent depression are multifaceted and the outcome of
relapse and recurrence is multidetermined (see Figure 17.1).
Joiner (2000) places the risk factors for depression into three distinct categories:
propagatory (i.e., risk factors in the classic sense), erosive (factors that erode over
time, those that are affected by the “scarring” process), and self-propagatory (or
individual-induced factors that increase their risk for depression). Dobson (2010) has
argued that the categories identified by Joiner may not be mutually exclusive, and
thus some factors may be viewed as both erosive and self-propagatory.
Cognitive Behavioral Therapy as Protection

against Relapse and Recurrence
There is strong evidence that some forms of psychotherapy successfully thwart the
chronic course of depression (Beshai et al., 2011; Guidi, Fava, Fava, & Papakostas,
2010; Vittengl, Clark, Dunn, & Jarrett, 2007). The models with the most evidence
Distal variables Proximal variables
Avoidant
coping
Negative Remission
Family history Familial Depressogenic life Depression
Genetic and residual Relapse
of experiences cognitive events/daily onset
vulnerability symptoms
psychopathology (e.g., trauma) style hassles
Rumination
Figure 17.1 Hypothesized causal model for relapsing depression.

to date include cognitive behavioral therapy (CBT), interpersonal psychotherapy

(IPT), and mindfulness-based cognitive therapy (MBCT). A thorough review of this
evidence is beyond the scope of this chapter, and can be found in other sources (see
Beshai et al., 2011). A brief overview of the protective effects of CBT is provided,
however, as it is pertinent in understanding treatment approaches to recurrent
depression.
First, acute-phase CBT targeted at symptom reduction shows a significantly higher
preventative effect against relapse and recurrence than acute-phase treatment with
antidepressant medication (Gloaguen, Cottraux, Cucherat, & Blackburn, 1998;
Hollon, 2003). For instance, Hollon (2003) found that remission rates after acute
phases of CBT and a course of selective serotonin reuptake inhibitor (SSRI) were
comparable at approximately 57%, but relapse rates in the CBT group (25%) were
significantly lower than those in the SSRI group (40%) after a 1-year follow-up. In a
similar vein, but even more telling, Dobson et al. (2008) reported that 1-year relapse
rates were 39% for patients successfully provided with a course of up to 20 sessions
of CBT during the acute phase of treatment, as compared to a 53% relapse rate for
patients who initially responded to, and were continued over the course of a year of
follow-up on, antidepressant medication.
Second, although acute phases of CBT fare better in reducing rates of relapse and
recurrence than their medication counterparts, it is clear that acute therapy alone
is largely unable to disrupt the chronic course of the disorder. For this reason, a
number of treatment protocols that directly target recurrence of depression (also
known as “maintenance” and “continuation” phase treatments) have been designed.
Studies to date have shown that continuation and maintenance phases of CBT, as
well as mindfulness-based protocols infused with cognitive behavioral elements, are
moderately effective in reducing relapse rates over and above acute-phase CBT (see
Beshai et al., 2011, and Vittengl et al., 2007, for reviews).
Third, a number of variables seem to moderate the effectiveness of therapy in the
reduction of relapse and recurrence. One relatively consistent finding has been that the
protective effects of continuation or maintenance CBT are augmented for individuals
with a history of three or more depressive episodes. In fact, targeted CBT efforts to
thwart the chronicity of depression appear largely ineffective for individuals with less
than three prior episodes (Bockting et al., 2005; Monroe, Slavich, Torres, & Gotlib,
2007; Teasdale et al., 2000; but see Bondolfi et al., 2010, for a failure to replicate).
Two Possible Types of Recurrent Depression
A few hypotheses have been forwarded to explain the emergent finding in the
recurrence prevention literature regarding the moderating effect of depressive history.
Beshai et al. (2011) suggested, for example, that some individuals with depression
may have a single episode or only a limited number of episodes, whereas other
individuals develop a more recurrent form of the disorder. Some treatment literature
has also examined the trajectories of patients with more and less recurrent depression.
For example, Bockting et al. (2005) randomly assigned 187 remitted depressed
patients to two groups: a treatment as usual condition, and treatment as usual in
combination with a continuation phase cognitive therapy condition. Consistent

with previous findings, the researchers found that the number of previous episodes
interacted with the group condition, as patients with five or more prior episodes
assigned to the CBT condition had significantly lower rates of recurrence in a 2-year
follow-up than did those assigned to the treatment as usual condition (46% vs.
71%, respectively). There was no significant difference in recurrence rates, however,
between the two conditions for those patients with a history of less than five episodes
(59% in the treatment as usual condition, and 63% in the CBT condition).
Bockting and colleagues (2005) proposed that different processes operate for
individuals with four or less and those with five or more prior episodes. Individuals with
a less severe history of depression have an “externally” propagated type of depression,
whereas those with a more severe history have an “internally” propagated type of
recurrent depression. This notion is congruent with Teasdale’s (1988) differential
activation hypothesis. It may be, then, that initial episodes of depression are largely
triggered by external events or factors. However, by the second or third episode, a
causal equilibrium between internal and external factors may be reached, and by the
third or fourth episode, the threshold for internal provocation may be surpassed. This
conceptual differentiation between “internally” and “externally” provoked recurrent
depression has both theoretical and clinical implications. Conceptually, it is possible
that many factors that are responsible for the onset of depression are not necessarily
involved in its maintenance or recurrence. Similarly, factors involved in recurrence may
be less implicated in early onset depressive episodes. The optimal clinical strategies
may also depend on where a particular patient is on this balance between external and
internal risk or vulnerability factors.
With this possible distinction between the types of recurrent depression in mind,
it is important to note that this distinction is most likely crude in nature, and one
that is only pragmatically significant. In reality, biological, psychological (internal),
and environmental/social (external) factors all coexist and interact in the onset,
maintenance, and recurrence of depression. To add to this complexity, the resultant
byproduct of such interactions is dependent on the severity of each individual risk
factor. Using this two-type distinction of recurrent depression as a guiding framework
for therapy, the next section focuses specifically on treatment approaches to relapse
and recurrence prevention of depression. This model is pertinent in the early phases
of treatment (assessment and case conceptualization), and becomes less so in the
intermediate and latter stages.
Cognitive Behavioral Therapy for Relapse Prevention
In this section, several intervention options are described from a cognitive behavioral
framework which can address relapse and recurrence prevention in depression. The
focus here is on unique elements of CBT that target known risk factors for relapse.
As such, a number of extrapolations from the literature are made to bridge the gap
between research and practice in the field. This section is organized in accordance with
the different stages of therapy (i.e., assessment, case conceptualization, intervention,
and evaluation).
Assessment
To date, the number of prior depressive episodes is the most consistent factor that
appears to mitigate the effects of preventative efforts. As such, it is also important
to develop a clear picture of the client’s history of depression in the initial stages of
therapy. We recommend that the clinician utilize a semistructured clinical interview.
In addition to other key elements of an intake interview, this interview should serve
to elucidate several aspects of the client’s condition: (a) the age of first onset of
depression and subsequent chronicity of the client’s depression, (b) the typical nature
and length of the intermediary periods between depressive episodes (e.g., the presence
of residual symptoms after the remission of depression, and how long the client has
been symptomatic or asymptomatic after the depression remission and/or recovery),
(c) potential risk, vulnerability, and resiliency factors associated with the onset and/or
recurrence of depressive episodes, and (d) the presence or absence of comorbid
conditions which have been shown to moderate recurrence. Moreover, collateral
information may be gathered to determine familial history of psychopathology and
early temperament.
Based on the interview, the therapist should form hypotheses regarding the presence
and severity of the risk factors and moderators of therapeutic success identified by the
literature. We recommend an investigation of these hypotheses, both at the beginning
stages of therapy and throughout the treatment as new information becomes available.
Further, if these factors are not clear following the interview, a series of tests can
be considered, which might include a measure of symptom severity (e.g., the Beck
Depression Inventory–II; Beck, Steer, & Brown, 1996), depressogenic cognitive
style (e.g., the Attributional Style Questionnaire; Peterson et al., 1982), neuroticism
(e.g., the NEO-PI-R Neuroticism Scale; Costa & McCrae, 1992), coping style (the
Utrecht Coping List; Schreurs, van de Willige, Brosschat, Tellegen, & Graus, 1988),
and negative life events (e.g., the Negative Life Events Questionnaire; Kraaij &
De Wilde, 2001). Furthermore, we recommend the use of instruments designed
to measure intermediary attitudes (e.g., the Dysfunctional Attitude Scale; Weissman
& Beck, 1978) and core beliefs (e.g., the Young Schema Questionnaire; Young &
Brown, 1994).
Case Conceptualization
Case conceptualization is typically an ongoing process in CBT (Kuyken, Padesky,
& Dudley, 2009). The case conceptualization is preferably developed in accordance
with a thorough and integrative assessment process (Persons & Davidson, 2001).
It is a part of standard CBT and should be also employed in CBT for relapse
prevention, as the case conceptualization permits the practitioner to identify optimal
therapeutic strategies to prevent depression. Given the hypothetical balance between
the “internal” and “external” factors that drive recurrent depression, the therapist
should first decide whether CBT is the best option for the individual client. Standard
CBT may not be the optimal preventative therapy for depression if the client reports
a history of one or two depressive episodes, as CBT protocols may be more effective
for the “internal” type of recurrent depression. In cases of depression where there
are more “external” factors, and although the evidence for this recommendation
is admittedly limited, the practitioner might consider other therapeutic approaches
designed to prevent relapse, such as behavioral activation or interpersonal therapy (see
Beshai et al., 2011).
In cases where the client reports a history of three or more episodes, however,
a CBT-based protocol is recommended. The cognitive behavioral case conceptual-
ization should present hypotheses regarding factors that are implicated in the onset
and maintenance of the depressive episode, and possible barriers to therapeutic suc-
cess. For instance, a client with a significant familial history of psychotic disorders,
heightened neuroticism, and residual symptoms between depressive episodes prob-
ably requires a different protocol than would an individual with low neuroticism,
heightened negative attributions, and asymptomatic recovery periods. As mentioned
above, it is likely that multiple risk and vulnerability factors operate simultaneously.
As such, the therapist should decide what elements to add or subtract from a protocol
depending on the hypothesized pathway to recurrence.
Intervention
A number of CBT protocols have been developed to address relapse and recurrence
in depression. Depending on the results of the assessment and the clinician’s case
formulation, there are multiple avenues to pursue in therapy.
Cognitive behavioral therapy for residual symptoms. This protocol was developed to
help resolve symptoms that were unresponsive to treatment in the acute phase (Fava,
Fabbri, & Sonino, 2002; Fava, Grandi, Zielezny, Canestrari, & Morphy, 1994).
Reports indicate that this approach is delivered in 10- to 40-minute sessions, with
a session occurring every other week. This protocol is founded on the premise that
residual symptoms (e.g., suicidality, disrupted sleep or appetite, poor concentra-
tion) function as a prodrome to future depression which, if left unmanaged, may
develop into a full-blown episode. A 4-year follow-up investigation of this protocol
(Fava, Grandi, Zeilezny, Rafanelli, & Canestrari, 1996) revealed that individuals in
the treatment condition experienced significantly lower relapse rates than those in the
nontreatment condition (35% vs. 70%, respectively). Unfortunately, results from the
6-year extension of this study (Fava, Rafanelli, Grandi, Canestrari, & Morphy, 1998)
indicated that the relapse rates between groups were comparable and the significant
differences found in the 4-year follow-up were attenuated. It is thus possible that
this approach delays, but does not prevent, relapse and recurrence. Further research
is needed to ascertain the benefits of this approach to treating residual symptoms in
depression.
Coping with depression. Coping with depression (CWP) is a group format CBT
prevention protocol designed by Kühner, Angermeyer, and Veiel (1996) and is
typically offered 4 weeks after the completion of acute phase therapy. The protocol
emphasizes the gains made in the acute phase of therapy, and assists with the creation
of plans to maintain treatment gains. Kühner et al. (1996) found that individuals who
received this treatment protocol experienced significantly lower relapse rates (14.3%)
than did matched controls (42.9%) over a 1-year follow-up period.
Continuation phase cognitive behavioral therapy. Continuation phase CBT emphasizes

the generalization of skills acquired during the acute phase of therapy, but with a
focus on the prevention of recurrence and relapse. A number of versions of this
protocol exist. Jarrett and colleagues (1998, 2001) designed an original version, but
variations have subsequently been offered by Paykel et al. (1999, 2004), and Bockting
et al. (2005). Jarrett and colleagues’ (1998) edition is provided for approximately
8 months following the completion of the acute phase, whereas in Paykel and
colleagues’ (1999) version, sessions are given once every 4 weeks for a 20-week
period after the completion of the acute period. The two protocols have shown
efficacy in preventing relapse over and above clinical management and treatment
as usual protocols (see Beshai et al., 2011, for a review). Bockting and colleagues’
(2005) version of continuation CBT targeted a specific vulnerability factor (the
cognitive content of negative thinking) and was delivered in a group format. Patients
with a history of five or more episodes of depression experienced significantly lower
relapse rates than did individuals with the same depressive history in the treatment as
usual condition (Bockting et al., 2005).
Maintenance cognitive behavioral therapy. This intervention is a slightly altered version

of acute-phase CBT. The focus of this protocol is on residual symptoms and enhance-
ment of coping skills to thwart relapse. Petersen et al. (2010) demonstrated, however,
that individuals in the maintenance CBT group did not show significantly lower rates
of relapse than those in the medication maintenance and placebo conditions.
Cognitive behavioral analysis system of psychotherapy. Cognitive behavioral analysis

system of psychotherapy (CBASP) is an eclectic intervention that was specifically
designed for chronic or recurrent depression, and combines cognitive behavioral,
interpersonal, and psychodynamic elements (McCullough, 2000). A key assumption of
CBASP is that patients with recurrent depression have distinct patterns of interpersonal
thinking and behavior which create the vulnerability to relapse and recurrence. A major
aspect of the treatment is the need for a situational analysis of the patient’s depression.
This analysis examines specific events, the thoughts that the patient has in these
situations, and his or her behavioral and emotional responses. The idea is to develop
a functional analysis of the characteristic manner in which the patient responds to
events. A second aspect of the analysis, however, is the remediation phase, in which
the patient is encouraged to explore whether or not his or her thoughts helped to
attain the ends or goals he or she had hoped for, and if not, what could change in the
future. Another aspect of CBASP is use of the therapeutic relationship. For example,
the therapist is encouraged to develop transference hypotheses about the relationships
between the patient and others in his or her world (including the therapist), and also
to openly discuss ways in which the therapist’s perceptions of interpersonal situations
may mirror or diverge from the patient’s.
CBASP is delivered weekly over a 52-week period, and is designed to augment
gains in the acute period of therapy. Results from an investigation by Klein et al.
(2004) revealed that individuals in the treatment condition experienced significantly

lower rates of relapse than those in the assessment only condition (10.7% vs. 32.0%,
respectively). Although CBASP is still a relatively recent addition to treatments to
reduce relapse, early indications (Arnow & Post, 2010) are that this treatment has
promise.
Mindfulness-based cognitive therapy. Mindfulness-based cognitive therapy (MBCT)

is based on Teasdale’s (1988) differential activation model, and thus maintains that
relapse does not necessarily develop in response to the content of negative thought,
but rather to the associative process which has been reinforced over time. Thus,
this intervention teaches remitted clients to recognize that, from time to time,
negative events will occur in their lives, and to foster an accepting attitude toward
experience, which includes negative thinking and depressive symptomatology that
may occur. Originally developed into a formal treatment by Segal, Williams, and
Teasdale (2002), MBCT is specifically designed to reduce relapse and recurrence
in depression. Furthermore, the protocol emphasizes to its trainees that negative
cognitions and emotions are an inevitable part of the human condition, and that
instead of actively struggling with such symptoms, it is necessary to adopt a more
mindful but disengaged and accepting stance toward them.
It is noteworthy that the developers of MBCT have insisted that a critical aspect
of the treatment is that the therapist has a mindfulness practice him- or herself. It
is argued that this practice is necessary to help the therapist respond effectively to
any questions or concerns raised by MBCT participants. This assumption has yet to
be evaluated empirically, but this potential requirement will limit the application of
MBCT in a way that is consistent with the developers of the approach.
A number of trials have evaluated the preventative power of MBCT, and the
results for those individuals with a history of three or more episodes of depression
appear promising (see Beshai et al., 2011). To date, however, the supportive trials
have been mostly published by the original developers of the approach, and a recent
replication in a separate country failed to demonstrate that MBCT was more effective
at preventing depression recurrence than treatment as usual (Bondolfi et al., 2010).
Further evidence is needed to know how effective MBCT is overall.
Intervention summary. As the above review demonstrates, a number of CBT-based

protocols for the prevention of relapse and recurrence have been developed, and a
number of these approaches appear promising in interrupting the depressive cycle.
In particular, continuation-phase CBT and CBT that addresses residual symptoms
appear highly promising. It is also clear, however, that a number of limitations exist
in the trials conducted to date. For example, there is a lack of consistency in the
manner that relapse and recurrence (and, relatedly, remission and recovery) have been
defined across studies. Second, a number of these prevention studies have employed
relatively small samples, precluding firm conclusions from the study results. Third, the
studies have employed different methodologies to allocate participants to conditions.
Moreover, the literature has typically compared preventative interventions to either
treatment as usual, which is often not quantified or evaluated thoroughly, or to
continuation medication. A number of trials have also permitted patients in the CBT
treatment to continue taking medications, making conclusions about the absolute

efficacy of these protocols difficult to establish. It is also important to note that the
efficacy of these prevention interventions is often limited to individuals with a chronic
history of depression, and that prevention of recurrence has been more difficult to
establish for people with a shorter history of depression.
Evaluation. In this phase of treatment, we recommend that therapists use the same
measure of symptom severity used in the assessment phase to evaluate the presence
and intensity of depression symptoms. Most prevention studies employing the Beck
Depression Inventory define remission as a score of 8 or less, whereas those that
utilized the Hamilton Rating Scale for Depression (Hamilton, 1960) employ a cut-off
score of 7 or less. We recommend that these cut-offs be followed to determine
treatment success. Furthermore, we recommend that the therapist also administer the
same measures of intermediary attitudes and/or core beliefs to examine the intactness
of those tightly wound depressive self-schemas (Dozois & Dobson, 2001).
Future Directions
It is clear that a number of theorists, clinicians, and researchers are beginning to

pay increased attention to the problem of depression relapse and recurrence. The
development of a literature on risk and vulnerability factors (Dobson & Dozois,
2008) is most welcome, as this literature can help to further develop different
models of depression recurrence, and provide some directions for the development
of treatments. Also, the fact that a number of emergent treatment methods exist,
some of which have good preliminary data to support them as effective tools to
reduce recurrence, should give hope for the many people who struggle with recurrent
depression. Notwithstanding these positive developments, a number of conceptual and
methodological issues can be observed in this field of research. The inconsistency of
the operationalization of “relapse” and “recurrence,” and the unfortunate conflation
of these constructs, remains a pertinent issue across studies. Further, the inconsistent
methodology across studies, especially regarding what type of intervention is offered in
the acute phase (e.g., psychotherapy vs. medication), is especially problematic. Many
of these investigations do not consider the potential cumulative effect of therapy.
In other words, those receiving medication in the acute phase and CBT in the
continuation phase might fare worse (or better) than those who receive some form
of CBT in both phases. As many studies do not formalize this potential cumulative
effect into a variable, the relative efficacy remains an open and unanswered question.
Future investigations should use more consistent methodology and build upon the
progress already achieved in the literature.
As highlighted elsewhere (Beshai et al., 2011), future research should focus on
intermediary and core levels of change in the cognitive system. It has been conjectured
that deep-seated change in the structure of negative self-schemas, which are often
relatively more dense and organized, is the mechanism that mediates the effect of
preventative CBT (Dozois et al., 2009). Alternatively, the effects of preventative CBT
may be mediated by the enhancement of cognitive organization and bolstering of
the density of positive (or constructive; Clark, Beck, & Alford, 1999) self-schemas.
As such, changes in self-schemas need to be measured, to enable evaluation of
these models of treatment change. Further, the study of constructs such as resilience
and thriving (i.e., the ability to learn from negative life events and adversity and
demonstrate functioning beyond baseline levels) becomes significant to understand
these compensatory mechanisms of mental health, and, in turn, individuals’ internal
ability to stave off depression.
It was noted above that acceptance of the chronic nature of one’s depression may
be positively correlated with the number of prior episodes, and that acceptance is
associated with treatment success. To the authors’ knowledge, this hypothesis has
never been empirically validated. In a related vein, it is possible that individuals with
perfectionistic and dichotomous cognitive patterns (e.g., “I need to be completely
healthy”; “If am not perfectly healthy at all times, I must be miserable”) benefit
less from preventative protocols, as they become distressed over being distressed.
In other words, these individuals might engage more frequently in “self-checking”
for depression symptoms, and if such symptoms are detected, the depressive cycle
is commenced. Finally, to the authors’ knowledge, relapse and recurrence patterns
have only been rarely examined in cultures outside of the Western world (cf. Dobson
& Mohammadkhani, 2007). As depression is a universally ubiquitous condition, we
believe that cross-cultural efforts to understand such patterns are in order.
Summary and Conclusions
Depression is often debilitating, prevalent, and chronic. Despite a number of efforts

to interrupt the cycle of depression (Bieling & Antony, 2003), the field does not yet
have a well-developed, conceptually sound, and evidence-based approach to disrupt
the chronicity of clinical depression. For humane, logical, and economic reasons,
several efforts are now underway to understand and prevent recurrent depression.
The result of these efforts is immensely productive; we are now aware of a number
of variables (e.g., familial history of psychopathology, neuroticism, negative cognitive
style, chronicity of depression) that increase the risk and vulnerability for relapse in
depression. Further, a number of hypotheses and models have been advanced to
elucidate the recurrent trajectory of depression, and some of these models (e.g., the
“scarring” and stress generation hypotheses) have received support in the literature.
Subsequently, this newly acquired knowledge regarding the course and nature
of major depression has allowed the design and implementation of a series of
relatively successful preventative CBT protocols for future depressive episodes. Despite
these tremendous strides, however, there remain a number of unanswered questions
regarding the efficacy of these relatively new protocols. For instance, it is still unclear
why such protocols work better for individuals with a more severe depressive history
(e.g., more than three episodes of depression). Also, the field is replete with a number
of methodological issues that need to be addressed in future studies to afford more
stable conclusions. In sum, we believe that while sound clinical practice is one that uses
scientific strides as a launching pad, the field has yet to evolve to the point that strong
recommendations can be made with respect to reducing the risk of recurrence in
depression. As such, we encourage the judicious utilization of the clinical approaches

described here to prevent the relapse and recurrence of depression, and strongly
endorse the need for well-conducted trials of interventions aimed at reducing the risk
of recurrent depression.
References
Arnow, B. A., & Post, L. I. (2010). Depression. In D. McKay, J. S. Abramowitz, & S. Taylor
(Eds.), Cognitive-behavioral therapy for refractory cases: Turning failure into success (pp.
183–210). Washington, DC: American Psychological Association Press.
Barnhofer, T., & Chittka, T. (2010). Cognitive reactivity mediates the relationship between
neuroticism and depression. Behaviour Research and Therapy, 48, 275–281.
Beck, A. T., Steer, R. A., & Brown, G. K. (1996). Manual for the Beck Depression Inventory-II .
San Antonio, TX: Psychological Corporation.
Bertschy, G., Haffen, E., Gervasoni, N., Gex-Farby, M., Osiek, C., Marra, M., … Bondolfi,
G. (2010). Self-rated residual symptoms do not predict 1-year recurrence of depression.
European Psychiatry, 25, 52–57.
Beshai, S., Dobson, K. S., Bockting, C. L. H., & Quigley, L. (2011). Relapse and recurrence
prevention in depression: Current research and future prospects. Clinical Psychology
Review, 31, 1349–1360.
Bieling, P. J., & Antony, M. M. (2003). Ending the depression cycle: A step-by-step guide for
preventing relapse. Oakland, CA: New Harbinger Publications.
Bockting, C. L. H., Schene, A. H., Spinhoven, P., Koeter, M., Wouters, L. F., Huyser, J.,
& Kamphuis, J. H. (2005). Preventing relapse/recurrence in recurrent depression with
cognitive therapy: A randomized controlled trial. Journal of Consulting and Clinical
Bockting , C. L. H., Spinhoven, P. H., Koeter, M. W. J., Wouters, L. F., Visser, I., Schene, A.
H., & the DELTA Study Group (2006). Differential predictors of response to preventive
cognitive therapy in recurrent depression: A 2-year prospective study. Psychotherapy and
Psychosomatics, 75, 229–236.
Bondolfi, G., Jermann, F., Van der Linden, M., Gex-Fabry, M., Bizzini, L., Weber Rouget, B.,
… Bertschy, G. (2010). Depression relapse prophylaxis with Mindfulness-Based Cognitive
Therapy: Replication and extension in the Swiss health care system. Journal of Affective
Disorders, 122, 224–231.
Burcusa, S. L., & Iacono, W. G. (2007). Risk for recurrence in depression. Clinical Psychology
Review, 27 , 959–985.
Clark, D., Beck, A. T., & Alford, B. A. (1999). Scientific foundations of cognitive theory and
therapy of depression. New York, NY: John Wiley & Sons, Inc.
Conradi, H. J., de Jonge, P., & Ormel, J. (2008). Prediction of the three-year course of
recurrent depression in primary care patients: Different risk factors for different outcomes.
Journal of Affective Disorders, 105, 267–271.
Costa, P. T., & McCrae, R. R. (1992). NEO PI-R. Professional manual. Odessa, FL:
Psychological Assessment Resources.
Dobson, K. S. (Ed.). (2010). Handbook of cognitive-behavioral therapies (3rd ed.). New York,
NY: Guilford Press.
Dobson, K. S., & Dozois, D. J. A. (Eds.). (2008). Risk factors in depression. San Diego, CA:
Academic Press.
Dobson, K. S., Hollon, S. D., Dimidjian, S., Schmaling, K. B., Kohlenberg, R. J., Gallop,
R. J., … Jacobson, N. S. (2008). Randomized trial of behavioral activation, cognitive
therapy, and antidepressant medication in the prevention of relapse and recurrence in
Dobson, K. S., & Ottenbreit, N. D. (2004). Tertiary intervention for depression and prevention
of relapse. In D. J. A. Dozois & K. S. Dobson (Eds.), The prevention of anxiety and
depression: Theory, research, and practice (pp. 233–256). Washington, DC: American
Dozois, D. J. A., Bieling, P. J., Patelis-Siotis, I., Hoar, L., Chudzik, S., McCabe, K., & Westra,
H. A. (2009). Changes in self-schema structure in cognitive therapy for major depressive
disorder: A randomized clinical trial. Journal of Consulting and Clinical Psychology, 77 ,
1078–1088.
Dozois, D. J. A., & Dobson, K. S. (2001). Information processing and cognitive organization
in unipolar depression: Specificity and comorbidity issues. Journal of Abnormal Psychology,
110, 236–246.
Dozois, D. J. A., & Dobson, K. S. (Eds.). (2004). The prevention of anxiety and depression:
Theory, research, and practice. Washington, DC: American Psychological Association.
Dozois, D. J. A., & Dobson, K. S. (2010). Depression. In M. M. Antony & D. H. Barlow
(Eds.), Handbook of assessment and treatment planning for psychological disorders (2nd ed.,
pp. 344–389). New York, NY: Guilford Press.
Duggan, C. F., Sham, P., Lee, A., Minne, C., & Murray, R. (1995). Neuroticism: A vulnerability
marker for depression evidence from a family study. Journal of Affective Disorders, 35,
139–143.
Fava, G. A., Fabbri, S., & Sonino, N. (2002). Residual symptoms in depression: An emerging
therapeutic target. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 26,
1019–1027.
Fava, G. A., Grandi, S., Zielezny, M., Canestrari, R., & Morphy, M. A. (1994). Cogni-
tive behavioral treatment of residual symptoms in primary major depressive disorder.
Fava, G. A., Grandi, S., Zielezny, M., Rafanelli, C., & Canestrari, R. (1996). Four-year outcome
for cognitive behavioral treatment of residual symptoms in major depression. American
Fava, G. A., Rafanelli, C., Grandi, S., Canestrari, R., & Morphy, M. A. (1998). Six-year
outcome for cognitive behavioral treatment of residual symptoms in major depression.
Frank, E., Prien, R. F., Jarrett, R. B., Keller, M. B., Kupfer, D. J., Lavori, P. W., …
Weissman, M. M. (1991). Conceptualization and rationale for consensus definitions of
terms in major depressive disorder: Remission, recovery, relapse, and recurrence. Archives
Gloaguen, V., Cottraux, J., Cucherat, M., & Blackburn, I. M. (1998). A meta-analysis of the
effects of cognitive-behavioral therapy in depressed patients. Journal of Affective Disorder,
49, 59–72.
Gotlib, I. H., & Joormann, J. (2010). Cognition and depression: Current status and future
directions. Annual Review of Clinical Psychology, 6, 285–312.
Guidi, G., Fava, G. A., Fava, M., & Papakostas, G. I. (2010). Efficacy of sequential integration
of psychotherapy and pharmacotherapy in major depressive disorder: A preliminary
meta-analysis. Psychological Medicine, 10, 1–11.
Hamilton, M. (1960). A rating scale for depression. Journal of Neurology, Neurosurgery and
Hammen, C. (1991). Generation of stress in the course of unipolar depression. Journal of

Hodgins, S., & Ellenbogen, M. (2003). Neuroticism and depression. British Journal of
Hollon, S. D. (2003). Does cognitive therapy have an enduring effect? Cognitive Therapy &
Research, 27 , 71–75.
Iacoviello, B. M., Alloy, L. B., Abramson, L. Y., Whitehouse, W. G., & Hogan, M. E. (2006).
The course of depression in individuals at high and low cognitive risk for depression: A
prospective study. Journal of Affective Disorders, 93, 61–69.
Ingram, R. E., Miranda, J., & Segal, Z. V. (1998). Cognitive vulnerability to depression. New
Institute of Medicine. (2009). Preventing mental, emotional, and behavioral disorders among
young people: Progress and possibilities. Washington, DC: National Academies Press.
Jarrett, R. B., Basco, M. R., Risser, R., Ramanan, J., Marwill, M., Kraft, D., & Rush, A. J.
(1998). Is there a role for continuation phase cognitive therapy of depressed outpatients?
Jarrett, R. B., Kraft, D., Doyle, J., Foster, B. M., Eaves, G. G., & Silver, P. C. (2001).
Preventing recurrent depression using cognitive therapy with and without a continuation
phase: A randomized clinical trial. Archives of General Psychiatry, 58, 381–388.
Joiner, T. E., Jr., (2000). Depression’s vicious scree: Self-propagatory and erosive factors in
depression chronicity. Clinical Psychology: Science & Practice, 7 , 203–218.
Judd, L. L., Akiskal, H. S., Schettler, P. J., Endicott, J., Maser, J., Solomon, D. A., … Keller,
M. B. (2002). The long-term natural history of the weekly symptomatic status of bipolar
I disorder. Archives of General Psychiatry, 59, 530–537.
Kendler, K. S., Karkowski, L. M., & Prescott, C. A. (1999). Causal relationship between
stressful life events and the onset of major depression. American Journal of Psychiatry,
156, 837–841.
Kendler, K. S., Thornton, L. M., & Gardner, C. O. (2000). Stressful life events and previous
episodes in the etiology of major depression in women: An evaluation of the “kindling”
hypothesis. American Journal of Psychiatry, 157 , 1243–1251.
Kessler, R. C., Berglund, P., Demler, O., Jin, R., Merikangas, K. R., & Walters, E. E. (2005).
Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National
Comorbidity Survey Replication. Archives of General Psychiatry, 62, 593–602.
Kessler, R. C., & Magee, W. J. (1994). Childhood family violence and adult recurrent
depression. Journal of Health and Social Behavior, 35, 13–27.
Klein, D. N., Santiago, N. J., Vivian, D., Arnow, B. A., Blalock, J. A., Dunner, D. L., … Keller,
M. B. (2004). Cognitive-behavioral analysis system of psychotherapy as a maintenance
treatment for chronic depression. Journal of Consulting and Clinical Psychology, 72,
681–688.
Kraaij, V., & De Wilde, E. J. (2001). Negative life events and depressive symptoms in the
elderly: A lifespan perspective. Aging Mental Health, 5, 84–91.
Kühner, C., Angermeyer, M. C., & Veiel, H. O. F. (1996). Cognitive-behavioral group
intervention as a means of tertiary prevention in depressed patients: Acceptance and
short-term efficacy. Cognitive Therapy and Research, 20, 391–409.
Kuyken, W., & Brewin, C. R. (1994). Intrusive memories of childhood abuse during depressive
episodes. Behaviour Research and Therapy, 32, 525–528.
Press.
Lewinsohn, P. M., Rohde, P., Seeley, J. R., Klein, D. N., & Gotlib, I. H. (2000). Natural
course of adolescent major depressive disorder in a community sample: Predictors of
recurrence in young adults. American Journal of Psychiatry, 157 , 1584–1591.
McCullough, J. P. (2000). Treatment for chronic depression: Cognitive behavioral analysis system
of psychotherapy (CBASP). New York, NY: Guilford Press.
Monroe, S. M., & Harkness, K. L. (2005). Life stress, the “kindling” hypothesis, and
the recurrence of depression: Considerations from a life stress perspective. Psychological
Review, 112, 417–45.
Monroe, S. M., & Harkness, K. L. (2011). Recurrence in major depression: A conceptual
analysis. Psychological Review, 118, 655–674.
Monroe, S. M., Slavich, G. M., Torres, L. D., & Gotlib, I. H. (2007). Major life events
and major chronic difficulties are differentially associated with history of major depressive
episodes. Journal of Abnormal Psychology, 116, 116–124.
Muñoz, R. F., Cuijpers, P., Smit, F., Barrera, A., & Leykin, Y. (2010). Prevention of major
depression. Annual Review of Clinical Psychology, 6, 181–212.
Murray, C. J. L., & Lopez, A. D. (1997). Global mortality, disability, and the contribution of
risk factors: Global Burden of Disease Study. Lancet, 349, 1436–1442.
Paykel, E. S., & Cooper, Z. (1992). Life events and social stress. In E. S. Paykel (Ed.),
Handbook of affective disorders (2nd ed., pp. 149–170). New York, NY: Guilford Press.
Paykel, E. S., Scott, J., Cornwall, P. L., Abbott, R., Crane, C., Pope, M., & Johnson, A.
L. (2004). Duration of relapse prevention after cognitive therapy in residual depression:
Follow-up of controlled trial. Psychological Medicine, 35, 59–68.
Paykel, E. S., Scott, J., Teasdale, J. D., Johnson, A. L., Garland, A., Moore, R., … Pope, M.
(1999). Prevention of relapse in residual depression by cognitive therapy: A controlled
trial. Archives of General Psychiatry, 56, 829–835.
Perris, C. (1992). Bipolar-unipolar distinction. In E. S. Paykel (Ed.), Handbook of affective
disorders (2nd ed., pp. 57–75). New York, NY: Guilford Press.
Persons, J. B., & Davidson, J. (2001). Cognitive-behavioral case-formulation. In K. S. Dobson
(Ed.), Handbook of cognitive-behavioral therapies (3rd ed., pp. 86–110). New York, NY:
Guilford Press.
Petersen, T. J., Pava, J. A., Buchin, J., Matthews, J. D., Papakostas, G. I., Nierenberg, A. A.,
… Fava, M. (2010). The role of cognitive-behavioral therapy and fluoxetine in prevention
of recurrence of major depressive disorder. Cognitive Therapy and Research, 34, 13–23.
Peterson, C., Semmel, A., von Baeyer, C., Abramson, L. Y., Metalsky, G. I., & Seligman, M.
E. P. (1982). The Attributional Style Questionnaire. Cognitive Therapy and Research, 6,
287–299.
Post, R. M., & Weiss, S. R. B. (1995). The neurobiology of treatment-resistant mood disorders.
In F. E. Bloom & D. J. Kupfer (Eds.), Psychopharmacology: The fourth generation of progress
(pp. 1155–1170). New York, NY: Raven Press.
Rowa, K., Bieling, P. J., & Segal, Z. V. (2005). Depression. In M. M. Antony, D. Roth
Ledley, & R. G. Heimberg (Eds.), Improving outcomes and preventing relapse in cognitive-
behavioral therapy (pp. 204–245). New York, NY: Guilford Press.
Schreurs, P. J. G., van de Willige, G., Brosschat, J. F., Tellegen, B., & Graus, G. M. H. (1988).
The Utrecht Coping List: UCL. Lisse, The Netherlands: Swets & Zeitlinger.
for depression: A new approach to preventing relapse. New York, NY: Guilford Press.
Stice, E., Ragan, J., & Randall, P. (2004). Prospective relations between social support
and depression: Differential direction of effects for parent and peer support? Journal of
Taylor, D. J., Walters, H. M., Vittengl, J. R., Krebaum, S., & Jarrett, R. B. (2010). Which
depressive symptoms remain after response to cognitive therapy of depression and predict
relapse and recurrence? Journal of Affective Disorders, 123, 181–187.
Teasdale, J. D. (1988). Cognitive vulnerability to persistent depression. Cognition & Emotion,
2, 247–274.
Teasdale, J. D., Segal, Z. V., Williams, J. M. G., Ridgeway, V. A., Soulsby, J. M., & Lau, M.
A. (2000). Prevention of relapse/recurrence in major depression by mindfulness-based
cognitive therapy. Journal of Consulting and Clinical Psychology, 68, 615–623.
Vittengl, J. R., Clark, L. A., Dunn, T. W., & Jarrett, R. B. (2007). Reducing relapse and
recurrence in unipolar depression: A comparative meta-analysis of cognitive-behavioral
therapy’s effects. Journal of Consulting and Clinical Psychology, 75, 475–488.
Weissman, A. N., & Beck, A. T. (1978, November). Development and validation of the
Dysfunctional Attitude Scale: A preliminary investigation. Paper presented at the meeting
of the Association for the Advancement of Behavior Therapy, Chicago, IL.
Young, J. E., & Brown, G. (1994). Young Schema-Questionnaire (2nd ed.). In J. E. Young
(Ed.), Cognitive therapy for personality disorders: A schema-focused approach (rev. ed., pp.
63–76). Sarasota, FL: Professional Resource Press.
18
Cultural Context
Devon E. Hinton
Massachusetts General Hospital, Harvard Medical School, and Arbour
Counseling Services, Lowell, United States
Martin La Roche
Children’s Hospital/Martha Eliot Health Center and Harvard Medical School,
United States
Introduction
There have been some attempts to develop treatments for refugee and ethnic
minority populations for depression disorders (for reviews, see Horrel, 2008;
Miranda et al., 2005) and for the anxiety disorders (Cardemil, 2008; Hinton, Pich,
Hofmann, & Otto, in press; Hinton, Rivera, Hofmann, Barlow, & Otto, 2012).
In this chapter we will illustrate how cognitive behavioral therapy (CBT) can be
adapted to treat ethnic minorities, particularly refugees, with anxiety and depres-
sive disorders. One of the central assumptions of culturally appropriate treatments
is that it is necessary to match the cultural characteristics of the treatment with
those of the patients (Bernal, Jiménez-Chafey, & Domenech Rodr ı́guez, 2009; La
Roche, 2013; D. Sue, Ivey, & Pedersen, 2008). We will first present a model
that describes the influences of culture on the generation of anxiety and depressive
disorders and, based on this model, describe various ways to make the treatment
culturally appropriate, giving examples from a treatment focused on posttraumatic
stress disorder (PTSD). The approach to developing culturally sensitive treatment
and most of the principles can be applied to other disorders, such as schizophrenia.
For example, in the case of schizophrenia, a model of the generation of disor-
der would include expressed emotion (Aguilera, Lopez, Breitborde, Kopelowicz, &
Zarate, 2010; Kopelowicz et al., 2006; Lopez et al., 2009), cultural differences on
that variable, and how that variable can be changed in a culturally sensitive way,
whereas for anxiety and depressive disorders, the construct of anxiety sensitivity will
loom large in the model of the generation of psychopathology and treatment, as we
will see.

DOI: 10.1002/9781118528563.wbcbt18
A Cultural Model of the Generation of Anxiety and

Depressive Disorders
In order to know how to intervene in a culturally sensitive way with anxiety and
depressive disorders, it is first necessary to develop an understanding of how anxiety
and depressive disorders are generated in different cultural populations. Culture pow-
erfully influences the ways in which anxiety and depression are generated, experienced,
and treated (Hinton & Good, 2009; Kleinman & Good, 1985). In Figure 18.1 we
present a general model of how episodes of anxiety and depressive disorders are
generated, all of which are culturally influenced processes.
Catastrophic Cognitions and Cultural Syndromes

Catastrophic cognitions constitute a key producer of anxiety and depressive disor-
ders (Figure 18.1). Catastrophic cognitions about anxiety- and depression-related
somatic and psychological symptoms worsen those disorders by generating arousal
and negative affect (D. M. Clark, 1986; Hedley, Hoffart, Dammen, Ekeberg, & Friis,
2000). To give some examples, catastrophic cognitions about PTSD-related symp-
toms worsen PTSD and lead to chronicity (D. M. Clark & Ehlers, 2004; Dunmore,
Clark, & Ehlers, 2001; Halligan, Michael, Clark, & Ehlers, 2003). Catastrophic
cognitions about the bodily and mental consequences of worry, and about the danger
posed by worry-induced somatic and psychological symptoms, may worsen—even
produce—generalized anxiety disorder, and may cause worry episodes to escalate
to panic (Wells, 2000, p. 160). Likewise, catastrophic cognitions about depressive
symptoms—such as concern that poor concentration indicates some permanent dam-
age to the brain, or that low energy is indicative of a permanently damaged physical
state—worsen the condition. More generally, catastrophic cognitions increase anxiety
sensitivity, which is known to be an important risk factor for and exacerbator of anxiety
and depressive disorders (Hinton, Pich, Safren, Pollack, & McNally, 2005, 2006).
How do these catastrophic cognitions arise? In many cases, these symptoms are
considered to indicate dangerous problems with the physiology of the body or the
functioning of the mind. In many cases, anxiety and depressive symptoms will be
attributed to cultural syndromes that then give rise to catastrophic cognitions. For
example, if a Cambodian considers anxiety symptoms such as dizziness to be the start
of a khyâl attack (in which khyâl and blood are thought to rush upward in the body
to cause various bodily disasters), or a Puerto Rican considers shakiness to be the start
of an ataque de nervios (in which disordered “nerves” are thought to result in loss of
control, asphyxia, and other disasters), multiple catastrophic cognitions may result.
How a patient evaluates and reacts to an anxiety- or depressive-type sensation
(e.g., blushing in a social situation, palpitations upon climbing stairs, a feeling of
profound lethargy) or cognitions (e.g., racing thoughts or poor concentration) will
depend on that individual’s understanding of what those sensations and cognitions
indicate, such as their attribution to disturbances of physiology and to locally specific
cultural syndromes (Hinton & Good, 2009; Kleinman & Good, 1985; Moss-Morris
& Wrapson, 2003). For example, if a Japanese patient interprets blushing as indicating
Cultural Context 401
Negative affect Cultural specific ways of

maintaining positive affect
Trigger of an episode of anxiety- or depressive-type distress

(e.g., thinking of a worry topic, depressive rumination, confronting a
feared social situation, thinking of a trauma, hearing a loud noise)
Somatic or psychological symptom
Catastrophic cognitions about

the symptom
Arousal- and attentional-caused (e.g., that it indicates the
increase of symptoms presence of a feared
syndrome)
Surveying the mind, body, and

environment for further evidence that
what is feared is occurring or will occur
Stresses and a sense of Cultural-specific ways of

insecurity handling stress
Stigma
(e.g., that it is an incurable condition, that medication and therapy will make you crazy)
Figure 18.1 A culturally sensitive model of how anxiety and depressive disorders occur in a
certain cultural context: Psychopathological mechanisms.
taijin kyofusho, or if a Chinese individual considers palpitations to indicate a “weak

heart” (xin xu), these attributions will cause the patient to imagine a specific
physiology generating those symptoms, to expect certain symptoms, to anticipate a
certain degree of danger, to imagine a certain illness course and prognosis, and to
seek out specific types of treatment. In addition, once a symptom is attributed to a
particular cultural syndrome, fears of having the cultural syndrome will increase that
symptom—and other syndrome-related symptoms—by increased arousal and/or by

attentional narrowing on the sensation (Figure 18.1). For example, a patient may
focus on depressive symptoms such as low energy or poor sleep and think these are
signs of permanent deterioration, and those ruminations will worsen the symptom.
Cultural syndromes vary across cultural groups and across time. Table 18.1 shows
some typical Asian syndromes and their overlap with the anxiety disorders (for
a discussion of these syndromes, see Hinton, Park, Hsia, Hofmann, & Pollack,
2009). A cultural syndrome may be diagnosable as multiple DSM-IV disorders, or
it may correspond highly to one DSM-IV diagnosis. Researchers often use the term
“functional somatic syndromes” to describe cultural syndromes; they might also be
called distress syndromes (Barsky & Borus, 1999; Kirmayer & Robbins, 1991). Such
functional somatic syndromes as fibromyalgia, chronic fatigue syndrome, multiple
chemical sensitivity, and Gulf War syndrome may be diagnosable as any one of a
number of DSM-IV diagnoses. These disorders may result from syndrome-related
fears and expectations interacting with the biology of anxiety: If a person considers
joint pain to be a key pathognomonic sign of a disorder (e.g., fibromyalgia), and fears
that the disorder is dangerous, the person will be hypervigilant to those sensations;
and if that person notes joint discomfort, the resulting fear will worsen joint pain by
increasing muscular tension and attentional amplification.
Degree of Stress and Insecurity

The context in which ethnic minorities and refugees live has a significant influence on
the levels of stress and insecurity they experience (Figure 18.1). Many ethnic minority
groups live in urban contexts in which there is great danger and stress, such as poverty,
poor housing, constant ambient noise, and violence; this will very likely increase their
level of stress and sense of insecurity that in turn can increase the severity of disorder
(Hinton & Nickerson, 2012; La Roche, 2013). Stress and insecurity worsen all
aspects of psychopathology, such as creating a state of arousability so that there is a
rapid induction of distress in various situations that include when the person engages
in dysphoric cognizing (e.g., worry, rumination, or hopelessness), confronts feared
bodily sensations (e.g., palpitations), confronts feared memories (e.g., trauma events),
or confronts feared situations (e.g., speaking in front of a group) (Hinton, Nickerson,
& Bryant, 2011).
Negative Affect
A dysphoric state is a processing mode that leads to withdrawal, rapid activation of
negative memory networks, scanning for danger cues, and a tendency toward negative
self-evaluation (Figure 18.1) (L. A. Clark & Watson, 1991; Ehrenreich, Fairholme,
Buzzella, Ellard, & Barlow, 2007).
Stigma and Negative Views of Treatment Effects

In a culture, there will be a certain attitude about a psychological condition. Because
of stigma concerns, patients may resist being “labeled” with a psychological disorder
Table 18.1 Anxiety-Related Distress Syndromes in Asia: Associated Catastrophic Cognitions, DSM-IV Diagnosis, and Panic Attack Subtype
Country Anxiety-related Usual DSM-IV Syndrome-generated Related panic-attack

syndrome anxiety diagnosis catastrophic cognitions subtype
East Asia
China Neurasthenia GAD, PD Dangerous weakening Worry-induced
“Weak heart” GAD, PD Heart arrest Heart-focused
“Weak kidney” GAD, PD Brain depletion Semen-loss-induced (e.g., in urine)
Japan Neurasthenia GAD, PD Dangerous weakening Worry-induced
Orthostatic dysregulation PD, SP (social phobia) Weakened nervous system, fainting Orthostasis-induced,
social-context-induced
Taijin kyofusho SP Offending others Social-context-induced
Korea Hwa byung GAD, PD Asphyxia, cardiac arrest Anger-induced
South Asia
India Semen loss GAD, PD Death from depletion Semen-loss-induced (e.g., in urine)
Southeast Asia
Cambodia “Weakness” GAD, PD, PTSD Dangerous weakening Worry-induced
“Weak heart” GAD, PD, PTSD Heart arrest Heart-focused
“Wind attack” GAD, PD, PTSD Syncope, vomiting Dizziness-focused
“Limb blockage” GAD, PD, PTSD Limb death, upward surge of wind Limb-focused
“Sore neck” GAD, PD, PTSD Neck-vessel rupture Neck-focused
“Abdominal wind” GAD, PD, PTSD Heart arrest, asphyxia Abdomen-focused
“Wind overload” GAD, PD, PTSD Syncope Orthostasis-induced
Country Anxiety-related Usual DSM-IV Syndrome-generated Related panic-attack

syndrome anxiety diagnosis catastrophic cognitions subtype
Northeastern “Weak heart” GAD, PD, PTSD Heart arrest Heart-focused

Thailand “Abdominal wind” GAD, PD, PTSD Heart arrest, asphyxia Abdomen-focused
Vietnam “Weakness” GAD, PD, PTSD Dangerous weakening Worry-induced
“Weak heart” GAD, PD, PTSD Heart arrest Heart-focused
“Weak kidney” GAD, PD, PTSD Brain depletion Semen-loss-induced (e.g., in urine)
“Orthostatic dizziness” GAD, PD, PTSD Syncope Orthostasis-induced
“Nerve fiber ripping” GAD, PD, PTSD Loss of mental power Headache-focused
“Hit by the wind” GAD, PD, PTSD Total bodily collapse Exterior-wind-induced
Notes. GAD = generalized anxiety disorder; PD = panic disorder; PTSD = posttraumatic stress disorder; SP = social phobia.
and also resist treatment (Figure 18.1). Patients may be afraid that they themselves
and their family may be labeled as being “insane” (each culture will have different
stigmatizing labels, such as “loco,” that is, “crazy” in Spanish) if they are receiving
treatment for the condition in question. They may fear that medication and psycho-
logical treatments may worsen their conditions. Stigma and fear of treatment at times
is created by cultural misunderstandings. For example, stigma and fear of treatment
is very pronounced in some African American communities because historically their
differences have often been construed as deficits; they have more frequently been
misdiagnosed with severe mental health disorders (e.g., schizophrenia) than any other
group and as a result they have had higher hospitalization rates that have led many to
fear mental health treatments (Snowden, 2012; Snowden & Cheung, 1993). Negative
views of treatment may include medication and lead to nonadherence.
Local Therapeutic Response to Distress

Every culture has various ways of decreasing distress and these will impact on whether
distress reaches the point of psychopathology and impacts on the pathological
processes outlined in Figure 18.1. Here we detail some of these local processes that
promote recovery.
Every culture has certain ways of promoting a positive emotional state, which range
from emotion regulation techniques (e.g., meditation) to more general activities such
as listening to certain kinds of music, eating certain types of foods in certain settings,
and watching certain television shows (e.g., telenovelas in Latino contexts).
Every culture has certain techniques for handling distress and anxiety and,
depending on how the disorder is interpreted (the cultural syndrome to which
it is attributed), the disorder will give rise to certain types of attempts at self-
cure, what might be called the local response to anxiety and its symptoms. For
example, in Buddhist societies, there will be meditation traditions, such as mind-
fulness and loving-kindness, that are useful in decreasing rumination and negative
affect (Hinton, Pich, Hofmann, et al., in press). In Japan, there is Morita ther-
apy, a Buddhist-influenced therapy that decreases distress in a variety of ways, such
as teaching the importance of attentional control and escalating panic in generat-
ing disorders (Maeda & Nathan, 1999). Cambodians use traditional healing with
“coining” (in which a camphor-menthol-dipped coin is rubbed along a limb) along
with yoga-like stretching to relieve muscle tension and symptoms of anxiety and
panic (Hinton, Pich, Marques, Nickerson, & Pollack, 2010). These emotion regu-
lation traditions vary across cultural contexts and have variable effects on decreasing
distress.
Key Components of the Culturally Sensitive Treatment of

Refugees and Ethnic Minorities
Now that we have outlined a model of some of the cultural factors that are involved
in generating anxiety and depressive disorders, we now turn to further discussion
of how CBT can be culturally adapted. The model of CBT intervention is given in
Cultural-specific and CBT ways of

Negative affect maintaining positive affect (e.g.,
prescribing pleasurable activity)
Trigger of an episode of anxiety- or depressive-type distress

(e.g., thinking of a worry topic, depressive rumination, confronting
a feared social situation, thinking of a trauma, hearing a loud noise)
Somatic or psychological symptom
• Education about the disorder

(e.g., PTSD) •
• Address catastrophic cognitions
(e.g., address cultural specific
cognitions and syndromes) •
• Teach about the role of
attentional focus and rumination
in generating the disorder •
• Teach arousal reduction Catastrophic cognitions
techniques • about the symptom
Arousal- and attentional-caused (e.g., that it indicates the
increase of symptoms • Teach ER techniques • presence of a feared
• Teach attentional management • syndrome)
• Exposure, including interoceptive
exposure to symptoms with
positive reassociations •
• Create positive expectancy about
the treatment •
• Build therapeutic rapport •
• Increase self-esteem •
Surveying the mind, body, and

environment for further evidence that
what is feared is occurring or will occur
Stresses and a sense of Cultural-specific and CBT-

insecurity based ways of handling stress
Stigma and negative ideas about treatment

(e.g., that it is an incurable condition, that medication and therapy will make you crazy)
Figure 18.2 A culturally sensitive model of how CBT can reduce the severity of anxiety and
depressive disorders.
Figure 18.2. We will mostly give examples of cultural adaptation used in our treatment
for anxiety disorders, culturally adapted CBT (CA-CBT) for PTSD, which we also
refer to as flexibility-focused CA-CBT, given its emphasis on promoting flexibility
(see Table 18.2 for an overview of the treatment). CA-CBT has been shown to
be effective in randomized controlled trials for traumatized Latino patients and for
Table 18.2 Sessions in CA-CBT and Key Components of the Sessions
Session Session title Emotional exposure followed by Applied stretching Mindfulness lesson
number practice of the indicated protocol lesson at session’s end at session’s end
1 Education about Trauma-Related Disorder Anxiety X X

2 Muscle Relaxation and Stretching with Anxiety X X
Visualization
3 Applied Stretching with Visualization Anxiety X X
Protocol
4 Flashback Protocol Anxiety X X
5 Education about Trauma-Related Disorder Anxiety and trauma X X
and Modifying Catastrophic Cognitions
6 Interoceptive Exposure I: Head Rotation Anxiety and trauma X X
7 Interoceptive Exposure II: Hyperventilation Anxiety and trauma X X
8 Education about Breathing and Its Use for Anxiety and trauma X X
Relaxation
9 Sleep Disturbance Anxiety and trauma X X
10 Generalized Anxiety Disorder Anxiety and trauma X X
11 Anger Anxiety and anger X X
12 Neck-, Shoulder-, and Headache-Focused Anxiety and anger X X
Dysphoria and Panic
13 Other Somatic Symptoms and Associated Anxiety and anger X X
Panic
14 Cultural Syndromes and Ethnophysiology Anxiety and anger X X
Related to Anxiety: Closing
Note. The stretching modules differ by muscle group that is targeted. The mindfulness modules differ as well, with most teaching different types of multisensorial
awareness; some involve performing loving-kindness. The applied stretching is practiced just before the mindfulness lesson
Southeast Asian refugee patients from Cambodia and Vietnam (Hinton, Chhean,
et al., 2005; Hinton, Hofmann, Rivera, Otto, & Pollack, 2011; Hinton et al., 2004).
We have recently adapted the treatment for both anxiety and depressive disorders
more generally. The treatment focuses on emotional flexibility, a paradigm equally
applicable to the anxiety and depressive disorders.
CA-CBT emphasizes emotion exposure and emotion regulation techniques such as
meditation and yoga-like stretching, and aims to promote emotional and psychologi-
cal flexibility (on an emotion-centered approach, see also Barlow’s Unified Protocol;
Ellard, Fairholme, Boisseau, Farchione, & Barlow, 2010). CA-CBT aims to provide
the patient with a range of new adaptive processing modes—such as mindfulness,
which involves attending to the present-moment sensorial experiencing of environ-
mental events—that differ from the usual mode of attending to threat. Below we
describe the ways in which CBT for anxiety disorders can be made more effective
and culturally appropriate for refugee and ethnic minority groups (for a summary, see
Table 18.3).
Creating Positive Expectancy and Treatment Credibility in a Culturally

Appropriate Way
Positive expectancy results when patients believe that the treatment will improve
the problems that are of most concern to them. It has two aspects: Patients
feel that the treatment addresses the problems of concern to them and they feel
that the treatment is capable of reducing those problems (this second aspect is
credibility).
To create positive expectancy, the clinician needs to know what patients think
their problem is (Lewis-Fernández & Diaz, 2002; Sue & Sue, 2008). For example,
Japanese individuals with social phobia may consider taijin kyofusho—with symptoms
such as fearing one’s odor is offending others being of greatest concern—rather than
“social phobia” as their key concern, or a Cambodian may see “weak heart,” dizziness,
sleep paralysis, and nightmares as the key problems rather than “PTSD,” a concept
with which they have little familiarity. If one tells the patient that the treatment will
address the problems of concern to him or her, positive expectancy will be greatly
increased.
To create positive expectancy, the clinician has to create credibility, the sense that
the treatment will actually address the problems: In the case of a Japanese patient
fearing taijin kyofusho, the clinician might give the explanation that seeking odors
constantly will lead to their perception, and that the fear of emitting an offending
odor leads to worsened social interaction by taking up all attentional resources and
by inducing multiple negative somatic and psychological symptoms; or in the case
of a Cambodian having generalized anxiety disorder and frequent khyâl attacks, the
clinician might explain that rumination on a problem increases arousal, which in turn
causes somatic symptoms, poor sleep, and dizziness (all typical symptoms of a khyâl
attack), and that muscle relaxation and stretching can decrease arousal and its somatic
aspects—in this way the patient will believe the treatment will address a key concern,
khyâl attacks.
Table 18.3 Ways to Make Cognitive Behavioral Therapy-Type Treatment of Anxiety Disorders for Various Cultural Groups More Efficacious and
Culturally Appropriate
Treatment intervention Examples of how the treatment intervention goal is accomplished
Create positive expectancy and treatment The clinician should frame the treatment as addressing issues of concern to the patient, which
credibility may include culturally emphasized symptoms (e.g., dizziness, poor sleep, shortness of breath)
and culturally specific syndromes (e.g., taijin kyofusho among social phobia patients in Japan or
khyâl attacks among panic disorder patients who are Cambodian).
Address catastrophic cognitions about anxiety Catastrophic cognitions about anxiety symptoms drive psychopathology. In different cultures the
symptoms specific catastrophic cognitions about anxiety symptoms must be addressed such as those about
arousal symptoms (e.g., Cambodians consider dizziness to indicate a dangerous khyâl attack
that may cause syncope and other disasters) and about PTSD symptoms (e.g., Cambodians
consider startle to indicate a “weak heart” and imminent cardiac arrest).
Address cultural syndromes Patients often consider anxiety symptoms to indicate a cultural syndrome. The clinician must
explain how the anxiety disorder relates to those syndromes (e.g., how the symptoms are part
of an anxiety disorder rather than a cultural syndrome) and alleviate the patient’s concerns
about the cultural syndrome.
Target somatic symptoms In many cultural contexts, somatic complaints are prominent (e.g., dizziness among Cambodian
refugees) and these must be specifically addressed in treatment, taking into account
catastrophic cognitions, metaphor meaning, and trauma associations.
Address sleep-related phenomenon In certain groups, sleep-related phenomena are quite prominent and have extensive meanings.
For example, sleep paralysis is extremely elevated in African American and Cambodian patients,
and Cambodian refugees give these events elaborate explanation. So too the culturally specific
interpretations of nightmares should be addressed.
Use culturally specific proverbs, local stories, CBT techniques should be presented in a culturally sensitive way, such as using proverbs and
and culturally appropriate analogies to expressions from the culture that express the information in question. For example, to teach a
convey CBT information and to create Latino patients the effect of attentional focus on mood, and the dangers of rumination, the
positive expectancy phrase “Don’t drown in a glass of water” (No se ahogue en un vaso de agua) can be used.
Treatment intervention Examples of how the treatment intervention goal is accomplished
Present CBT information and techniques in terms of Each culture will have certain ideas about how psychological disorder occurs. This may
the local psychology and physiology be rooted in local religious traditions such as Islam, Christianity, or Buddhism. The
clinician should try to frame CBT information in terms of those local psychologies
and related physiologies. For example, in Buddhism coldness is considered to be the
ideal state, suggesting a centered mind unperturbed by worry, and so the CBT
treatments can be presented as “cooling” and helping to center the mind.
Include techniques from the local religious and Each culture will have certain methods to relieve distress. If possible, techniques from
spiritual tradition local religious traditions should be incorporated in the treatment (or at least the CBT
techniques should be framed in terms of local religious traditions). Examples would
be to include yoga among Indian populations, meditation among Buddhists, or the
practice of repeatedly saying the name of Allah (dhikr) in Islamic groups.
Promote a sense of self-esteem and self-efficacy in a Low self-esteem and self-efficacy drives psychopathology. It is important to create
culturally appropriate way positive self-images that promote a positive sense of self and a sense of self-efficacy.
For example, in CA-CBT the image of the flexile wind-moved lotus is used as a
positive self-image that promotes a sense of being able to adjust.
Address stress and security issues Living in a state of stress and insecurity will have a major impact on psychopathology,
such as increasing arousal and arousability. Every group will have particular sources of
stress and insecurity and higher rates of certain types, for example, domestic abuse.
Knowledge of these issues and teaching how to practically handle these issues is
important. Emotion regulation techniques also need to be taught.
Worry and GAD as important treatment targets Uncontrollable worry drives multiple types of psychopathology, including somatic
symptoms, generalized anxiety disorder, and panic. Patients from other cultural
groups may have specific worry domains and great severity of worry, and they may
have great catastrophic cognitions about worry and its symptoms, which must be
addressed, or great arousal and psychopathology will result.
Conduct exposure in a culturally acceptable way Patients from other cultural contexts may tolerate poorly traditional exposure for several
reasons, including high current stress. A phase approach is suggested and the use of
novel techniques to make exposure more acceptable such as immediately practicing
emotion regulation techniques after exposure. This is done in CA-CBT.
Emotion exposure paired with practice of emotion Given that emotion regulation deficits are a key treatment in the emotion disorders, it
regulation makes sense to use exposure as an opportunity to practice emotion regulation
techniques. This makes exposure much more acceptable. This is done in CA-CBT.
Use emotion regulation techniques from the As indicated above, often a group will have healing traditions rooted in religious traditions.
patient’s religious and cultural healing tradition These can be incorporated into treatment as emotion regulation techniques. Examples
include the following: among Buddhists, practicing meditation or loving-kindness, or
among Christians, opening the Bible at random to read a passage or praying the Rosary.
Cultural adaptation of key CBT techniques CBT techniques should be adapted as far a possible to the group in question. For example,
when doing positive reassociation during interoceptive exposure, we introduce culturally
appropriate imagery: when inducing dizziness in head rolling we have Latino patients
think of the piñata game, a traditional game in which dizziness is induced.
Increase cognitive and emotion flexibility in a Psychological flexibility is a key aspect of psychological health and it is particularly
culturally appropriate way important for refugees and minorities who need to negotiate between multiple cultural
domains. Ideally, culturally appropriate analogies and self-imagery should be taught to
promote this skill.
Reduce stigma To reduce self-caused stigma, it is important to explain to patients that psychological
disorders are treatable and to address local ideas about mental illness.
Culturally indicated transitional rituals At the end of treatment, culturally appropriate transition may be utilized. This creates a
sense of positive expectancy about recovery. Also, these rituals through use of local
religious and psychological ideas often present a self-image and world image that create a
sense of having recovered, producing more positive self-schemas and world schemas.
Addressing Catastrophic Cognitions about Anxiety and Posttraumatic

Stress Disorder Symptoms
See Figure 18.1 for an illustration of the role of these catastrophic cognitions in
worsening anxiety disorders. In CA-CBT we ask patients about their understanding
of what produces their anxiety symptoms, including their conceptualization of the
physiology that produces those symptoms, and we ask about their fears about the
danger posed by those symptoms. Cambodian patients often fear that dizziness
indicates the start of a khyâl attack (Hinton et al., 2010), and Latino patients
that shakiness of the limbs or racing thoughts indicate a problem with nervios
or an imminent ataque de nervios (Hinton & Lewis-Fernández, 2010; Hinton,
Lewis-Fernández, & Pollack, 2009).
Let us take the example of PTSD. Every PTSD symptom—from nightmares to
startle—may give rise to such catastrophic cognitions. Many cultural groups fear
that trauma recall indicates imminent insanity (e.g., Cambodian refugees; Hinton,
Rasmussen, Nou, Pollack, & Good, 2009), and many groups fear that trauma recall
results from persecution by dangerous spirits of the dead (e.g., Cambodian refugees
and Rwandan trauma survivors; Hagengimana & Hinton, 2009; Hinton, Hinton,
et al., 2009). Some groups consider startle to have the power to dislodge the soul
and to cause death or serious illness (e.g., Latino and Southeast Asian populations;
for a review, see Hinton & Lewis-Fernández, 2010), and some groups that startle
indicates a dangerous “weakness” of the heart that brings about a general cardiac
hyperreactivity that may lead to death (e.g., Cambodian and Vietnamese refugees;
for a review, see Hinton & Lewis-Fernández, 2010). (In the CA-CBT manual,
catastrophic cognitions about anxiety and PTSD symptoms for certain groups are
specified, namely, for several Asian groups [Cambodian, Chinese, and Vietnamese]
and for Latino populations.)
Addressing Cultural Syndromes

We devote one session in our treatment to evaluating and treating anxiety- and PTSD-
related cultural syndromes. Patients often attribute PTSD and anxiety symptoms to
a cultural syndrome, and this attribution produces catastrophic cognitions that
the symptoms indicate a serious bodily dysfunction or imminent insanity. These
catastrophic cognitions start an escalating spiral of arousal, panic, somatic symptoms,
and PTSD (see Figure 18.1).
Assessing cultural syndromes gives the clinician a better sense of the patient’s
experiencing of anxiety and PTSD and the effects of anxiety and PTSD on his or
her life-world and relationships. This also allows the clinician to assess and modify
key catastrophic cognitions. It also increases treatment adherence because some of
the patient’s key concerns are being addressed (on the clinical utility of assessing and
treating cultural syndromes, see Hinton & Lewis-Fernández, 2010).
As some examples, in our treatment of Cambodian speakers we specifically ask
whether the patient fears having “weak heart” or “khyâl attacks,” how they treat
episodes of those cultural syndromes, and what fears they have about them (for a
review of these syndromes, see Hinton & Lewis-Fernández, 2010). CA-CBT has
attempted to develop culturally sensitive measures to examine cultural syndromes.

The Cambodian Somatic Symptom and Syndrome Inventory (SSI; Hinton, Kredlow,
Bui, Pollack, & Hofmann, 2012; Hinton, Pich, Kredlow, Bui, & Hofmann, in press)
is one such measure. The SSI aims not only to assess key symptoms measured in the
DSM-IV but also specific Cambodian cultural syndromes. As these cultural syndromes
are assessed they can be addressed in CA-CBT. Likewise, in our treatment of Latino
speakers, we specially address concerns about nervios and ataque de nervios through
these same questions.
Targeting Somatic Symptoms

Studies show that somatic complaints are particularly prominent among many non-
English speakers (Hinton & Lewis-Fernández, 2011; Hinton & Otto, 2006).
Figure 18.1 illustrates how such symptoms are produced, and Figure 18.2 how
they are addressed through CBT.
Addressing Sleep-Related Phenomena

In CA-CBT one session specifically addresses several sleep-related phenomena, namely,
nightmares, sleep paralysis, and nocturnal panic. Sleep paralysis occurs upon falling
asleep or awakening. The person suddenly can neither move nor speak even though
awake, and often sees a black shadow approaching the body. In nocturnal panic, the
person awakens in a panic but is able to move (ruling out sleep paralysis) and the
person cannot recall a nightmare.
We evaluate the meaning of nightmares according to the patient. In many cultural
contexts, the nightmares are considered the visitation of a deceased person or an
indication that the dreamer is in a physically and spiritually vulnerable state (Hinton,
Hinton, et al., 2009). We specifically ask about sleep paralysis and its meaning. Sleep
paralysis worsens anxiety and PTSD and is caused by them, and in certain cultural
groups, sleep paralysis is given extensive cultural elaboration and is quite common
(Hinton, Pich, Chhean, & Pollack, 2005). Distressed Cambodian refugees often have
sleep paralysis and it is usually attributed to the visitation of a malevolent spirit or
to dangerous physiological problems; African American groups likewise often have
sleep paralysis and frequently give it a catastrophic interpretation (Hinton, Pich,
Chhean, et al., 2005). We assess for nocturnal panic and its interpretation. In order to
improve sleep, we also have patients do yoga-like stretching before sleeping to prevent
cramping and decrease arousal (Patra & Telles, 2009). Those yoga-like stretching
methods are taught at the end of every session (see Table 18.2).
Using Culturally Specific Proverbs, Local Stories, and Culturally

Appropriate Analogies to Convey Cognitive Behavioral Therapy
Information and to Create Positive Expectancy
Proverbs can serve as adaptive cognitive sets to interpret reality that promote positive
affect and serve as primers to adaptive functioning (Aviera, 1996; Hyman, Ortiz, Añez,
Paris, & Davidson, 2006; Otto, 2000). The proverbs can result in positive expectancy
and alleviate negative affect, and may help the person to handle stress and negative
emotions. They can be used to teach CBT information and may function as a form of
emotion regulation. For example, in trying to teach Latino patients the importance
of decentering and the negative spiral created by narrowly focusing on a negative
cognition, one can use the proverb, “No se ahogue en un vaso de agua,” meaning, “Do
not drown in a glass of water.” This is an example of tapping into the local model
of mind and traditional ways of handling distress enshrined in a proverb that teaches
about the danger of attending too narrowly to one subject or issue. Or to help a
Cambodian patient to better regulate anger, one can use the Cambodian proverb,
“If you don’t become angry one time, it gains you a hundred days of happiness.”
Similarly, to help a Cambodian patient to talk about current issues of distress, one can
use the proverb, “Don’t reek by yourself,” in which reek means “to carry a package
at either end of a pole that is balanced at the shoulder.” Or among African American
teenagers the term “rebound” is a powerful motivator that is increasingly used as a
reminder that you can recover after a missed “shot” or opportunity.
Appropriate cultural analogies can also be used to create positive expectancy about
treatment and to promote adherence. It should be noted that there is much evidence
that CBT efficacy is greatly influenced by positive expectancy (Woodhead, Ivan, &
Emery, 2012). At the beginning of therapy to help the Cambodian patient to be
adherent to treatment and to create positive expectancy, we state that the treatment
is like making a certain traditional noodle dish. To make that dish, there are several
steps, which include making a paste, making noodles from the paste, and multiple
Table 18.4 Examples of Proverbs and Culturally Salient Expressions that Can Be Used
Therapeutically
Group Proverb or culturally salient idiom Therapeutic meaning
Latino “Don’t drown in a glass of water” Do not ruminate on an issue or

(No se ahogue en un vaso de agua) problem to the point it causes you
great distress.
Latino “Undrown yourself” (Desahogarse) Say what bothers you or you will
drown in your unspoken distress
(i.e., in this idiom, an unspoken
topic of distress is analogized to a
drowning water).
Cambodian “If you don’t get angry one time, you Realize the negative consequences of
gain a hundred days of happiness” anger episodes in which the person
(Gom kheung medoong baan sok says or does something that has
merooy thngay). long-term negative effects.
Cambodian “Don’t reek by yourself” (reek means Share your problems with others or
“to carry the pole at the shoulder, you will become overburdened and
with a weight balanced at either overwhelmed.
side”)
African “Rebound” You can rebound after a missed
American “shot,” that is, you can recover
from a reversal or mistake if you
engage and mobilize to recover.
steps to make the sauce. We explain that each part of the therapy, each lesson taught,
is like one step in making this dish, and that one needs to wait until the end of therapy
to know exactly what has been accomplished.
The examples given above (Table 18.4) show how proverbs, cultural stories, and
appropriate culturally grounded analogies are useful in decreasing negative affect,
creating positive expectancy, and promoting emotion regulation. Using proverbs,
cultural stories, and culturally appropriate analogies also helps to promote cultural
self-esteem, that is, the sense that one comes from a culture with a rich and important
tradition of knowledge, which further decreases negative affect. Additionally, using
proverbs, cultural stories, and culturally appropriate analogies can improve the ther-
apeutic alliance; the patient feels the therapist understands and appreciates his or her
cultural background.
Presenting Cognitive Behavioral Therapy Information and Techniques

in Terms of Local Psychology and Physiology
Every culture has a certain set of ideas about how to manage negative affect and
negative events. These can be used to promote treatment and positive expectancy.
In the Spanish language, multiple tropes describe negative events in terms of images
of suffocation or drowning (Hinton, Lewis-Fernández, et al., 2009). To encourage a
patient to talk about trauma memories, one may use the word “desahogarse,” which
literally means to “undrown yourself,” and refers to talking about what is bothering
you, with the connotation that if you do not, you will find it intolerable, analogous
to drowning. In the Cambodian language, anger and other negative states are often
compared to a “fire,” and in fact many traditional treatments involve a sort of cooling
technology, such as anointing with waters that are considered supernaturally cooled.
So then one can tell the patient that getting angry is like “bringing a fire into one’s
house,” and one can give the analogy that when angry, often there are two fires: the
one fire is the anger caused by what the person did (e.g., a child not listening) that
is added to the fire of other similar events that are recalled to mind (e.g., the child’s
father treating her badly). More generally, framing “anger” in the cultural imagery
of fire helps the patient distance from that emotion and treat it with more caution.
Contrariwise, certain proverbs may need to be specifically addressed and countered. In
Cambodia, there is a proverb, “Don’t open your chest and let the crow eat it,” meaning
“Do not share private information to those outside the family.” More generally, the
patient can be asked how or he or she manages negative affect. This information can
be used to better frame the teaching of CBT-type emotion regulation techniques.
Incorporating Therapeutic Techniques from the Local Religious and

Spiritual Tradition
As much as possible the treatment should be couched in terms of the traditional
spiritual and religious traditions, and the patient should be asked specifically if he
or she is involved in those traditions and whether they have been helpful, and if so,
how (Lewis-Fernández & Diaz, 2002). Every culture will have a certain spiritual and
religious tradition, which may be used to promote therapy. An obvious case would
be Buddhist societies that have a tradition of meditation, or Indic societies with a

yoga tradition. These techniques have proven to be effective in multiple studies and
their efficacy has been explained in terms of CBT principles (Hinton, Pich, Hofmann,
et al., in press), so clearly they should be incorporated into treatment protocols for
these groups. It should be noted that, although these techniques are part of these
cultural traditions, often members of these groups have used them minimally, and
teaching them in the context of a structured therapy can have extremely positive
effects. Moreover, for CBT purposes, those techniques can be distilled so that they
will be efficacious according to CBT principles. More generally, societies often have
traditions that aim to develop emotion regulation. For example, praying the Rosary
in the Catholic tradition of certain Latino groups is an example of placing the mind
on a positive attentional object, or likewise the religious tradition of opening the
Bible at random to a passage when feeling distressed. In Islam, there is the example
of repeatedly saying dhikr, the name of Allah (see below). In the Native American
traditions, there are several healing rituals that can be conceptualized in terms of CBT
(Gone, 2010). The Indian steam ritual can be conceived of as interoceptive exposure
to symptoms of autonomic arousal and as creating positive associations to symptoms
of autonomic arousal, given that it results in asphyxia. Among Cambodian patients,
to create a sense of agency and positive affect, and to decrease suicide ideation, the
treater can remind patients of the need to make “merit” for the deceased. Merit can
be made by donating objects to monks, meditating, or performing any positive action,
and this “merit” can be sent to the deceased to promote rebirth; it is mandatory to
do this in certainly yearly rituals.
These spiritual and religious rituals create positive expectancy and a sense of
being healed, and so increase self-esteem and help to decrease negative affect. These
healing rituals often articulate the traditional cosmology and what is considered ideal
personhood (i.e., what are considered good forms of action), and these self-schemas
and world-schemas can have a very positive effect (Benish, Quintana, & Wampold,
2011). Through these rituals, part of the self-referential imagery involves the rituals
themselves (i.e., the memory of having done the ritual becomes a key part of the
self-concept; moreover the rituals often involve self-imagery), and additionally, part
of the world-schema is the rituals themselves (the rituals almost always represent a
cosmology), and furthermore, there is a sense of having been healed and protected.
These changes can have important effects; for example, in PTSD, it has been found that
negative self-schemas and world-schemas are very important predictors of worsening
(Foa & Rothbaum, 1998).
Promoting a Sense of Self-Esteem and Self-Efficacy in a Culturally

Appropriate Way
One key way to decrease negative affect is to increase self-esteem and a sense
of self-efficacy. This would also be expected to help emotional regulation ability
(Gyurak et al., 2012), among other effects. Culturally appropriate visualization can
be used to create positive self-images and promote a sense of self-efficacy. The aim
of such imagery is not “relaxation,” but rather the creation of positive self-images
and a sense of self-efficacy—as well as positive expectancy (which shows the close
link between self-esteem and other constructs). In CA-CBT, the treatment teaches
self-images that promote cognitive flexibility (see section on “Culturally Adapted
Emotion Regulation Techniques”).
Addressing Stress and Security Issues

As indicated above in relation to the generation of psychopathology, it is increasingly
realized that ethnic minorities and refugees confront multiple practical issues that
range from medical problems, financial problems, children difficulties (truancy and
fears of drug abuse and gang involvement), and safety issues. In treating patients
from other cultural contexts, it is important to ensure that these problems are being
addressed (Ell et al., 2011; Lesser et al., 2008; Miranda, Azocar, Organista, Dwyer,
& Areane, 2003). It is important to be aware of the extent to which these issues are
still salient and are being properly addressed. For example, if a woman is still in an
abusive relationship, it may be difficult to make treatment gains, and the treatment
approach should take account of this situation. In some cases, it may be imperative
to conduct a hybrid therapy in which these safety and practical issues are discussed
to some extent in each session. Given these safety and practical issues, particular
emphasis should be placed on teaching techniques to handle emotional arousal before
conducting exposures.
Worry and Generalized Anxiety Disorder as

Important Treatment Targets
Regardless of the patient’s primary anxiety disorder, uncontrollable worry itself is a
key treatment target among refugee and minority populations. As described above,
refugees and ethnic minorities often engage in worry because of life circumstances
(they often live in dangerous localities and frequently confront financial problems and
other stresses), and stress results in the person having difficulty disengaging from worry
and the tendency to experience arousal—and not uncommonly panic attacks—upon
engaging in worry, what might be called “arousal inducibility” (Hinton, Nickerson,
et al., 2011). The arousal induced by worry may give rise to catastrophic cognitions
and trauma recall, and worry also brings about a state of ruminative hypervigilance to
threat. In CA-CBT we elicit worry themes, address catastrophic cognitions about the
negative effects of worry, and determine whether the worry episodes induce trauma
recall or panic attack. Learning the patient’s worry themes builds the patient–clinician
empathic bond (the patient feels his or her problems are understood by the clinician)
and improves the therapeutic alliance. In CA-CBT, we specifically teach emotion
regulation techniques to decrease worry that have been proven to be effective for
generalized anxiety disorder such as meditation (Roemer, Orsillo, & Salters-Pedneault,
2008) and for PTSD (Follette, Palm, & Pearson, 2006).
Conducting “Exposure” in a Culturally Acceptable Way

Exposure is a central part of the treatment of the anxiety disorders, but there are
several reasons to think that it should be conducted in a culturally acceptable way.
To illustrate this point, we give the example of exposure therapy in the case of
PTSD.
Probably the best-known CBT treatment of PTSD, prolonged exposure therapy (Foa
& Rothbaum, 1998), takes exposure to trauma memories to be the central part
of treatment for PTSD. Therapy mainly consists in repetitive exposure to a trauma
memory that is evoked in all its sensorial aspects until the person is quite distressed.
Vivid reliving and high distress are thought to be necessary for efficacy, with cure
resulting from the extinction of anxiety and fear associated with memories. In another
prominent protocol, cognitive processing therapy (Resick & Schnicke, 1996), exposure
is also a central component: The person writes down the trauma event in detail and
repeatedly reads it. The only published manual for treatment of refugees that has been
empirically tested is narrative exposure therapy (Schauer, Neuner, & Elbert, 2005).
It is based on the prolonged exposure approach but is much briefer (usually three
to six sessions; prolonged exposure therapy is 12 sessions and cognitive processing
therapy 12 sessions). This intervention focuses almost exclusively on exposure with
multisensorial reliving in the context of constructing the person’s trauma narrative
and aims to achieve extinction. For several reasons, none of these three treatments
conducts exposure in a manner that is optimal for traumatized refugees and ethnic
minorities.
First, even English-speaking Western populations who are highly educated often
find traditional exposure hard to tolerate and experience worsening at certain points
of the treatment (for a review, see Cahill, Foa, Hembree, Marshall, & Nacash,
2006; Markowitz, 2010). Given that ethnic minorities and refugees are often highly
distressed, these techniques would seem more likely to have negative results, such as
worsening of symptoms and increasing drop-out. In one study, traditional exposure
was poorly tolerated by ethnic minorities and refugees, with African Americans
dropping out twice as often as Caucasian patients (55% vs. 27%; Lester, Resick,
Young-Xu, & Artz, 2010).
Second, the theory of how exposure works has changed. Previously it was believed
that exposure was effective owing to the simple fact of exposure to the memory
reducing its automaticity, activatibility, and “hotness,” and that a key part of “extinc-
tion” was having the person experience the memory with high levels of multisensorial
vividness and distress (Foa & Rothbaum, 1998). Now it has been found instead
that the trauma memory is never erased through treatment (Craske et al., 2008;
Hofmann, 2008). Exposure works by creating new nonthreatening associations to
the trauma memory network and by creating new verbal links to and representations
of the trauma memory that decrease the memory’s uncontrollability and “hotness”
(Brewin, Dalgleish, & Joseph, 1996; Craske et al., 2008). The person does not need
to experience high levels of distress to get this result—rather, the goal is to create the
expectancy that the trauma memory can be tolerated (Craske, et al., 2008; Hofmann,
2008). This suggests new and less distressful treatments are possible.
Third, researchers have increasingly realized that emotion regulation techniques
should be taught prior to conducting exposure so that the patient’s level of arousal
is reduced. Otherwise the person will be unable to tolerate exposure. This is often
called a phase approach and is used in one new 16-session treatment (Cloitre, Cohen,
& Koenen, 2006; Cloitre, Koenen, Cohen, & Han, 2002). Phase treatment is
especially important in highly traumatized populations and with patients under great
stress (Markowitz, 2010), which is commonly the case among refugees and ethnic
minorities.
Fourth, it has been increasingly realized that exposure should be conducted not
only for certain event memories but also for somatic sensations (Hinton, Hofmann,
Pitman, Pollack, & Barlow, 2008; Otto & Hinton, 2006; Wald & Taylor, 2007,
2008). Interoceptive exposure is especially indicated for those patients with promi-
nent somatic complaints, extensive catastrophic cognitions about somatic symptoms,
extensive trauma associations to somatic sensations (e.g., each trauma results in the
encoding of the trauma by somatic sensations), and many comorbid anxiety disorders,
all of which are commonly found in ethnic minority and refugee populations. Intero-
ceptive exposure to sensations decreases catastrophic cognitions about them, reduces
their ability to recall trauma events, and reduces panic attacks and panic disorder—as
well as somatization more generally (Barlow, 2002; Craske et al., 2009; Wald &
Taylor, 2007, 2008).
Taking into account these recent theories about exposure, we make our exposure
in CA-CBT acceptable and efficacious in the following ways:
• Phase approach: We use a phase approach, teaching emotion regulation skills, such
as applied muscle relaxation, applied stretching, and meditation, before starting
exposure. See Table 18.2 for a description of the first three sessions that precede
exposure and the emotion regulation techniques that are introduced.
• Trauma protocol: To promote acceptability of exposure during verbal recounting
and to make it more effective, in CA-CBT we have the patient discuss trauma
memories at the beginning of several sessions (sessions 5–10), and then when
the patient becomes upset, we have the patient perform a trauma protocol.
This protocol consists of a series of emotion regulation techniques, including
mindfulness and applied stretching with a visualization (the reasons for the efficacy
of the trauma protocol and the culturally adapted techniques used in this protocol
are discussed more fully later in the chapter).
• Interoceptive exposure with reassociation: We conduct interoceptive exposure to
sensations such as dizziness while creating positive reassociations to them to
compete with sensation-type trauma associations and catastrophic cognitions.
Creating positive reassociations to sensations increases acceptability and efficacy.
Emotion Exposure Paired with Practice of Emotion Regulation

Emotion regulation deficits are a key treatment issue among persons with emotional
disorders (Fairholme, Boisseau, Ellard, Ehrenreich, & Barlow, 2010; King & Sloan,
2010) and form a key part of our model of how anxiety disorders are perpetuated (see
Figure 18.1). In addition to the emotion of fear, refugees or ethnic minorities with
anxiety disorders often have problems with anger, general anxiety, and worry (Hinton,
Nickerson, et al., 2011; Hinton, Rasmussen, et al., 2009). These emotions often give
rise to arousal, trauma recall, and catastrophic cognitions, which start vicious cycles
of worsening.
Recent research suggests that an important treatment approach for emotional

disorders consists of exposure to intense emotions in such a way that the patient
learns to tolerate the affect and to utilize more adaptive ways of reacting to it, an
approach that is a central part of Barlow’s Unified Protocol in which he expands his
work on interoceptive exposure to include emotional exposure (Ellard et al., 2010;
Fairholme et al., 2010; Otto, Powers, & Fischmann, 2005; Wilamowska et al., 2010).
Emotion exposure is easily accomplished with various cultural groups if it is framed
as being a way to practice the emotion regulation techniques, and this then also
gives an opportunity to practice emotion regulation. We consider emotion exposure
to be both the exposure to negative affect and the induction of and exposure to
positive affect such as compassion and loving-kindness. Exposure creates a broader
behavioral-emotional repertoire because those states become action options under
greater volitional control.
In CA-CBT, we elicit certain emotions in a vivid way. Some emotions are induced
during trauma recall at the beginning of sessions. Other emotions, namely, anxiety,
anger, and worry, are induced by asking about recent experiencing of the emotion,
the events that caused the emotion, and the somatic sensations associated with the
emotion. After the emotion is induced during the CA-CBT session, we have the
patient practice shifting state by using an emotion regulation technique. Almost every
session of CA-CBT begins with an enquiry about anxiety states in the previous week,
followed by practice of the anxiety protocol. As discussed above, several sessions
of CA-CBT (sessions 5–10) begin with trauma exposure during which the patient
experiences fear and other trauma-recall-related emotions, followed by practice of the
trauma protocol. Several sessions involve the review of causes of anger, which will
invoke that emotion, followed by practice of the anger protocol (sessions 11–14: for
a description of key components of CA-CBT, see Table 18.2).
In particular, we think that trauma exposure—which elicits a number of negative
emotions—followed by practicing emotion regulation through the trauma protocol
has several positive effects. The patient is able to verbalize the trauma and thereby
creates frontal representations that should decrease automaticity of recall (Brewin
et al., 1996; D. M. Clark & Ehlers, 2004). The patient is able to practice the emotion
regulation and acceptance techniques, techniques that can be used whenever trauma
recall occurs and whenever any dysphoric state is experienced. Through the exposure
protocol, the patient pairs a positive memory state to the trauma memory, with the
positive memory being characterized by a sense of agency and self-esteem and by
adaptive emotional states such as curious, detached observance, loving-kindness, com-
passion, and aesthetic engagement with the sensorial surround. The patient changes
his or her self-image to one of mastery and ability to cope with the trauma memory.
Culturally Adapted Emotion Regulation Techniques

Poor emotion regulation is a key aspect of PTSD and the anxiety disorders more
generally (Fairholme et al., 2010). In this section we describe several emotion
regulation techniques we teach in CA-CBT and how they are culturally adapted.
The anxiety protocol is practiced at the beginning of most sessions after asking about
recent events that produced anxiety (see Table 18.2), and it can be used whenever the
patient becomes anxious or distressed in any way. This anxiety protocol not only serves
as a means to regulate emotion. It also serves as exposure to dizziness sensations,
creates positive reassociations to dizziness (e.g., dizziness becomes associated to the
image of the lotus that competes with catastrophic images), and acts as a visual
analog of flexibility, a self-image of flexible adjustment. In the first part of the anxiety
protocol, the patient uses applied stretching to relax any tense areas, and then uses
applied stretching and muscle relaxation to relax the shoulders. The imagery in the
next section depends on the cultural group. We have the patient straighten the spine
through tightening the stomach muscles and then do head rolling. While doing the
head rolling with the straight spine, we have Southeast Asian patients imagine a lotus
flower circling in the wind on its stem and compare the spine to the stem and the
flower to the head. At the same time we have the patient make self-statements of
flexibility: “May I flexibly adjust to each situation just as the lotus flower is able to
adjust to each new breeze.” For Latino patients, we use the image of a palm tree at
the beach, with its long trunk and its fronds moving and circling in the wind. The
self-statement is the following: “May I flexibly adjust to each situation just as the
fronds of the palm tree adjust to each new breeze.”
We teach a loving-kindness meditation to help decrease anger (for a review of the
efficacy of loving-kindness meditation, see Hofmann, Grossman, & Hinton, 2011).
We change the imagery depending on the cultural group. We have Southeast Asian
patients imagine love spreading outward in all directions like water. This is because in
Buddhism water and coolness are associated with values of love, kindness, nurturing,
and “merit-making,” that is, doing good deeds such as making donations to the poor
or to the temple. In many Buddhist rituals, water is poured into a bowl to symbolize
the merit being made by participating in the rite and the “cooling” influence of the
merit-making for the dead and the living. We have Latino patients imagine love as
a warmth and light that spreads from the heart and body in all directions. We refer
to the image of the “Sacred Heart of Jesus,” or Sagrado Corazón de Jésus, one of the
best-known images in Christian iconography. In the image, Christ points a finger to
his flame-surrounded heart that emanates light; often the heart is surrounded by a
wreath of thorns that further symbolizes the overcoming of difficulties. In Western
European ethnopsychology and iconography, warmth connotes love and affection
and has extensive positive symbolic meanings (for one review, see Hinton, 2000).
The trauma protocol also varies by cultural group. The trauma protocol begins
with acceptance of having endured the trauma, followed by self- and other-directed
compassion, then loving-kindness, and next multisensorial mindfulness meditation.
After that, we use a technique that aims to bring about the multichannel embodying
of flexibility. The technique pairs together bodily representations of flexibility (actual
stretching and rotational movements), self-statements of flexibility, and musical
analogs of flexibility, that is, acoustic images of flexibility. The 5-step multichannel
flexibility protocol is as follows:
1. Applied stretching. The patient stretches any area of sensed tension.

2. Arm stretching that emphasizes flexibility icons. The patient stretches the arms
and their joints by extending the arms out and rotating them with the wrists
bent back, by rotating the wrists, and by extending and fluttering the fingers (for
further discussion of the efficacy of such body-based flexibility techniques, see

Hinton, 2008).
3. Evocation of an acoustic icon of flexibility. These arm-stretching motions have a
dance-like quality, particularly the wrist rotations and finger fluttering, and next
we have the patient think of music appropriate for the patient’s cultural group.
For Cambodian patients, we suggest imagining the arms dancing to the songs
of a famous singer, Seng Sii Samut; that dancing can occur at the level of the
whole arm, forearm, wrist, or fingers (this highlights the highly flexile aspect of
the human body). For Caribbean-Latino patients, we use the example of salsa
and bachata; for Mexican-Americans, ranchero music. In the salsa example, we
instruct the patient to imagine the rhythm of the singer’s voice and that of the
conga drum, bongos, timbales, horns, cowbells, piano, and maracas; and in the
ranchero example, the rhythm of the singer’s voice and that of the polka-like
oompah sound of the accordion, the sound of the guitar, and so on. We mention
several musical genres of the group in question in order to bring about further
cognitive shifts: from salsa to bachata to bolero.
4. Embodying the acoustic icon of flexibility. We describe each of the music’s sound
layers, stating that the patient can choose to dance to any of these music layers
and that making these movements is practice in flexible adjustment (it is a form
of set-switching).
5. Self-image of flexibility paired to music-listening. We conclude by commenting
that the music is a reminder to stay flexible, to know how to adjust.
This 5-step multichannel flexibility protocol has several effects other than shifting
from the dysphoric states induced by trauma recall. It pairs bodily flexibility to a
musical metaphor that emphasizes psychological flexibility; it teaches the powerful
effect of attention on experiencing because the patient attends to one layer and then
another layer of music, for example, from one instrument to another; it teaches
set-switching, as the patient switches between musical layers; it creates cultural pride
because a certain cultural music is presented; and it creates a prompt—hearing
music—to remind the person to be flexible, a prompt that will often be experienced
in the everyday world.
Utilizing Emotion Regulation Techniques from the Patient’s

Religious or Cultural Healing Traditions
To make the treatment culturally acceptable and to improve efficacy, we try to
utilize emotion regulation techniques from the culture in question and frame our
techniques in terms of locally prominent emotion regulation techniques. In CA-CBT,
we determine the emotion regulation techniques in that cultural group that can be
used in treatment: As mentioned above, some Islamic groups repetitively recite Allah’s
name, a ritual called “dhikr,” to bring about a peaceful state of mind.
Our treatment involves the use of many Buddhist-type techniques, so in the case of
a Buddhist patient, the treatment already includes a key aspect of his or her religious
tradition. The treatment includes “loving-kindness” (metta) and many meditation
techniques, with a new mindfulness exercise being provided at the end of every session
(Table 18.2). A key Buddhist principle, “equanimity” (upekkha), that is, practice in
distancing from emotions and mental content, treating them as like clouds in the
sky, is also a part of the treatment. For a Buddhist patient, these acts can be referred
to by the term used in that tradition, and it can be stated that performing these
actions is “merit-making” and that this “merit” can be shared with oneself and others.
This “merit-making” promotes a sense of agency and greatly decreases suicidality and
depression. If a patient has survivor guilt, he or she can be reminded of the culturally
indicated duty to make merit at least yearly for the person about whom the patient
feels guilty in order to ensure the deceased will have a good rebirth and spiritual
health.
To promote flexibility among Christian Latino patients, we instruct them to note
how the flexile flame of votive candles moves in each breeze and assert that this
motion is a reminder to stay flexible—the image in question serves as a flexibility
primer (Hinton, 2008). As indicated above, we use Christian imagery in the loving-
kindness meditation. In addition, we suggest that the Christian Latino patient use
other religious-type techniques of emotion regulation such as random opening of
the Bible to select a passage to be read or reciting the Rosary (e.g., if the patient is
Catholic). If the patient is a Pentecostalist, we suggest that speaking in tongues, with
its layers of voices, is a reminder that there are many paths to God, many ways of
acting and feeling.
We consider emotion regulation techniques in the broad sense, ranging from
proverbs in a culture that are used to deal with negative affects, to healing rituals.
In the anger module of our treatment, we use a Cambodian proverb to help teach
anger restraint, which was mentioned earlier: “If you control your anger once, you
gain a hundred days of happiness.” We specifically ask about how patients cope with
anxiety, anger, and trauma recall in order to elicit the patient’s typical ways of dealing
with distress, including culturally specific healing traditions and emotion regulation
techniques. In CA-CBT we also suggest that the patient be encouraged to participate
in healing rites from his or her culture that may improve emotion regulation: among
Buddhists, relevant healing ceremonies, such as anointing with lustral waters or
listening to Buddhist tapes; among Latinos, going to church services, lighting a votive
candle, or reciting the Rosary; and among Native American groups, participation in
traditional ceremonies such as the sweat lodge. Ideally therapeutic metaphors, ideas
of causation (e.g., “historical trauma”), ideas of cure, and ideas about ontology (i.e.,
the nature of personhood) from that tradition should be integrated into treatment.
(For further discussion of the incorporation of traditional healing into treatments, see
Gone, 2009, 2010.)
Cultural Adaptation of Key Cognitive Behavioral Therapy Techniques

CBT techniques should be adapted for the group in question to promote treatment
adherence. We have described how relaxation imagery and exposure are adapted
for a particular group. Here we will examine in more detail the cultural adaptation
of a particular aspect of exposure, namely, interoceptive exposure. In interoceptive
exposure in CA-CBT, we make positive reassociations of somatic sensations to
culturally appropriate images. Among Cambodian refugees, when doing head rolling,
we have the patient imagine various traditional games: a game in which a person
is made to run around in circles while holding a scarf (lea geunsaeng), or another
game in which the person runs to get a stick that has been hit into the distance,
all the while humming, making it impossible to inhale. Among Latinos, we have
the patient imagine playing traditional games that induce considerable dizziness:
playing the piñata game, which involves being blindfolded and spun around, or
playing galliñita ciega. In these games, the person is spun until very dizzy. La Roche,
D’Angelo, Gualdron, and Leavell (2006) found that relaxation imagery involving
an allocentric (the idea that one defines through social relationships) rather than an
individualistic (the idea that one defines through self-attributes) orientation was more
effective.
Increasing Emotional and Cognitive Flexibility in a Culturally

Appropriate Way
Psychological flexibility—defined as the ability to distance from current mindsets
and consider other possible mindsets (Kashdan, 2010)—is a metalevel processing
mode that CA-CBT tries to create as a default mode of processing. Psychological
inflexibility is a key cause of psychopathology (Ehrenreich et al., 2007; Hinton,
Hofmann, Pollack, & Otto, 2009). Psychological flexibility creates a new adaptive
processing mode that competes with the threat mode (Hinton, Pich, Hofmann, et al.,
in press; Kashdan, 2010; Kok & Fredrickson, 2010). It is a key aspect of emotion
regulation.
Psychological flexibility is a crucial skill for refugees and ethnic minorities who are
dealing with multiple adaptations that require great flexibility: They must reconcile
their own culture and their new one, learn a new social and geographic location,
learn to switch language registers, and deal with different ideas about proper behavior
and social interaction, such as how children should behave. One theoretician of
adapting cultural treatments among Native American groups emphasized as a key
goal the achieving of “postcolonial hybridity,” given the complex bricolage necessary
to construct identity in such localities (for a discussion of Duran’s use of this term,
see Gone, 2010).
CA-CBT aims to increase psychological flexibility in the following ways:
• through teaching emotional distancing, a key aspect of emotional flexibility, by

practicing the labeling and distancing from affect (Ayduk & Kross, 2010; Hinton,
2008);
• through the emotion and trauma protocols by practicing distancing from one
affect and taking on another one—that is, emotion switching;
• through the visualization part of the anxiety protocol;
• through applied muscle relaxation with self-statement of relaxation;
• in a multichannel way through the “dancing” part of the trauma protocol; and
• through decreasing anxiety (e.g., through the anxiety and trauma-recall protocols),
which is an emotional state characterized by narrowed attention and a rigid
responding style.
We have the used the “multisystem network” (MSN) model of emotional state
to depict the psychological-flexibility processing mode induced by applied stretching
and by the visualization part of the anxiety protocol. The model is based on recent
research on emotion (Fairholme et al., 2010; Teasdale, 1996). Figure 18.3 shows a
negative processing mode centering on negative affect and a sense of being trapped
and inflexible, and Figure 18.4 the positive processing mode induced by the anxiety
protocol or applied stretching more generally. This nodal network is constantly
activated during CA-CBT. Applied muscle stretching is practiced at the end of each
session, each night before sleep, and whenever the person is anxious. The anxiety
protocol is practiced in every session (see Table 18.2) and outside of the sessions
whenever the patient feels dysphoric. More generally, whenever a state of psychological
flexibility is experienced (e.g., when the patient distances from a negative affect during
the practice of equanimity) this type of network will tend to be activated but focused
on that psychological flexibility in question.
Reducing Stigma
Stigma can be reduced by informing the patient that the anxiety disorder in question
is treatable and that treatments such as medication will not lead to worsening. It
is also extremely helpful in reducing stigma to frame the treatment as reducing the
symptoms of most concern to the patient that are less stigmatizing. For example,
one can frame the treatment as reducing a somatic symptom such as dizziness or
improving vegetative functions such as sleep or appetite. These symptom conditions
are not stigmatizing. The patient then may describe their treatment to others in their
family or social network as targeting those nonstigmatizing symptoms.
Culturally Indicated Transitional Rituals

If the culture has “purification” or transitional rites, such as steam bath rituals among
Cambodian refugees, Vietnamese refugees, and certain Native American groups (Silver
& Wilson, 1988), the patient should be encouraged to perform that rite at the end
of treatment. This creates a sense of closure, and of positive transformation. These
rituals also have healing properties in themselves. For example, the steaming ritual
induces a somatic state that is analogous to an anxiety state: flushing and shortness
of breath. It thus acts as exposure to those sensations and as a positive reimagining
of them; the steaming ritual often involves odiferous substances and symbolic objects
that become associated with—conditioned to—the somatic sensations. This type
of healing semiotizes certain sensations, that is, creates new positive associations to
sensations.
Conclusion
In this chapter we have tried to illustrate how CBT can be adapted to treat refugees and
ethnic minorities with anxiety and depressive disorders. The manner of development of
culturally sensitive treatment illustrated in the chapter can be applied to other disorders
Activation of the biologically associated state of the CNS: decreased vagal tone and
decreased HRV (heart rate variability), associated with a decreased ability to
disengage from ongoing experiencing and to consider other mind-sets
Activation of the biologically

Associated psychological appraised: a sense associated state of the ANS:
of being threatened, of inadequacy, of low shortness of breath, chest
self-worth, of having few options; a sense of tightness, cold extremities
being unable to adjust to challenges, of
desperation; a sense of anger, of taking on
Muscular/tendon state:
more than one can handle, of being trapped
tightness in the muscles, at
the joints, bodily rigidity,
Attentional bias: attention certain posture
to threat (symptoms,
threat cues) and insult
Particular mood state:
Negative affective state: anxiety, panic, anger,
Mental-content Focus on inflexibility aspects sadness
processing mode:
rumination/worry
Associated biographical
memory: memory of a trauma,
of anger topics
Set-shift ability: poor set-shift ability
Associated imagery: a rod, a

branch that breaks rather
Distancing ability: over-identification with than bends; an explosion, a
mental content, poor decentering boiling pot, a bursting boiler
distancing, poor metacognitive awareness or gasket
Associated self-statements: I am about

Associated action predisposition: to snap, I feel tense, I can't adjust; I will
withdrawal, non-engagement, hostility explode
Associated metaphors: inflexible, rigid, trapped, uptight; a sense

of imminent explosion, a gasket about to burst (particularly in
respect to the tension in the neck and head)
Figure 18.3 The Nodal Network Model of Negative Affect: Focus on Inflexibility Aspects.
This is a nodal network model of negative affect, showing how multiple nodes interact to create
a negative affective state. At one point in time, one or another node may be the object of
attention or may be more active in determining the current mode of processing. As one node
becomes active, all the other nodes tend to be so as well; if one node shifts, all the others tend
to as well.
such as schizophrenia, and the same is true of many of the therapeutic principles
adduced in the chapter. A model of the cultural influences on the development of
anxiety and depressive disorders was presented (Figure 18.1), as was a model of
how culturally sensitive CBT can be conducted based on this cultural understanding
(Figure 18.2). We described key treatment components based on the model of how
anxiety and depression disorders are generated and on our treatment model. We
illustrated these treatment components using examples from our culturally adapted
CBT for PTSD.
Activation of the biologically associated state of the CNS: Increased vagal tone and
increased HRV (heart rate variability) that increases the ability to distance from
mind-sets and consider other mind-sets
Activation of the biologically

associated state of the ANS:
Associated psychological appraisal: a warm extremities, slowed
sense of new possibilities, of many breathing, etc...
action options, a sense of being able
to adjust to challenges, of hope; a
sense of relaxation, of not being Muscular/tendon state:
overwhelmed relaxation in the muscles,
flexibility at the joints
Attentional bias: attention
to positive cues
Mental-content Particular mood state:

processing mode: Positive state: anxiety, panic, anger,
nonrumination Focus on flexibility aspects sadness
mode, present-
moment focus
Associated biographical
memory: memory of positive
events that are encoded by
Set-shift ability: good set-shift ability muscle relaxation and bodily
flexibility
Associated imagery: flexible

Distancing ability: ability to distance from objects such as rice plants in
mental content, good decentering the wind, leaves in the wind,
distancing, good metacognitive awareness a candle flame in the wind
Associated self-statements: I am
Associated action predisposition: relaxed; I can adjust; I can handle
prosocial, active engagement things
Associated metaphors: flexible, having options,

loose; the sense of possibility, of multiple
motions
Figure 18.4 The Nodal Network Model of Positive Affect: Focus on Flexibility Aspects. This
is a nodal network model of positive affect, showing how multiple nodes interact to create a
positive affective state. At one point in time, one or another node may be the object of attention
or may be more active in determining the current mode of processing. As one node becomes
active, all the other nodes tend to be so as well; if one node shifts, all the others tend to as well.
The approach in this chapter is consistent with recommendations as to how to

make treatment more culturally competent (La Roche, 2013; La Roche & Lustig,
2010; Sue et al., 2008), one of the basic ideas of which is that the efficacy of
treatment increases as local responses are not only respected but integrated into
interventions: proverbs, religious traditions, and locally emphasized somatic symptoms
and syndromes (Hinton, Kredlow, et al., 2012). The incorporation of the cultural
characteristics endorsed by each patient is crucial in the design of individualized
and effective treatment. It is not that patients’ race or ethnicity is used to predict
outcomes, but rather that the utilization of their cultural characteristics increases the
efficacy of treatment.
Future studies should examine through meditational analyses and dismantling
studies whether the model of the cultural influences on the generation of anxiety
and depressive disorders is accurate, and whether the interventions identified in the
model lead to improvement. Future studies should explore how the recommendations
advanced in this chapter are applicable to psychological disorders other than anxiety
and depression. Future studies need to explore the efficacy of culturally adapted
treatments to standard protocols (Foa & Rothbaum, 1998; Resick & Schnicke, 1996).
References
Aguilera, A., Lopez, S. R., Breitborde, N. J., Kopelowicz, A., & Zarate, R. (2010). Expressed
emotion and sociocultural moderation in the course of schizophrenia. Journal of Abnormal
Aviera, A. (1996). “Dichos” therapy group: A therapeutic use of Spanish language proverbs
with hospitalized Spanish-speaking psychiatric patients. Cultural Diversity and Mental
Health, 2, 73–87.
Ayduk, O., & Kross, E. (2010). From a distance: Implications of spontaneous self-distancing
for adaptive self-reflection. Journal of Personality and Social Psychology, 98, 809–829.
Barlow, D. H. (2002). Anxiety and its disorders: The nature and treatment of anxiety and panic
Barsky, A. J., & Borus, J. (1999). Functional somatic syndromes. Annals of Internal Medicine,
130, 910–921.
Benish, S. G., Quintana, S., & Wampold, B. E. (2011). Culturally adapted psychotherapy
and the legitimacy of myth: A direct-comparison meta-analysis. Journal of Counseling
Bernal, G., Jiménez-Chafey, M. I., & Domenech Rodr ı́guez, M. D. (2009). Cultural adaptation
of treatments: A resource for considering culture in evidence-based practic. Professional
Psychology: Research and Practice, 40, 361–368.
Brewin, C., Dalgleish, T., & Joseph, S. (1996). A dual representation theory of posttraumatic
stress disorder. Psychological Review, 103, 670–686.
Cahill, S. P., Foa, E. B., Hembree, E. A., Marshall, R. D., & Nacash, N. (2006). Dissemination
of exposure therapy in the treatment of posttraumatic stress disorder. Journal of Traumatic
Stress, 19, 597–610.
Cardemil, E. (2008). Culturally sensitive treatments. Culture & Psychology, 14, 357–367.
Clark, D. M. (1986). A cognitive approach to panic. Behaviour Research and Therapy, 24,
461–470.
Clark, D. M., & Ehlers, A. (2004). Posttraumatic stress disorder: From cognitive theory to
therapy. In R. L. Leahy (Ed.), Contemporary cognitive therapy (pp. 141–160). New York,
NY: Guilford Press.
Clark, L. A., & Watson, D. (1991). Tripartite model of anxiety and depression: Psychometric
evidence and taxonomic implications. Journal of Abnormal Psychology, 100, 316–336.
Cloitre, M., Cohen, L. R., & Koenen, K. C. (2006). Treating survivors of childhood abuse:
Psychotherapy for the interrupted life. New York, NY: Guilford Press.
Cloitre, M., Koenen, K. C., Cohen, L. R., & Han, H. (2002). Skills training in affective and
to childhood abuse. Journal of Consulting and Clinical Psychology, 70, 1067–1074.
Craske, M. G., Kircanski, K., Zelikowsky, M., Mystkowski, J., Chowdhury, N., & Baker, A.
(2008). Optimizing inhibitory learning during exposure therapy. Behaviour Research and
Therapy, 46, 5–27.
Craske, M. G., Roy-Byrne, P. P., Stein, M. B., Sullivan, G., Sherbourne, C., &
Bystritsky, A. (2009). Treatment for anxiety disorders: Efficacy to effectiveness to imple-
mentation. Behaviour Research and Therapy, 47 , 931–937.
Dunmore, E., Clark, D. M., & Ehlers, A. (2001). A prospective investigation of the role of
cognitive factors in persistent posttraumatic stress disorder (PTSD) after physical and
sexual assault. Behaviour Research and Therapy, 39, 1063–1084.
Ehrenreich, J. T., Fairholme, C. P., Buzzella, B. A., Ellard, K. K., & Barlow, D. H. (2007).
The role of emotion in psychological therapy. Clinical Psychology: Science and Practice,
14, 422–428.
Ell, K., Xie, B., Kapetanovic, S., Quinn, D. I., Lee, P. J., Wells, A., & Chou, C. P. (2011). One-
year follow-up of collaborative depression care for low-income, predominantly Hispanic
patients with cancer. Psychiatric Services, 62, 162–170.
Ellard, K. K., Fairholme, C. P., Boisseau, C. L., Farchione, T. J., & Barlow, D. H. (2010).
Unified protocol for the transdiagnostic treatment of emotional disorders: Protocol
development and initial outcome data. Cognitive and Behavioral Practice, 77 , 88–101.
Fairholme, C. P., Boisseau, C. L., Ellard, K. K., Ehrenreich, J. T., & Barlow, D. H. (2010).
Emotions, emotion regulation, and psychological treatment: A unified perspective. In A.
M. King & D. M. Sloan (Eds.), Emotion regulation and psychopathology: A transdiagnostic
approach to etiology and treatment (pp. 283–309). New York, NY: Guilford Press.
Foa, E. B., & Rothbaum, B. O. (1998). Treating the trauma of rape: Cognitive-behavioral
therapy for PTSD. New York, NY: Guilford Press.
Follette, V., Palm, K. M., & Pearson, A. N. (2006). Mindfulness and trauma: Implications for
treatment. Journal of Rational-Emotive & Cognitive-Behavior Therapy, 24, 45–61.
Gone, J. P. (2009). A community-based treatment for Native American historical trauma:
Prospects for evidence-based practice. Journal of Consulting and Clinical Psychology, 77 ,
751–761.
Gone, J. P. (2010). Psychotherapy and traditional healing for American Indians: Exploring the
prospects for therapeutic integration. Counseling Psychologist, 38, 166–235.
Gyurak, A., Hooker, C. I., Miyakawa, A., Verosky, S., Luerssen, A., & Ayduk, O. N. (2012).
Individual differences in neural responses to social rejection: The joint effect of self-esteem
and attentional control. Social Cognition and Affective Neuroscience, 7 , 322–331.
Hagengimana, A., & Hinton, D. (2009). Ihahamuka, a Rwandan syndrome of response to
the genocide: Blocked flow, spirit assault, and shortness of breath. In D. E. Hinton &
B. J. Good (Eds.), Culture and panic disorder (pp. 205–229). Stanford, CA: Stanford
University Press.
Halligan, S. L., Michael, T., Clark, D. M., & Ehlers, A. (2003). Posttraumatic stress disorder
following assault: The role of cognitive processing, trauma memory, and appraisal. Journal
Hedley, L., Hoffart, A., Dammen, T., Ekeberg, O., & Friis, S. (2000). The relationship between
cognitions and panic attack intensity. Acta Psychiatrica Scandinavica, 102, 300–302.
Hinton, D. E. (2000). Musical healing and cultural syndromes in Isan: Landscape, conceptual
metaphor, and embodiment. Cambridge, MA: Harvard University Press.
Hinton, D. E. (2008). Healing through flexibility primers. In B. Keon (Ed.), The Oxford
handbook of medical ethnomusicology (pp. 121–163). Oxford, England: Oxford University
Press.
Hinton, D. E., Chhean, D., Pich, V., Safren, S. A., Hofmann, S. G., & Pollack, M. H. (2005).
A randomized controlled trial of cognitive-behavior therapy for Cambodian refugees with
treatment-resistant PTSD and panic attacks: A cross-over design. Journal of Traumatic

Stress, 18, 617–629.
Hinton, D. E., & Good, B. J. (Eds.). (2009). Culture and panic disorder. Palo Alto, CA:
Stanford University Press.
Hinton, D. E., Hinton, A., Chhean, D., Pich, V., Loeum, J. R., & Pollack, M. H. (2009).
Nightmares among Cambodian refugees: The breaching of concentric ontological security.
Culture, Medicine, and Psychiatry, 33, 219–265.
Hinton, D. E., Hofmann, S. G., Pitman, R. K., Pollack, M. H., & Barlow, D. H. (2008). The
panic attack–PTSD model: Applicability to orthostatic panic among Cambodian refugees.
Cognitive Behaviour Therapy, 27 , 101–116.
Hinton, D. E., Hofmann, S. G., Pollack, M. H., & Otto, M. W. (2009). Mechanisms of efficacy
of CBT for Cambodian refugees with PTSD: Improvement in emotion regulation and
orthostatic blood pressure response. CNS Neuroscience and Therapeutics, 15, 255–263.
Hinton, D. E., Hofmann, S. G., Rivera, E., Otto, M. W., & Pollack, M. H. (2011). Culturally
adapted CBT for Latino women with treatment-resistant PTSD: A pilot study comparing
CA-CBT to Applied Muscle Relaxation. Behaviour Research and Therapy, 49, 275–280.
Hinton, D. E., Kredlow, M. A., Bui, E., Pollack, M. H., & Hofmann, S. G. (2012). Treatment
change of somatic symptoms and cultural syndromes among Cambodian refugees with
PTSD. Depression and Anxiety, 29, 148–155.
Hinton, D. E., & Lewis-Fernández, R. (2010). Idioms of distress among trauma survivors:
Subtypes and clinical utility. Culture, Medicine and Psychiatry, 34, 209–218.
Hinton, D. E., & Lewis-Fernández, R. (2011). The cross-cultural validity of posttraumatic
stress disorder: Implications for DSM-5. Depression and Anxiety, 28, 783–801.
Hinton, D. E., Lewis-Fernández, R., & Pollack, M. H. (2009). A model of the generation of
ataque de nervios: The role of fear of negative affect and fear of arousal symptoms. CNS
Neuroscience and Therapeutics, 15, 264–275.
Hinton, D. E., & Nickerson, A. (2012). Treating trauma-related symptoms in special popula-
tions. In J. G. Beck & D. Sloan (Eds.), The Oxford handbook of traumatic stress disorders
(pp. 5014–5012). Oxford, England: Oxford University Press.
Hinton, D. E., Nickerson, A., & Bryant, R. A. (2011). Worry, worry attacks, and PTSD
among Cambodian refugees: A path analysis investigation. Social Science and Medicine,
72, 1817–1825.
Hinton, D. E., & Otto, M. W. (2006). Symptom presentation and symptom meaning among
traumatized Cambodian refugees: Relevance to a somatically focused cognitive-behavior
therapy. Cognitive and Behavioral Practice, 13, 249–260.
Hinton, D. E., Park, L., Hsia, C., Hofmann, S., & Pollack, M. H. (2009). Anxiety disorder
presentations in Asian populations: A review. CNS Neuroscience and Therapeutics, 15,
295–303.
Hinton, D. E., Pham, T., Tran, M., Safren, S. A., Otto, M. W., & Pollack, M. H. (2004). CBT
for Vietnamese refugees with treatment-resistant PTSD and panic attacks: A pilot study.
Journal of Traumatic Stress, 17 , 429–433.
Hinton, D. E., Pich, V., Chhean, D., & Pollack, M. H. (2005). “The ghost pushes you down”:
Sleep paralysis-type panic attacks in a Khmer refugee population. Transcultural Psychiatry,
42, 46–78.
Hinton, D. E., Pich, V., Hofmann, S. G., & Otto, M. W. (in press). Mindfulness and
acceptance techniques as applied to refugee and ethnic minority populations: Examples
from culturally adapted CBT (CA-CBT). Cognitive and Behavioral Practice.
Hinton, D. E., Pich, V., Kredlow, M. A., Bui, E., & Hofmann, S. G. (in press). The relationship
of PTSD to key somatic complaints and cultural syndromes among Cambodian refugees
attending a psychiatric clinic: The Cambodian Somatic Symptom and Syndrome Inventory
(SSI). Transcultural Psychiatry.
Hinton, D. E., Pich, V., Marques, L., Nickerson, A., & Pollack, M. H. (2010). Khyâl attacks:
A key idiom of distress among traumatized Cambodia refugees. Culture, Medicine and
Hinton, D. E., Pich, V., Safren, S. A., Pollack, M. H., & McNally, R. J. (2005). Anxiety
sensitivity in traumatized Cambodian refugees: A discriminant function and factor analytic
investigation. Behaviour Research and Therapy, 43, 1631–1643.
Hinton, D. E., Pich, V., Safren, S. A., Pollack, M. H., & McNally, R. J. (2006). Anxiety
sensitivity among Cambodian refugees with panic disorder: A factor analytic investigation.
Hinton, D. E., Rasmussen, A., Nou, L., Pollack, M. H., & Good, M. J. (2009). Anger, PTSD,
and the nuclear family: A study of Cambodian refugees. Social Science and Medicine, 69,
1387–1394.
Hinton, D. E., Rivera, E., Hofmann, S. G., Barlow, D. H., & Otto, M. W. (2012). Adapting
CBT for traumatized refugees and ethnic minority patients: Examples from culturally
adapted CBT (CA-CBT). Transcultural Psychiatry, 49, 340–365.
Hofmann, S. G. (2008). Cognitive processes during fear acquisition and extinction in animals
and humans: Implications for exposure therapy of anxiety disorders. Clinical Psychology
Review, 28, 199–210.
Hofmann, S. G., Grossman, P., & Hinton, D. E. (2011). Loving-kindness and compassion
meditation: Potential for cognitive behavioral therapy. Clinical Psychology Review, 31,
1126–1132.
Horrel, S. C. (2008). Effectiveness of cognitive-behavioral therapy with adult ethnic minority
clients: A review. Professional Psychology: Research and Practice, 39, 160–168.
Hyman, R., Ortiz, J., Añez, L., Paris, M., & Davidson, L. (2006). Culture and clinical practice
recommendations for working with Puerto Ricans and other Latinos in the United States.
Professional Psychology: Research Practice, 37 , 694–701.
Kashdan, T. B. (2010). Psychological flexibility as a fundamental aspect of health. Clinical
King, A. M., & Sloan, D. M. (Eds.). (2010). Emotion regulation and psychopathology: A
transdiagnostic approach to etiology and treatment. New York, NY: Guilford Press.
Kirmayer, L., & Robbins, J. (1991). Functional somatic syndromes. In L. Kirmayer & J.
Robbins (Eds.), Current concepts of somatization: Research and clinical perspectives (pp.
79–106). Washington, DC: American Psychiatric Press.
Kleinman, A., & Good, B. J. (Eds.). (1985). Culture and depression: Studies in anthropology
and cross-cultural psychiatry of affect and disorder. Berkeley, CA: University of California
Press.
Kok, B. E., & Fredrickson, B. L. (2010). Upward spirals of the heart: Autonomic flexibility, as
indexed by vagal tone, reciprocally and prospectively predicts positive emotions and social
connectedness. Biological Psychology, 85, 432–436.
Kopelowicz, A., Lopez, S. R., Zarate, R., O’Brien, M., Gordon, J., Chang, C., & Gonzalez-
Smith, V. (2006). Expressed emotion and family interactions in Mexican Americans with
schizophrenia. Journal of Nervous and Mental Disease, 194, 330–334.
La Roche, M. (2013). Cultural psychotherapy: Theory, methods and practice. Thousand Oaks,
CA: Sage.
La Roche, M., D’Angelo, E., Gualdron, L., & Leavell, J. (2006). Culturally sensitive guided
imagery for allocentric Latinos: A pilot study. Psychotherapy: Theory, Research, Practice,
Training, 43, 555–560.
La Roche, M., & Lustig, K. (2010). Cultural adaptations: Unpacking the meaning of culture.
Scientific Review of Mental Health Practice, 7 , 26–30.
Lesser, I., Rosales, A., Zisook, S., Gonzalez, C., Flores, D., Trivedi, M., … Epstein, M. (2008).
Depression outcomes of Spanish- and English-speaking Hispanic outpatients in STAR*D.
Psychiatric Services, 59, 1273–1284.
Lester, K., Resick, P. A., Young-Xu, Y., & Artz, C. (2010). Impact of race on early treatment
termination and outcomes in posttraumatic stress disorder treatment. Journal of Consulting
Lewis-Fernández, R., & Diaz, N. (2002). The cultural formulation: A method for
assessing cultural factors affecting the clinical encounter. Psychiatric Quarterly, 73,
271–295.
Lopez, S. R., Ramirez Garcia, J. I., Ullman, J. B., Kopelowicz, A., Jenkins, J., Breitborde,
N. J., & Placencia, P. (2009). Cultural variability in the manifestation of expressed
emotion. Family Process, 48, 179–194.
Maeda, F., & Nathan, J. (1999). Understanding taijin kyofusho through its treatment, Morita
therapy. Journal of Psychosomatic Research, 46, 525–530.
Markowitz, J. C. (2010). IPT and PTSD. Depression and Anxiety, 27 , 879–881.
Miranda, J., Azocar, F., Organista, K. C., Dwyer, E., & Areane, P. (2003). Treatment
of depression among impoverished primary care patients from ethnic minority groups.
Psychiatric Services, 54, 219–225.
Miranda, J., Bernal, G., Lau, A., Kohn, L., Hwang, W. C., & LaFromboise, T. (2005). State of
the science on psychosocial interventions for ethnic minorities. Annual Review of Clinical
Moss-Morris, R., & Wrapson, W. (2003). Representational beliefs about functional somatic
syndromes. In L. Cameron & H. Leventhal (Eds.), The self-regulation of health and illness
behaviour (pp. 119–137). New York, NY: Routledge.
Otto, M. W. (2000). Stories and metaphors in therapy. Cognitive and Behavioral Practice, 7 ,
166–172.
Otto, M. W., & Hinton, D. E. (2006). Modifying exposure-based CBT for Cambodian refugees
with posttraumatic stress disorder. Cognitive and Behavioral Practice, 13, 261–270.
Otto, M. W., Powers, M. B., & Fischmann, D. (2005). Emotional exposure in the treatment
of substance use disorders: Conceptual model, evidence, and future directions. Clinical
Patra, S., & Telles, S. (2009). Positive impact of cyclic meditation on subsequent sleep. Medical
Science Monitor, 15, 375–381.
Resick, P., & Schnicke, M. (1996). Cognitive processing therapy for rape victims. London,
England, and New Delhi, India: Sage.
Roemer, L., Orsillo, S. M., & Salters-Pedneault, K. (2008). Efficacy of an acceptance-based
behavior therapy for generalized anxiety disorder: Evaluation in a randomized controlled
trial. Journal of Consulting and Clinical Psychology, 76, 1083–1089.
Schauer, M., Neuner, F., & Elbert, T. (2005). Narrative exposure therapy: A short term
intervention for traumatic stress disorders after war, terror or torture. Göttingen, Germany:
Hogrefe & Huber.
Silver, S. M., & Wilson, J. P. (1988). Native American healing and purification rituals for war
stress. In J. P. Wilson, Z. Harel, & B. Kahana (Eds.), Human adaptation to extreme stress:
From the Holocaust to Vietnam (pp. 337–356). New York, NY: Plenum.
Snowden, L. (2012). Health and mental health policies’ role in better understanding and
closing African American–White American disparities in treatment access and quality of
care. American Psychologist, 67 , 524–531.
Snowden, L., & Cheung, F. (1993). Use of impatient mental health services by members of
ethnic minority groups. American Psychologist, 45, 347–355.
Sue, D., Ivey, A., & Pedersen, P. (2008). Theories of multicultural counseling and therapy.
Mason, OH: Cengage Learning Press.
Sue, D. W., & Sue, D. (2008). Counseling the culturally diverse: Theory and practice. Hoboken,
NJ: John Wiley & Sons, Inc.
Teasdale, J. D. (1996). Clinically relevant theory: Integrating clinical insight with cognitive
science. In P. M. Salkovskis (Ed.), Frontiers of cogntiive therapy (pp. 26–47). New York,
NY: Guilford Press.
Wald, J., & Taylor, S. (2007). Efficacy of interoceptive exposure therapy combined with
trauma-related exposure therapy for posttraumatic stress disorder: A pilot study. Journal
of Anxiety Disorders, 21, 1050–1060.
Wald, J., & Taylor, S. (2008). Responses to interoceptive exposure in people with posttraumatic
stress disorder (PTSD): A preliminary analysis of induced anxiety reactions and trauma
memories and their relationship to anxiety sensitivity and PTSD symptom severity.
Cognitive Behaviour Therapy, 37 , 90–100.
Wells, A. (2000). Emotional disorder and metacognitions: Innovative cognitive therapy. Chich-
Wilamowska, Z. A., Thompson-Hollands, J., Fairholme, C. P., Ellard, K. K., Farchione, T. J.,
& Barlow, D. H. (2010). Conceptual background, development, and preliminary data
from the unified protocol for transdiagnostic treatment of emotional disorders. Depression
and Anxiety, 27 , 882–890.
Woodhead, E. L., Ivan, I. I., & Emery, E. E. (2012). An exploratory study of inducing positive
expectancies for psychotherapy. Aging and Mental Health, 16, 162–166.
19
Psychosis
Tania Lincoln
University of Hamburg, Germany
Aaron T. Beck
University of Pennsylvania, United States
Introduction
The difficulties faced by patients with psychotic disorders are diverse and complex.
On the one hand, there are the symptoms per se, such as persecutory delusions,
hearing threatening voices, feeling driven, or—if negative symptoms dominate—the
loss of drive and motivation. These tend to go along with distressing emotions,
such as anxiety, anger, or shame, and with concerns related to the meaning or the
consequences of symptoms. The symptoms are also accompanied by an array of
interpersonal problems, such as perceiving others to be untrustworthy, not empathic,
or even alienated and difficult to communicate with.
Moreover, the experience of an acute episode that might involve voluntary or
involuntary hospitalization can be traumatizing. Many patients report a continuous
worry about a possible relapse. The experience of psychosis can leave a person with the
impression that there is something fundamentally wrong with him or her, that he or she
as a person is “somehow defective” or “forever ill” and will never be able to live a nor-
mal life again. Such assumptions are generally accompanied by a sense of hopelessness.
Unfortunately, this hopelessness is often shared by mental health professionals.
Psychotic disorders, in contrast to affective disorders that show similar courses
overall, are more likely to be classified as chronic and are habitually diagnosed
as lifetime disorders. Furthermore, in contrast to other psychological disorders,
schizophrenia tends to be seen as almost exclusively biologically determined. This
view of psychosis provides the basis for a treatment reality that focuses strongly
on medical treatment. The efficacy of pharmacological treatment of schizophrenia
is empirically well supported with small to moderate effect sizes for positive and
negative symptoms in comparison to placebo (Leucht, Arbter, Engel, Kissling, &
Davis, 2009). However, antipsychotic medication has adverse side effects for many

Edited by Stefan G. Hofmann. Volume II edited by Winfried Rief.
DOI: 10.1002/9781118528563.wbcbt19
438 Specific Disorders
and does not help everyone (e.g., the overall number of patients needed to be treated
for one patient to improve relevantly is about six; Leucht et al., 2009), while some
symptoms tend to be treatment resistant. Although most of the patients nevertheless
do not completely disapprove of medical treatment, many would appreciate additional
psychological therapy that takes into account the social and psychological aspects of
their symptomatology. Some case examples demonstrating different problems that
patients present with in therapy are provided in Box 19.1. All case examples in this
chapter stem from an outpatient intervention study (Lincoln et al., 2012) and have
been slightly modified to prevent the possibility of identifying the patient.
Cognitive Behavioral Interventions for Psychotic Symptoms:

A Feasible Approach?
Most of the earlier clinical text books that describe cognitive behavioral interventions
for psychological disorders note that these interventions are contraindicated when
it comes to schizophrenia. For schizophrenia the recommendations, if any, have
been restricted to non-symptom-oriented interventions, such as family interventions
based on improving knowledge of the disorder, problem solving and communica-
tion (Pilling et al., 2002), cognitive remediation (Wykes, Huddy, Cellard, McGurk,
& Czobor, 2011), or combinations of cognitive remediation and skills training
(Roder, Mueller, Mueser, & Brenner, 2006), while there was a concern that targeting
symptoms directly was likely to make matters worse. At the root of this concern
was the assumption that psychotic symptoms such as delusions or hallucinations
are qualitatively different from normal experiences, are purely biologically deter-
mined, and are therefore not amenable to reason or normal mechanisms of learning.
Indeed, the concern that delusions might even deteriorate when discussed with the
patient remains widespread. Meanwhile, the idea that there is a qualitative differ-
ence between delusional and normal beliefs and between hallucinations and normal
perceptions has been strongly questioned by epidemiological studies that find high
rates of delusion-like beliefs and hallucinations in healthy populations (McGovern
& Turkington, 2001; van Os, Linscott, Myin-Germeys, Delespaul, & Krabbendam,
2009). For example, in a survey with a representative population sample in Germany
(Lincoln, Keller, & Rief, 2009) a quarter of the participants indicated that they
had the impression that others are trying consciously to harm them at least occa-
sionally. A similar proportion indicated that they at least occasionally believe that
they have to fulfill a special mission in life. About 7% said they were, at least
occasionally, convinced they were being persecuted, 10% knew from their own expe-
rience the phenomenon that thoughts could get so loud that others could hear
them, and 35% confessed to believing in telepathic communication. As in other
studies (Freeman, 2006), prevalence rates of the “symptoms” considered to be
typical for psychosis range from about 5% up to 30% in the general population,
depending on which phenomenon is regarded and how exactly the question is
phrased. Although only a small proportion of these delusion-like beliefs qualifies
as clinically relevant, such research demonstrates impressively that it is difficult to
Psychosis 439
Box 19.1 Case examples: Reasons for coming into treatment

Andreas, 25, student
Andreas sought outpatient psychotherapy after being in hospital with his fourth
psychotic episode. Inpatient psychiatric treatment had considerably decreased
his acute psychotic symptoms. However, he still reported low mood, lack of
drive, and feelings of insecurity. He felt incapable at present of picking up the
pieces of life he had left behind and pursuing his studies. He hoped therapy
would support him in achieving this. Furthermore, Andreas reported that he was
constantly worrying about relapsing. Despite all of his efforts and the massive
support provided by his parents he had not been able to prevent relapse so far
and he hoped that therapy would help him to “get a grip” on his psychosis.
Evelyn, 52, retired early, used to be a freelancer in the field of gastronomy

Evelyn sought treatment in our outpatient unit without explicitly registering
for the psychosis unit. She described problems with her family, her colleagues,
and advisors in different psychosocial institutions. She reported having been
harassed, taken advantage of, betrayed, and laughed at by them. The disrespect
and maltreatment by her family members was getting to her in a way that she
felt she could no longer endure. As a consequence she had moved from the
town she had been living in with them. Evelyn had received counseling once
before and had found it helpful to have someone to open up to. She hoped that
therapy would help to stabilize her mood. She also reported that the diagnosis
“schizophrenia” in the report issued by her general practitioner made her angry
as she felt that it did not apply to her. She also refused to take the medication
he had prescribed.
Johanna, 26, student

Johanna perceived her neighbors from the flat next door to be abusing her. She
could hear them discussing her in the night which caused her to lie awake in
bed feeling tense and anxious. She also felt distressed because she kept hearing
people on the street talking badly about her. She experienced this as extremely
distressing and felt that it was interfering with her academic achievements
at university. According to her medical report, she had developed paranoid
schizophrenia a few years back. She acknowledged this and reported being afraid
that all the stress she was having with the neighbors might cause a new episode.
draw a clear borderline even for the core psychotic symptoms such as delusions
and hallucinations. The assumption of a continuum between normal and psychotic
experiences indicates that normal reasoning could be involved in the formation
and maintenance of delusional beliefs and has therefore been one of the main
prerequisites for the systematic development of cognitive behavioral therapy (CBT)
for schizophrenia.
A further supposition for cognitive interventions is provided by findings from

fundamental research on cognitive and emotional correlates of psychotic symptoms,
which have been integrated into cognitive models. One of the most influential
early models in this area, proposed by Garety et al. (2001), explains the devel-
opment and maintenance of positive symptoms. This model develops existing
vulnerability–stress models of psychosis (Nuechterlein & Dawson, 1984; Zubin
& Spring, 1977) and postulates that psychotic symptoms evolve when life events
or daily stressors lead to an overload in a vulnerable person, causing this person
to have unusual experiences, such as increased arousal, bodily sensations, or hal-
lucinations. According to this model, it is not the unusual experience itself that
is the key point but the dysfunctional appraisal by the patient of the experience.
For example, patients might not see acoustic hallucinations as a result of increased
stress exposure, but attribute them to external factors. The appraisal is assumed to
be influenced by the emotional condition of the person on the one hand and by
cognitive biases that have been shown to be associated with delusions on the other
hand. The findings on which these models are based indicate that normal mecha-
nisms of perception and reasoning could be involved in delusional interpretations
and patients with psychosis might thus be susceptible to adaptations of a cognitive
approach.
The Prominent Techniques
CBT for psychotic symptoms has been adapted from cognitive therapy, originally
developed by A. T. Beck for depression and then broadened and adapted to numer-
ous other disorders in the course of the last 30 years (Beck, 2005). In CBT
for psychosis an important focus is on the development of a stable therapeutic
relationship as well as on the development of individual explanation models. Dis-
tressing symptoms are conceptualized as a part of a chain of preceding and resulting
thoughts and feelings. Core cognitions may be the delusional beliefs per se, thoughts
about the symptoms, or thoughts related to the self or other persons. Essentially,
the therapy consists of building a relationship, developing a shared understanding
of how symptoms might have arisen and are being maintained, using cognitive
interventions for working with psychotic symptoms as well as for changing dysfunc-
tional assumptions about the self and other persons, and interventions to prevent
relapse.
The following descriptions and illustrations of the intervention used for pos-
itive symptoms are based on manuals of the leading British researchers in this
area (Chadwick, Birchwood, & Trower, 1996; Fowler, Garety, & Kuipers, 1995;
Kingdon & Turkington, 2004; Morrison, Renton, Dunn, Williams, & Bentall,
2004), a German treatment manual (Lincoln, 2006), and clinical experience. Due
to space limitations the descriptions and case examples have been slightly simplified
and restricted to their central points.
Psychosis 441
Building a Stable Relationship
The essence of establishing a stable relationship is listening to the patient and

attempting to understand. Thus, the therapist strives to see the world through the
eyes of the patient and thereby to understand how symptoms developed, regardless of
how bizarre or unreasonable some beliefs might seem at first. In attempting to build
rapport, a normalizing approach is taken. The therapist does this by emphasizing
that symptoms occur frequently in many people and can be considered as fairly
normal (e.g., “Hearing voices does not necessarily mean you are crazy, because a
substantial number of healthy people report hearing voices and still lead a normal
life”). Furthermore, the therapist conveys understanding and empathy toward the
reactions and feelings that arise from the symptoms (e.g., “I can understand that you
were really scared when you got the impression that the persecutors had surrounded
your house and that you felt you needed to withdraw or hide”). Patients are far more
likely to scrutinize their interpretations in the ongoing therapy if they feel validated
and understood at the beginning of it. As depicted in the case example of Evelyn (see
Box 19.2), if the therapist engages in a questioning role too early, he or she runs the
risk of pushing the patient into a defensive role and thereby possibly even reinforcing
the delusional conviction. Another important aim in the first part of therapy is to
convey hope for recovery and thereby enhance the patient’s motivation to engage
actively in promoting change.
Box 19.2 Building rapport with Evelyn

Evelyn’s extremely hostile depictions of her family members enticed her therapist
to begin questioning some of her delusional assumptions at a very early point
(e.g., “Could another explanation for the behavior of your brother exist,
other than him wanting to get rid of you?”). Evelyn reacted very sensitively
to such questioning and adopted a defensive position immediately, which
also manifested in a louder tone of voice (e.g., “No, I am sure that he
wanted to get rid of me. Why else should he have behaved like that?”).
After this incident the therapist refrained from further questioning of delusions
in this phase of therapy and focused again on building rapport by taking
an understanding-based position. Herein, it was additionally helpful that the
therapist anticipated some of Evelyn’s concerns related to therapy (e.g., “Do you
have the concern about me, as well, that I will not take you seriously or may pass
information on to others?”) and therefore demonstrated her understanding.
The therapeutic relationship was strengthened notably by talking about the
interpersonal conflicts that formed the basis of the delusions and arose from
them, because in this way the therapist found it much easier to validate Evelyn’s
emotional experiences.
Developing and Working with Formulations
Another part of therapy is the development of an explanatory formulation which

refers to psychological mechanisms that explain how symptoms might have arisen
and are maintained. In doing so, the models derived from basic research or aspects
of these models are linked to patient information. These models constitute working
models that hold plausible alternative explanations of experiences for the patient
and build a foundation for an individualized problem-oriented approach in therapy.
Figure 19.1 illustrates a prototype model including an application example, which
postulates psychological mechanisms for the explanation of anxiety and suspiciousness
leading up to persecutory delusions.
Immediate stressors Interaction of genetic and early environmental factors

Frank: taking on his father’s firm, Frank: shy, grandfather with psychosis, parents both died
arguing with his sister about it when Frank was an adolescent, occasionally bullied in
school
Feeling exhausted and worried

Negative beliefs about self and others
Anomalous experiences
Frank: feels low in social rank, vulnerable to
Frank: unexplained physical somatic illness
symptoms, such as swollen feet,
aches
Reasoning biases (jumping to conclusions, personalized

attributions, difficulties in taking perspective of others)
Frank: “Something might be wrong with the coffee I’m
drinking,” “The machine needs cleaning,” “Maybe they left it
dirty on purpose,” “They don’t care about me,” “Maybe they
even want to get rid of me.”
Negative reactions to other

Selective attention Anxiety, suspicion, persons and social withdrawal—
to threat paranoid thoughts, lack of corrective feedback
later: persecutory
delusions Frank: stops going out with
Frank: watching for
colleagues, keeps distance from
signs that his sister
sister
is hostile toward
him, selective
attention to
physical symptoms Avoidance and safety behavior
Frank: stops drinking coffee from the
shared machine
Figure 19.1 Individual formulation for persecutory delusions. This model draws on the
cognitive model of persecutory delusions outlined by Freeman, Garety, Kuipers, Fowler, &
Bebbington (2002), but is modified to fit Frank’s case.
Psychosis 443
Interventions for Auditory Hallucinations
Basically, therapeutic strategies for hallucinations aim at reducing the feeling of not
being able to control hallucinations and challenge dysfunctional appraisals of the hal-
lucination. All of the described approaches act on the assumption that hallucinations
appear in a certain context, which is characterized by emotional, cognitive, physio-
logical, and behavioral factors within the patient or the environment. One group of
interventions targets the behavior that follows from the voice and aims at enhancing
the specific exertion of coping strategies (Tarrier et al., 1993). Patients are guided
to write baseline reports about the voices, their volume and duration, as well as their
reaction to the voices. In doing this, existing as well as new coping strategies, such as
social communication, relaxation, music, and withdrawal, are evaluated in regard to
the influence they have on frequency and duration of the hallucination as well as the
distress caused by it. The aim is to adopt the strategies that prove to be the most helpful.
Another approach, the so-called metacognitive approach (Chadwick & Birchwood,
1994), challenges the appraisals of hallucinations. Such appraisals can either be
catastrophizing (e.g., “Hearing voices means that I am crazy, need to go to hospital,
and will never live a normal life again”) or delusional (“Hearing voices means that
aliens must have implanted a chip, that the neighbors are talking to me through the
walls to frighten me”). Figure 19.2 illustrates how such catastrophizing or delusional
appraisals lead to further arousal and tension and thereby to the subsistence of voices.
In response to catastrophizing interpretations of voices, Chadwick et al. (1996)
suggest using normalizing techniques and enlightening patients about the fact that
healthy persons can hear voices occasionally without being classified as ill or crazy.
Some interesting web sites now provide numerous examples of how voice hearers
cope with their voices (e.g., www.intervoiceonline.org) and can be used to underline
the normalizing approach. In this context, it is also helpful to explain that generally
perceptions are a construction of the environment which does not necessarily match
the exact facts but is affected by expectation effects. For this, examples from the
genre of optical illusions can be useful since they illustrate that misperceptions are
Stress Stress
Hearing voices that Hearing voices that

others do not hear others do not hear
“I have gone mad.” “Something’s going on.”
“My life has been ruined.” “The others are not telling
Arousal Arousal me the truth.”
social withdrawal “Better not tell anyone social withdrawal “Others are conspiring
about the voices.” against me.”
Figure 19.2 Cognitive formulations for the development and maintenance of voices by
catastrophizing (top) and delusional (bottom) interpretations. Used with permission from Dr.
Alison Brabban.
part of a natural physiological process in many situations. As further emotionally

stressing appraisals of hallucinations, Chadwick and colleagues describe omniscience
and omnipotence appraisals as well as dysfunctional compliance beliefs. Persons with
omniscience beliefs are convinced that their voices know everything about their
thoughts, behavior, fears, and experiences. Persons with omnipotence beliefs perceive
their voices to be almighty and to be exerting power over them. Dysfunctional
compliance beliefs become evident in the concern about being punished if one does
not do as the voice commands. The modification of such beliefs basically relies on
common methods of cognitive restructuring. The therapist questions the beliefs using
gentle and empathic Socratic questioning (e.g., “What is the evidence that your voice
has power over you? Is there anything that seems to question the power of your
voices?”) and guided discovery (e.g., “You told me last week that you did not respond
to your voice during your conversation with Caren and that this helped you to
concentrate better on what she was saying. What do you make of that in terms of the
power of your voice?”). Furthermore, the implementation of behavioral experiments
can be helpful. For example, the belief that the voice is uncontrollable and unswayable
may be challenged by an exercise in which the patient discovers that he or she can
suppress the voice by reading out loud or talking. Group settings have been suggested
because sharing the experiences with others can be relieving and provides patients
with a variety of different appraisals of voices which can help patients to question their
own beliefs (Chadwick, Sambrooke, Rasch, & Davies, 2000). The aim of all these
cognitive interventions for hallucinations is for the patient to adopt a more functional
appraisal of the voices and thereby breach the vicious circle (compare Table 19.1).
Box 19.3 describes a case of working with voices.
Working with Delusions
Working with delusional beliefs can be indicated once the delusion leads to severe
distress or is accompanied by potential harm to the self or others. It is essential to
prepare the work on delusions thoroughly. Most importantly, and as described in the
section entitled “Building a Stable Relationship,” an important premise is that the
therapist is able to understand how and why the delusions developed from their onset
onward and how they are linked to the patient’s background. Often, the beginnings
Table 19.1 Result of a Successful ABC Model in Dealing with Voices
Event Thoughts Feelings
“That’s a result of all the stress I’ve been through

lately.”
Hearing voices that “People who are not considered ‘crazy’ also Relief
others do not hear sometimes hear voices and live a normal life.”
“I can regain control of my life.”
Note. Adapted from Lincoln, Hohenhaus, & Hartmann (2013).

Psychosis 445
Box 19.3 Working with auditory hallucinations with Johanna

To reduce the strain caused by auditory hallucinations, Johanna’s therapist
began by supporting Johanna to use coping strategies in a more systematic
manner. To set out, they used self-monitoring reports in which Johanna noted
the appearance of hallucinations, the subjective sense of distress associated with
them, and the coping strategies she was employing. By keeping a record of
the precipitating events it became evident that Johanna’s voices occurred most
frequently when she was worrying about her upcoming exams and ruminating
over the exhausting internship in which she was currently enrolled. The protocols
also demonstrated that not all of the coping strategies she was currently using
were being helpful on a longer-term basis. For example, in order to cope with
voices that were bothering her in the evening and the resulting difficulties
in falling asleep Johanna often drank several glasses of wine. To escape from
the voices on the street she withdrew into her room and listened to loud
music. Johanna identified the “drinking wine” strategy to be unhelpful, since
it was only effective in the short term and she often felt hung over in the
morning. Similarly, she identified social withdrawal as not helpful, because it
was accompanied by mood deterioration. She tested out several new strategies,
of which two (“talking to room-mates” and “distraction through chores or
learning”) turned out to be more helpful, leading to reductions in distress and
volume of voices. However, Johanna’s conviction that a conspiracy against her
was in progress made it difficult for her to adopt the new strategies, specially the
strategy of talking to room-mates, and caused an increase in focus on the voices.
As a consequence, the therapist then began to intensify the work on delusions
and delusional appraisals of the hallucinations.
Box 19.4 The beginning of delusion development in Evelyn

Evelyn developed the idea that other family members were conspiring against
her in a phase that was characterized by intense family conflicts. One day, she
came back home and overheard her brother talking to her mother on the phone,
mentioning her name. The first thought that occurred to her was that they were
probably saying something negative about her.
of a delusion development are easier to follow and validate than the final complex
conspiracy system that the patients present. A case example of how delusions can
begin to develop is presented in Box 19.4.
Another step in preparing to challenge delusional beliefs is to clarify the motivational
base for the modification of the delusions. At this point the therapist refrains
from discussing the evidence for or against the delusion but rather treats it as a
hypothesis that can be correct, noncorrect, or partly correct. The therapist and patient
collaboratively explore the positive and negative consequences that holding on to or

giving up the delusional beliefs might have. From the point of view of the patient, two
options are particularly relevant. First, there is the option of giving up the belief (e.g.,
if Evelyn adopts the belief that she was only stressed and feeling insecure and therefore
misinterpreted the behavior of other family members as a conspiracy) even though
it is actually consistent with the truth (e.g., the family members are indeed talking
about her in a negative way and planning how to get rid of her). In this case—and
this is the fear many patients have—the patient would run the risk of trusting others
mistakenly and becoming a naive victim. Alternatively, the patient could make the
mistake of holding on to the delusional belief even though, when viewed objectively,
it is unsubstantiated. In this case, he or she would risk investing time and effort
(e.g., moving town, giving up social contacts, etc.) for a false conviction. Moreover,
he or she would miss the chance to take care sufficiently about other important
areas in life, such as doing or obtaining meaningful work or seeking professional
help.
Identifying possible consequences of abandoning or sticking with the delusional
belief is not only relevant in order to enhance the motivation to change. It also helps
the therapist to gain a clearer picture of the function that the delusions might be
serving and the reasons a patient might not (yet) be ready to question the validity
of his or her beliefs. Even though there is no scientific evidence as yet to show
that working with delusions can have possible adverse effects, the restructuring of
delusions hardly seems promising if there is little to gain for the patient but a lot to be
lost. This might be especially likely for delusions of grandeur. Other patients might
find it difficult to let go of a delusional belief because they believe that confessing
to having been mistaken is equal to confessing to being crazy and needing help. To
address this concern, the therapist discusses the normal mechanisms of how opinions
are formed by using examples such as religious or political beliefs, which make clear
that it is normal to adhere to opinions with strong conviction and not to abandon
them even though evidence may be lacking. A case example of this is provided in
Box 19.5.
Once a sufficient motivational basis has been established, the therapist can proceed
to a more direct questioning of delusional appraisals. One way of doing this is by
collecting alternative explanations and assessing the impact that these explanations
have on the strength of the belief. Furthermore, the therapist can encourage the
patient to collect falsifying information in similar situations in the future or use
role-play techniques in which the patient is encouraged to engage in the role of a
“contra-part” and question his or her beliefs. In order to visualize the impact that
dysfunctional and functional interpretations of events have on feelings and actions,
the therapist can use the ABC model of cognitive therapy. In working with delusional
beliefs it is advisable to begin with a belief that is recent and less determined. A case
example of working with delusional beliefs is provided in Box 19.6.
Meanwhile, as an alternative to the classic cognitive approach that focuses directly
on the delusional belief and attempts to modify it, several more recent develop-
ments focus on metacognitive beliefs that patients may have in regard to their
delusional beliefs, and on styles of information processing, such as reasoning
biases and attention to thoughts, as well as on preoccupation with the delusion.
Psychosis 447
Box 19.5 Preparing for the questioning of delusions in

Wolfgang
Wolfgang showed up at one therapy session feeling insecure about attending
a planned weekend trip with an acquaintance. He had thought about this
acquaintance and concluded that the acquaintance worked as a secret agent for
the government and was planning to spy on him. Wolfgang was also convinced
that his acquaintance had the power to put him back into a psychiatric hospital
against his will. The therapist used a fourfold table to support Wolfgang in
considering the consequences of this belief (see Table 19.2). The negative con-
sequences of mistakenly assuming the hypothesis to be correct (“Acquaintance
is a secret agent”) became very obvious, especially once Wolfgang figured out
that in this case, he could hardly satisfy his need for social contacts. He therefore
decided to go on the weekend trip and was able to note positive implications of
the activity on his mood. Although the intervention in itself did not result in
a strong reduction of delusion conviction (he remained careful and distrustful
even on the trip), it helped Wolfgang to consider the alternative hypothesis and
see his own belief as a hypothesis rather than a fact and thereby provided the
basis for further questioning of delusional beliefs.
Table 19.2 Result of Using the Fourfold Scheme with Wolfgang
Reality: Reality:
Acquaintance is a spy Acquaintance is trustworthy
Hypothesis: • “I would lose a potential

Acquaintance is friend.”
trustworthy • “I will remain lonely.”
• “I will miss a nice day out.”
• “I will miss the opportunity
to meet other people.”
• “I will be sad sitting at
home.”
Hypothesis: • “He would be spying on me
Acquaintance is a without me realizing.”
spy • “He could make sure I get
put back in hospital.”
• “I won’t be able to protect
myself.”
• “I am not in control.”
Note. Adapted from T. M. Lincoln (2012), Ambulante KVT bei psychotischen Störungen. In
Stavemann (Hrsg.), KVT update. Neue Entwicklungen und Behandlungsansätze in der Kognitiven
Verhaltenstherapie, S179–200. Weinheim, Germany: Beltz Verlag.
Box 19.6 Working with delusional beliefs with Tom

THERAPIST: Tom, you described that you were feeling anxious on the bus
yesterday when you felt that several people were looking at you. You were
thinking that these people might be Scientologists and out there to keep an eye
on you. In the previous sessions we have already talked about why you are
susceptible to believing that Scientologists are after you. Does it seem plausible
that somebody else who has had less negative experiences with Scientology
would have felt and thought differently from you in the same situation?
TOM: Yes, possibly. My friend might have just been annoyed about the bus being
so crowded and would not have noticed people staring. But then, he’s not being
followed by them, is he?
THERAPIST: How would he have been feeling then?
TOM: Different, well, normal. Might have been a bit angry about the bus being
full.
THERAPIST: Is it OK with you if we have a closer look at the evidence for and
against your assumption that you are being spied on by Scientologists and that
they were on that bus with you?
TOM: Yes, OK.
THERAPIST: Just to begin with, how convinced are you right now that
Scientologists were there and spying on you on that bus? Can you indicate how
convinced you were on a scale from 1 to 100%?
TOM: Well, at least 80%.
THERAPIST: OK, let’s note all the pieces of evidence you have that support your
assumption. And maybe there are also some facts that do not support it and we
can note those as well, on another piece of paper. Is that OK with you?
TOM: Yes, that’s fine.
THERAPIST: OK, what evidence is there that Scientologists were spying on you in
the bus?
TOM: Well, basically the fact that people in the bus were all staring at me.
THERAPIST: Were they all staring at you or only some of them?
TOM: Well, maybe not all of them, but many of them.
THERAPIST: Could you describe some of the people who you noticed staring at
you?
TOM: Well, I didn’t even really look at them that closely. I was just scared.
THERAPIST: I can imagine that. It’s not nice to feel stared at by people you don’t
know. I would also find it rather worrying. I wonder, though, whether it’s
possible that you were feeling so distressed that you did not get the chance to
actually check how many of the other passengers were really staring at you or if
they were staring at you at all.
TOM: I suppose that’s possible. I was looking at the floor most of the time,
although I’m positive that at least one man looked right at me when I came in.
THERAPIST: Is it OK with you if we note, then, that the evidence for the
hypothesis that Scientologists were after you in the bus is that you felt that
several people were staring at you but it could have been just one?
TOM: Yes, OK.
Psychosis 449
THERAPIST: Can you think of further evidence for the belief that you were being
spied on by Scientologists in the bus?
(The therapist and Tom collect and note further evidence.)
THERAPIST: If you now look at the paper with the evidence do you think it is
complete or is there anything we should add?
TOM: No, I think that’s all.
THERAPIST: Well, maybe if you take it home with you, you might still come up
with some further evidence. Meanwhile, I’d like to collect some facts with you
that might speak against the beliefs that you were being spied on by
Scientologists on the bus. Can you think of any?
TOM: Well, sometimes my mum says that I am just imagining it all, and that it is
all just psychosis.
THERAPIST: What do you think your mother means when she says that? Do you
think she means that you are being hyper careful because you are already
convinced that something is going on and that therefore you might be seeing
things where there is really nothing?
TOM: Yes, that’s possible. Once, when I began to think that Scientologists were
on a bus I noticed more and more people who looked strange or suspect to me
and that made me really frightened.
THERAPIST: OK, so can we note: “I tend to be quick to interpret things as a
threat”?
TOM: Yes, note that. Although that doesn’t necessarily mean that there is no
threat.
THERAPIST: No, I agree with you. What about alternative explanations? Are there
any other reasons that people might look at you on a bus other than them being
Scientologists?
(The therapist and Tom continue to collect evidence against the belief and the
therapist then assesses the strength of the conviction in the belief which is now
at 65%.)
THERAPIST: Although you still think it’s likely that there were people on the bus
that were spying on you and that these people were Scientologists it seems that
you are slightly less convinced of this than at the beginning. Right?
TOM: Yes, I think that thinking about other reasons why people might have
looked at me was helpful. I certainly do not feel so sure any more that the
bus was full of Scientologists, though of course there might well have been
some.
One of these approaches is the metacognitive training developed by Moritz and

Woodward (2007). Herein, patients are trained to modify their cognitive processing
styles; for example, to draw less hasty conclusions or to conduct a more balanced
attribution for causes in distressing and ambiguous situations. Other metacognitive
approaches identify and work on thoughts about the symptoms that tend to be
associated with the presence of delusional beliefs (e.g., “better to be distrustful than
naive” or “because of my paranoia, I am on the safe side”) and are hypothesized to
be a maintaining factor (Morrison, French, & Wells, 2007).
Working on Dysfunctional Self-Related Schemas
Numerous studies now suggest that delusional symptoms are associated with a
negative appraisal of the self and other persons (Kesting & Lincoln, in press). Persons
with delusions ascribe more negative attributes to themselves and see themselves as
inferior, lower in the social hierarchy, less respected, and less accepted in comparison
to other people. Also, several studies have shown that the self-esteem of persons with
delusions is unstable, with decreases in self-esteem being preceded by increases in
delusional interpretations (Thewissen, Bentall, Lecomte, van Os, & Myin-Germeys,
2008; Thewissen et al., 2007). As a consequence of low self-esteem and high
levels of suspiciousness, patients with delusions tend to withdraw from people and
experience sparse positive social reinforcement. Thus, working on improving self-
esteem, self-acceptance, and acceptance of others is a vital aspect of therapy. Life
charts and downward arrow techniques are used to assess core assumptions and the
circumstances that have been feeding them. In the next step, these beliefs are linked
to the delusional beliefs or the content of distressing voices. The aim of therapy is
to get patients to question and abandon these beliefs. This is achieved by disputing
these assumptions by Socratic dialogue techniques, reality testing, and discussing the
implications of the beliefs. Because patients with psychosis often have difficulties in
describing their emotions, it can be helpful to work with specific life experiences and
imagery. In our work we found that schema therapy approaches (Young, Klosko,
& Weishaar, 2003) or techniques from compassion-focused therapy (Gilbert, 2010)
can be very useful. However, evaluation of such approaches for psychotic disorders is
needed. Finally, in order to achieve a stable growth in self-esteem and self-acceptance,
it is necessary to motivate patients to reengage in social interactions and support them
in finding meaningful work. A case example of working with self-esteem is presented
in Box 19.7.
Relapse Prevention
One aim of relapse prevention is to prepare patients to recognize early signs of

relapse and respond to these signs. The therapist and patient collaboratively review
the times leading up to previously experienced psychotic episodes. This involves
a fairly accurate reconstruction of events, thoughts, and feelings occurring prior
to previous psychotic episodes. It is helpful to use calendars or diaries, and note
important markers, such as birthdays, travel, parties, having visitors, and so on, that
the patient can remember. As patients sometimes find it difficult to reconstruct these
periods in their memory, it can be helpful to encourage them to involve friends
or relatives in the search for significant changes and signals. In the next step the
therapist gently probes for the more subtle experiences, thoughts, and feelings.
Although this kind of reconstruction can be time-consuming, it is an extremely
helpful way of increasing the patients’ awareness of individual risk factors, early
signals, and the development of symptoms. Patients are then encouraged to use this
knowledge to recognize the signals and apply the therapeutic strategies (e.g., “I know
Psychosis 451
Box 19.7 Self-esteem focused interventions with Andreas

The therapist used imagery work that focused on childhood memories to help
Andreas to understand from where the feelings of helplessness and inferiority
arise. In the imagery exercises Andreas imagined scenes in which his father was
looking down on him, shouting and threatening to beat him up. In doing so,
Andreas was able to describe the anxiety and feelings of defenselessness that
went along with these types of experiences he had had with his father. Andreas
realized that the extreme fear of others he experienced in his psychotic phases,
as well as the fact that he generally is easily intimidated by other people, might
originate in the feelings of helplessness toward the outbursts of his father. In
therapy, the self-schema of the “defenseless boy” could be revised to concord
with many current experiences and a more functional self-schema could be
established. In the end, Andreas was able to verbalize the fact that he is now
a grown-up, taller in fact than his father, and able to stick up for himself. He
began to feel more confident about being able to stand up to his father in future
disagreements as well as to other persons if they crossed his boundaries. In order
to further strengthen his sense of being able to defend himself he also took up
more sports and enrolled in a karate course.
that when I am very stressed in my academic studies and several papers are due
simultaneously, I tend to hear my name or to easily get the impression that other
people are talking about me behind my back. Therefore, in such situations when
I get the impression that other people are whispering about me, I remember that
this is probably a stress symptom and it could be helpful to take things easier for a
while”).
At the same time, it is crucial to reduce catastrophic appraisals of relapse, which
are easily triggered by the awareness of early signals (e.g., “I am sleeping poorly, this
means I am going to relapse”) and are likely to increase anxiety, thereby rendering
relapse more, rather than less, likely. The manual Staying Well After Psychosis (Gumley
& Schwannauer, 2006) offers many valuable insights into the mechanisms of relapse
and its prevention. A case example of relapse prevention is provided in Box 19.8.
The Empirical Evidence
The first description of a cognitive approach to delusions was provided by Beck

(1952) in a case study. Since then, the bulk of intervention studies have been
conducted in the United Kingdom, driven by various research groups (Kuipers et al.,
1998; Tarrier, 1998; Turkington, Kingdon, & Turner, 2002). Today, the efficacy
of cognitive behavioral interventions has been demonstrated in approximately 30
intervention trials of differing quality and focus. These trials typically compare CBT
for psychosis in combination with medication to medication alone (treatment as
usual) or to medication in combination with another psychological intervention
Box 19.8 Relapse prevention with Andreas

Andreas and the therapist determined the preconditions, thoughts, feelings,
and reactions that occurred prior to several previous psychotic episodes. In
addition to his own recapitulation of events, Andreas also questioned his friends
and parents about what they remembered from the times preceding his last
psychotic episode.
According to the detailed picture that could be gained with regard to triggers,
early warning signs, and first symptoms, Andreas and the therapist were able
to identify some similarities in the time prior to the episodes. For example, it
became evident that distressing life circumstances (e.g., many exams coming
up, relationship conflicts) tended to have a triggering effect for Andreas. Also,
Andreas discovered that his tendency to attach greater importance to minor
things (e.g., interpreting things as special cues) might be a warning signal or
an early symptom. Talking about these phases was also helpful in identifying
some responses to stress that had helped Andreas in the past, such as relaxing
activities and meeting friends that he had known for a long time and felt safe
with, and strategies that had turned out to be unhelpful or even increased
tensions and arousal, such as certain complicated social relationships. Andreas
then noted these “early warning signals” as well as a number of helpful strategies
for handling these. He involved his closest friends by giving them advice about
what types of support he would prefer should a new episode occur. This also
included the permission to contact his doctor.
(e.g., psychoeducation) or placebo intervention (e.g., befriending). A representative

example of one of the first randomized controlled trials is presented in Box 19.9.
Most of the interventions have been directed to patients with medication-resistant
positive symptoms who were treated in outpatient settings. However, trials have also
produced promising results for inpatients in the acute phase of psychosis (Bechdolf,
Köhn, Knost, Pukrop, & Klosterkötter, 2005; Drury, Birchwood, Cochrane, &
Macmillan, 1996; Lewis et al., 2002; Startup, Jackson, & Bendix, 2004) and for
patients with prodromal symptoms of psychosis (Morrison, French, et al., 2004).
These pioneer studies have been followed by some larger-scale multicenter studies
that have received better funding and could therefore be conducted with more
methodological rigor. In Germany a large multicenter efficacy study (called “Positive-
Studie”) (Klingberg et al., 2011) has just been completed successfully. In this
study, CBT was demonstrated to be superior to supportive therapy in reducing
positive symptoms in patients with persistent positive symptoms. Another rigorous
multicenter trial (Garety et al., 2001) did not produce positive results for CBT in
reducing relapse and improving symptoms in patients who had previously relapsed,
which raises the question whether CBT is equally suited for all patient populations.
Several meta-analyses have been conducted to integrate the findings from the
randomized controlled trials of cognitive therapy for psychosis. The first meta-
analysis by Rector and Beck (2001) analyzed the effects from seven randomized
Psychosis 453
Box 19.9 The London–East Anglia Randomized Controlled

Trial of CBT for Psychosis (Kuipers et al., 1997)
In this trial the group around Philippa Garety and Elizabeth Kuipers compared
CBT for psychosis to treatment as usual (TAU) in 60 participants who were
experiencing at least one stable positive symptom that was distressing and had
not improved during the previous 6 months. In order to recruit this sample,
they screened 152 patients who had been referred by community teams and
from inpatient settings. The majority of these had to be excluded because they
had no distressing positive symptom (47), were not on stable medication (10),
lived too far away (26), or refused to participate (9). The remaining sample
of 60 patients were diagnosed with schizophrenia (39), schizoaffective disorder
(2), delusional disorder (13), or other psychotic disorders (6), and had been
living with this condition for 13 years on average.
Patients were assessed at baseline, at intermediate time-points (3 months and
6 months), at the end of treatment at 9 months, and at 18-month follow-up.
The outcome measures included—among others—the Brief Psychiatric Rating
Scale, the Present State Examination, and Beck’s Depression, Anxiety, and
Hopelessness Scales and were rated by persons who were not involved in the
trial but were not blind to the treatment conditions.
Treatment consisted of the CBT interventions as described above and was
conducted by experienced clinicians who were receiving supervision from col-
leagues. TAU consisted of medication and case management. Patients received
15 sessions of CBT overall on a weekly basis at first, followed by one session
every 2 weeks. However, the number of sessions each patient received varied
considerably, with some patients receiving as many as 50 sessions. Doctors were
asked to keep medication stable during the time of the trial and any changes
were protocolled.
In the CBT group, 14% dropped out during treatment, most of them at
the beginning. In the TAU group 22% dropped out. By posttreatment the
score on the Brief Psychiatric Rating Scale was reduced by a significantly larger
amount in the CBT group compared to the control group. Fifty percent of
the CBT sample demonstrated reliable improvement, with changes being most
prominent for suspiciousness, delusions, and hallucinations. More increases in
medication were documented for the TAU compared to the CBT group. There
were no significant changes on any of the other measures employed, however.
At 18 months, 65% of the CBT group had improved reliably and significant
differences between the groups in favor of CBT could be demonstrated for
delusion distress, preoccupation, and conviction. In addition, the CBT group
spent fewer days in hospital in the course of the intervention (15 days) in
comparison to the TAU group (26 days).
Threats to the validity of the study might be seen in the lack of blind
assessors, the fact that medication could not be kept entirely stable, and the
fact that treatment duration varied considerably between the patients. However,
there was no indication that longer treatments produced better results.
controlled trials and effect sizes were calculated for the comparison of CBT to
supportive therapy, revealing a high effect size of d = 0.91 in favor of CBT.
However, later meta-analyses that included larger numbers of studies and used
different methodology slightly dampened the initial optimism by finding small to
medium overall effect sizes (Jones, Cormac, Silveira da Mota Neto, & Campbell,
2004; Lincoln, Suttner, & Nestoriuc, 2008; Pilling et al., 2002; Wykes, Steel,
Everitt, & Tarrier, 2008; Zimmermann, Favrod, Trieu, & Pomini, 2005). The meta-
analysis by Wykes et al. (2008) also found that the methodological rigor of the
studies impacted on the results. In particular, studies that used blind raters to assess
symptoms were characterized by lower effect sizes. The meta-analysis conducted by
Lincoln et al. (2008) used a moderator analysis to investigate whether interventions
that relied more heavily on cognitive elements, such as working with a cognitive
model, cognitive restructuring of delusions and dysfunctional self-concepts, cognitive
symptom-monitoring, and metacognitive approaches, were more effective than those
using fewer cognitive elements. In this analysis, the mean weighted pre-post effect sizes
for the overall symptomatology was significantly correlated with a cognitive emphasis
in the interventions (r = .75, p ≤ .001, k = 18), indicating that interventions with a
stronger cognitive focus were more effective.
Furthermore, several studies have investigated how well the effects from the
randomized controlled trials hold up in clinical practice (Farhall, Freeman, Shawyer, &
Trauer, 2009; Peters et al., 2010). Lincoln et al. (2012) randomized 80 patients with
DSM-IV schizophrenia spectrum disorders who were seeking outpatient treatment
for psychosis in a primary care setting to a CBT plus treatment as usual or a wait-
list treatment as usual condition. This study found that the CBT group showed
significant improvement over the wait-list group for the total Positive and Negative
Syndrome Scale (PANSS) score at posttreatment/post waiting period. CBT was also
superior to the wait-list with regard to depression and functioning, but not with
regard to negative symptoms. Notably, the number of dropouts during the treatment
phases was low (11.3%), which further emphasizes the high treatment acceptability
of this approach by patients with psychosis. The positive effects of treatment on the
main outcomes could be maintained at 1-year follow-up, which demonstrates that
the efficacy of CBT for psychosis can be generalized to clinical practice despite the
differences in patients, therapists, and delivery.
Recent Developments
The results of almost two decades of research on cognitive behavioral interventions

for psychosis have demonstrated that psychotic symptoms respond to psychological
interventions. Consequently, CBT has been incorporated into various national treat-
ment guidelines. However, the first generation of CBT trials has also raised a number
of open questions and the reported effect sizes clearly leave room for improve-
ment. This has inspired further research on and refinements of the therapeutic
approaches.
For one, the designs that compare the combination of CBT with medical treatment
are not easy to interpret. Rigorous validity considerations would have required a
Psychosis 455
third treatment arm in which patients receive CBT without simultaneously receiving
medication. This treatment arm was not put into practice in the first generation of
trials for ethical and practical reasons. Therefore, the conclusions drawn with regard
to the efficacy of CBT are only correct if one assumes that CBT and TAU work
in an independent and additive manner. This is not necessarily the case. It is also
plausible to assume that medication is a necessary precondition for effective CBT to
occur (e.g., by its positive effect on disorganization, arousal, etc.). Alternatively, it is
conceivable that CBT would have a stronger effect as a stand-alone if one assumes
that patients who are not taking medication find it easier to be aware of and express
feelings, an essential part of any talking therapy. A recent and noteworthy pilot trial
(Morrison et al., 2011) used a pre-post design to investigate CBT for a group of
20 patients with psychotic disorders or attenuated psychotic symptoms who were
registered within the mental health system but had been refusing medication for
at least 6 months. Cognitive therapy took place for 26 sessions over a 9-month
period. The study found significant and large pre-post effect sizes for the total PANSS
score that were found to have increased at follow-up 6 months later. At follow-up
50% of the included patients showed a symptom reduction of 50% or more on the
PANSS. These results seem to indicate that the overall effect of CBT might have been
underestimated in trials that combine CBT and medication. However, several design
and methodological issues limit the generalizability of these results, and replications
are needed.
Furthermore, in regard to the interventions suggested for working with psychotic
symptoms, the established CBT manuals lag behind the transformation that has taken
part in recent years concerning our understanding of symptoms. Also, the complex
nature of the interventions and the global and broad outcome measures make it
difficult to identify the effective ingredients and to quantify the extent to which they
impact on individual symptoms or syndromes per se. These aims are more likely to be
achieved by tailoring interventions specifically to individual symptoms or syndromes
and the factors that are known to play a crucial role in their development and
maintenance.
With regard to persecutory delusions, reasoning biases (Fine, Gardner, Craigie, &
Gold, 2007), difficulties in emotion regulation (Lincoln, Lange, Burau, Exner, &
Moritz, 2010; Oliver, O’Connor, Jose, McLachlan, & Peters, 2011; Westermann,
Kesting, & Lincoln, 2012), and low and unstable self-esteem (Palmier-Claus, Dunn,
Drake, & Lewis, 2011; Thewissen et al., 2008) have been found to be strongly
associated with and possibly even causal to delusions. Also, both negative emotions
and reasoning biases tend to increase under stress (Keefe & Warman, 2011; Lincoln
et al., 2010; Moritz, Burnette, et al., 2011) and might mediate the impact of stressors
on paranoid beliefs (Lincoln et al., 2010). A recent line of intervention research has
thus begun to train patients to collect more information and is producing promising
effects on various dimensions of delusions (Moritz, Veckenstedt, Randjbar, von
Vitzthum, & Woodward, 2011; Waller, Freeman, Jolley, Dunn, & Garety, 2011).
Other studies have begun to focus on emotional factors relevant to delusions by
working with worry (Foster, Startup, Potts, & Freeman, 2010), emotion regulation
(Lincoln, Hohenhaus, & Hartmann, 2013), and distress associated with delusions
(Hepworth, Startup, & Freeman, 2011). However, these are pilot trials and more
work is required in this domain.
With regard to hallucinations, empirical findings support the cognitive model put
forward by Chadwick and Birchwood (1994), stating that the affect generated by
voices is not linked to the content or form but rather to the beliefs patients hold
about them. Specifically, beliefs about the power and meaning of voices were shown
to be closely related with coping and affect (Birchwood & Chadwick, 1997). Many
researchers have based specific interventions for hallucinations on this assumption
and have also followed suggestions by the recommendations (Chadwick et al.,
1994) to use a group format (Chadwick et al., 2000; Wykes et al., 2005). Cognitive
behavioral models are now being elaborated and broadened by including interpersonal
perspectives, such as social rank theory, to understand more fully the relationships that
voice hearers experience with their voices. For example, Trower et al. (2004) evaluated
the effects of a cognitive therapy grounded in the principles of social rank theory and
found it to be effective in reducing compliance with command hallucinations as well
as the degree of conviction of power and superiority of the voices. Larger-scale studies
using a similar approach are currently underway (Birchwood et al., 2011).
Another recent line of research is attempting to untangle the psychological processes
involved in negative symptoms, aiming to identify more specific targets for treatment.
Negative symptoms have been shown to be associated with a reduced sense of self-
efficacy (Bentall et al., 2010), low expectations of success (Beck, Rector, Stolar, &
Grant, 2009; Rector, Beck, & Stolar, 2005), low self-esteem (Lincoln, Mehl, Kesting,
& Rief, 2011), and social anxiety or insecurity (Bell, Tsang, Greig, & Bryson,
2009; Grant & Beck, 2010). Furthermore, several studies have demonstrated that
dysfunctional attitudes (e.g., “Finding new friends is not worth the energy I would
have to invest”; “Nothing will work out for me anyway”) mediate the association
between the neurocognitive deficits on the one hand and psychosocial functioning
on the other (Bell et al., 2009; Grant & Beck, 2009; Horan et al., 2010; McGlade
et al., 2008). Based on these findings, a study by Grant, Huh, Perivoliotis, Stolar,
and Beck (2012) used a cognitive approach to deal with negative symptoms in
a sample of low-functioning patients with psychotic disorders. Sixty patients were
randomized to CBT plus medication or to a medication alone condition. The authors
could demonstrate a significant improvement in functioning at the end of a 9-month
period. With regard to negative symptoms the authors found improvements in some
domains, such as apathy and avolition, whereas anhedonia, flat affect, and alogia did
not improve significantly. Overall, the results of this study are promising because they
demonstrate that CBT can achieve clinically meaningful changes for low-functioning
patients who do not respond well to medication.
Summary and Outlook
The research on CBT for psychotic disorders has come a long way since an early case
study by Beck in the 1950s (Beck, 1952) and the first case studies by U.K. pioneers in
the early 1990s. We now have numerous treatment manuals offering detailed descrip-
tions of how to deal with psychotic symptoms and a wealth of evidence demonstrating
Psychosis 457
their effectiveness. Based on the results and the positive experiences of clinical practice
studies, we argue that more efforts should be undertaken to incorporate CBT for
psychosis into the regular training programs for clinical psychologists and for psychi-
atrists and to make it widely available to patients. Finally, it will be exciting to see
whether the attempts that are underway to refine cognitive interventions by tailoring
them more specifically to symptoms and syndromes will be successful in improving
the overall effectiveness of cognitive interventions in the future.
Acknowledgements
We would like to thank Stephanie Mehl, Esther Jung, and Martin Wiesjahn for
providing some of the case examples, Annika Clamor and Margaret Lincoln for their
help with translations and language editing, and Dr. Alison Brabban for providing
the cognitive formulations for voices.
References
Bechdolf, A., Köhn, D., Knost, B., Pukrop, R., & Klosterkötter, J. (2005). A randomized
comparison of group cognitive-behavioural therapy and group psychoeducation in acute
patients with schizophrenia: Outcome at 24 months. Acta Psychiatrica Scandinavica, 112,
173–179.
Beck, A. T. (1952). Successful outpatient psychotherapy of a chronic schizophrenic with a
delusion based on borrowed guilt. Psychiatry, 15, 305–312.
Beck, A. T. (2005). The current state of cognitive therapy. A 40-year retrospective. Archives of
Beck, A. T., Rector, N. A., Stolar, N., & Grant, P. M. (2009). Schizophrenia: Cognitive theory,
research and therapy. New York, NY: Guilford Press.
Bell, M., Tsang, H. W. H., Greig, T. C., & Bryson, G. J. (2009). Neurocognition, social cogni-
tion, perceived social discomfort, and vocational outcomes in schizophrenia. Schizophrenia
Bulletin, 35, 738–747.
Bentall, R. P., Simpson, P. W., Lee, D. A., Williams, S., Elves, S., Brabbins, C., & Morrison,
A. P. (2010). Motivation and avolition in schizophrenia patients: The role of self-efficacy.
Psychosis, 2, 12–22.
Birchwood, M., & Chadwick, P. (1997). The omnipotence of voices: Testing the validity of
cognitive model. Psychological Medicine, 27 , 1345–1355.
Birchwood, M., Peters, E., Tarrier, N., Dunn, G., Lewis, S., Wykes, T., … Michail, M. (2011).
A multi-centre, randomised controlled trial of cognitive therapy to prevent harmful
compliance with command hallucinations. BMC Psychiatry, 11, 155. doi:10.1186/1471-
1244X-1111-1155
Chadwick, P., & Birchwood, M. (1994). The omnipotence of voices: A cognitive approach to
auditory hallucinations. British Journal of Psychiatry, 165, 190–201.
Chadwick, P., Birchwood, M., & Trower, P. (1996). Cognitive therapy for delusions, voices and
paranoia. Chichester, England: John Wiley & Sons, Ltd.
Chadwick, P., Sambrooke, S., Rasch, S., & Davies, E. (2000). Challenging the omnipotence
of voices: Group cognitive behavior therapy for voices. Behaviour, Research and Therapy,
38, 993–1003.
Drury, V., Birchwood, M., Cochrane, R., & Macmillan, F. (1996). Cognitive therapy and
recovery from acute psychosis: A controlled trial. I. Impact on psychotic symptoms. British
Farhall, J., Freeman, N. C., Shawyer, F., & Trauer, T. (2009). An effectiveness trial of cognitive
behaviour therapy in a representative sample of outpatients with psychosis. British Journal
of Clinical Psychology, 48, 47–62.
Fine, C., Gardner, M., Craigie, J., & Gold, I. (2007). Hopping, skipping or jumping to
conclusions. Clarifying the role of the JTC bias in delusions. Cognitive Neuropsychiatry,
12, 46–77.
Foster, C., Startup, H., Potts, L., & Freeman, D. (2010). A randomised controlled trial
of a worry intervention for individuals with persistent persecutory delusions. Journal of
Behavior Therapy and Experimental Psychiatry, 41, 45–51.
Fowler, D., Garety, P., & Kuipers, E. (1995). Cognitive behaviour therapy for psychosis: Theory
and practice. Chichester, England: John Wiley & Sons, Ltd.
Freeman, D. (2006). Delusions in the nonclinical population. Current Psychiatry Reports, 8,
191–204.
Freeman, D., Garety, P., Kuipers, E., Fowler, D., & Bebbington, P. (2002). A cognitive model
of persecutory delusions. British Journal of Clinical Psychology, 41, 331–347.
Garety, P. A., Kuipers, L., Fowler, D., Freeman, D., & Bebbington, P. (2001). A cognitive
model of the positive symptoms of psychosis. Psychological Medicine, 31, 189–195.
Gilbert, P. (2010). Compassion focused therapy. New York, NY: Routledge Chapman & Hall.
Grant, P. M., & Beck, A. T. (2009). Defeatist beliefs as a mediator of cognitive impairment,
negative symptoms, and functioning in schizophrenia. Schizophrenia Bulletin, 35, 798.
Grant, P. M., & Beck, A. T. (2010). Asocial beliefs as predictors of asocial behavior in
schizophrenia. Psychiatry Research, 177 , 65–70.
Grant, P., Huh, G. A., Perivoliotis, D., Stolar, N. M., & Beck, A. T. (2012). Randomized trial to
evaluate the efficacy of cognitive therapy for low-functioning patients with schizophrenia.
Gumley, A., & Schwannauer, M. (2006). Staying well after psychosis: A cognitive interpersonal
approach to recovery and relapse prevention. Chichester, England: John Wiley & Sons, Ltd.
Hepworth, C., Startup, H., & Freeman, D. (2011). Developing treatments of persistent
persecutory delusions: The impact of an emotional processing and metacognitive awareness
intervention. Journal of Nervous and Mental Disease, 199, 599–720.
Horan, W. P., Rassovsky, Y., Kern, R. S., Lee, J., Wynn, J. K., & Green, M. F. (2010). Further
support for the role of dysfunctional attitudes in models of real-world functioning in
schizophrenia. Journal of Psychiatric Research, 44, 499–505.
Jones, C., Cormac, I., Silveira da Mota Neto, J. I., & Campbell, C. (2004). Cognitive therapy
for schizophrenia. Cochrane Database of Systematic Reviews, 4, CD000524.
Keefe, K. M., & Warman, D. M. (2011). Reasoning, delusion proneness and stress: An
experimental investigation. Clinical Psychology and Psychotherapy, 18, 138–147.
Kesting, M. L., & Lincoln, T. M. (in press). The relevance of self-esteem and self-schemata in
individuals with persecutory delusions. Comprehensive Psychiatry.
Kingdon, D. G., & Turkington, D. (2004). Cognitive therapy of schizophrenia. New York, NY:
Guilford Press.
Klingberg, S., Wittdorf, A., Meisner, C., Wölwer, W., Wiedemann, G., Herrlich, J., …
Buchkremer, G. (2011). Cognitive behavioral therapy versus supportive therapy for
persistent positive symptoms in psychotic disorders: Major results of the POSITIVE
study. European Archives of Psychiatry and Clinical Neuroscience, Suppl. 1, 13.
Kuipers, E., Fowler, D., Garety, P., Chisolm, D., Freeman, D., Dunn, G., … Hadley, C.
(1998). London-East Anglia randomised controlled trial of cognitive-behavioural therapy
Psychosis 459
for psychosis. III: Follow-up and economical evaluation at 18 months. British Journal of
Kuipers, E., Garety, P. A., Fowler, D., Dunn, G., Bebbington, P., Freeman, D., & Hadley,
C. (1997). London-East Anglia randomised controlled trial of cognitive-behavioural
therapy for psychosis: I. Effects of the treatment phase. British Journal of Psychiatry, 171,
319–327.
Leucht, S., Arbter, D., Engel, R. R., Kissling, W., & Davis, J. M. (2009). How effective
are second-generation antipsychotic drugs? A meta-analysis of placebo-controlled trials.
Molecular Psychiatry, 14, 429–447.
Lewis, S., Tarrier, N., Haddock, G., Bentall, R., Kinderman, P., Kingdon, D., … Dunn, G.
(2002). Randomised controlled trial of cognitive-behavioural therapy in early schizophre-
nia: Acute-phase outcomes. British Journal of Psychiatry, 181, 91–97.
Lincoln, T. (2006). Kognitive Verhaltenstherapie der Schizophrenie: Ein individuenzentri-
erter Ansatz zur Veränderung von Wahn, Halluzinationen und Negativsymptomatik.
Göttingen, Germany: Hogrefe.
Lincoln, T. M., Hohenhaus, F., & Hartmann, M. (2013). Can persecutory beliefs be reduced
by targeting anxiety and self-esteem? An experimental investigation of a brief compassion
focused intervention. Cognitive Therapy & Research, 37 , 390–402.
Lincoln, T. M., Keller, E., & Rief, W. (2009). Die Erfassung von Wahn und Halluzinationen
in der Normalbevölkerung: Deutsche Adaptationen des Peters et al. Delusions Inventory
(PDI) und der Launay Slade Hallucination Scale (LSHS-R). Diagnostica, 55, 29–40.
Lincoln, T. M., Lange, J., Burau, J., Exner, C., & Moritz, S. (2010). The effect of state-
anxiety on paranoid ideation and jumping to conclusions: An experimental investigation.
Schizophrenia Bulletin, 36, 1140–1148.
Lincoln, T. M., Mehl, S., Kesting, M.-L., & Rief, W. (2011). Negative symptoms and
social cognition: Detecting suitable targets for psychological interventions. Schizophrenia
Bulletin, 37 , S23–S32.
Lincoln, T. M., Suttner, C., & Nestoriuc, Y. (2008). Wirksamkeit kognitiver Interventionen in
der Reduktion schizophrener Symptomatik: Eine Meta-Analyse. Psychologische Rundschau,
4, 217–232.
Lincoln, T. M., Ziegler, M., Mehl, S., Lüllmann, E., Kesting, M. L., Westermann, S., &
Rief, W. (2012). Moving from efficacy to effectiveness in CBT for psychosis: A
randomized-controlled clinical practice trial. Journal of Consulting and Clinical Psychology,
80, 674–686.
McGlade, N., Behan, C., Hayden, J., O’Donoghue, T., Peel, R., Haq, F., … Donohoe, G.
(2008). Mental state decoding v. mental state reasoning as a mediator between cognitive
and social function in psychosis. British Journal of Psychiatry, 193, 77–78.
McGovern, J., & Turkington, D. (2001). “Seeing the wood from the trees”: A continuum
model of psychopathology advocating cognitive behaviour therapy for schizophrenia.
Clinical Psychology and Psychotherapy, 8, 149–175.
Moritz, S., Burnette, P., Sperber, S., Köther, U., Hagemann-Goebel, M., Hartmann, M., &
Lincoln, T. M. (2011). Elucidating the black box from stress to paranoia. Schizophrenia
Bulletin, 37 , 1311–1317.
Moritz, S., Veckenstedt, R., Randjbar, S., von Vitzthum, F., & Woodward, T. (2011b). Antipsy-
chotic treatment beyond antipsychotics: Metacognitive intervention for schizophrenia
patients improves delusional symptoms. Psychological Medicine, 41, 1823–1832.
Moritz, S., & Woodward, T. S. (2007). Metacognitive training in schizophrenia: From basic
research to knowledge translation and intervention. Current Opinion in Psychiatry, 20,
619–625.
Morrison, A. P., French, P., Walford, L., Lewis, S. W., Kilcommons, A., Green, J., … Bentall,
R. P. (2004). Cognitive therapy for the prevention of psychosis in people at ultra-high
risk. British Journal of Psychiatry, 185, 291–297.
Morrison, A. P., French, P., & Wells, A. (2007). Metacognitive beliefs across the continuum of
psychosis: Comparisons between patients with psychotic disorders, patients at ultra-high
risk and non-patients. Behaviour Research and Therapy, 45, 2241–2246.
Morrison, A. P., Hutton, P., Wardle, M., Spencer, H., Barratt, S., Brabban, A., …
Turkington, D. (2011). Cognitive therapy for people with a schizophrenia spectrum diag-
nosis not taking antipsychotic medication: An exploratory trial. Psychological Medicine,
42, 1049–1056. doi:10.1017/S0033291711001899
Morrison, A. P., Renton, J. C., Dunn, H., Williams, S., & Bentall, R. P. (2004b). Cognitive
therapy for psychosis: A formulation-based approach. New York, NY: Brunner-Routledge.
Nuechterlein, K. H., & Dawson, M. E. (1984). A heuristic vulnerability/stress model of
schizophrenic episodes. Schizophrenia Bulletin, 10, 300–312.
Oliver, J. E., O’Connor, J. A., Jose, P. E., McLachlan, K., & Peters, E. (2011). The impact
of negative schemas, mood and psychological flexibility on delusional ideation: Mediating
and moderating effects. Psychosis, 4, 1–13.
Palmier-Claus, J., Dunn, G., Drake, R., & Lewis, S. (2011). The negative and positive self: A
longitudinal study examining self-esteem, paranoia and negative symptoms in individuals
with first-episode psychosis. Early Intervention in Psychiatry, 5, 150–155.
Peters, E., Landau, S., McCrone, P., Cooke, M. A., Fisher, P., Steel, C., … Kuipers, E. (2010).
A randomized controlled trial of cognitive behavior therapy for psychosis in a routine
clinical service. Acta Psychiatrica Scandinavica, 122, 302–318.
Pilling, S., Bebbington, P., Kuipers, E., Garety, P., Geddes, J., Orbach, G., & Morgan, C.
(2002). Psychological treatments in schizophrenia: I. Meta-analysis of family interventions
and cognitive behaviour therapy. Psychological Medicine, 31, 763–782.
Rector, N. A., & Beck, A. T. (2001). Cognitive behavioural therapy for schizophrenia: An
empirical review. Journal of Nervous and Mental Disease, 189, 278–287.
Rector, N. A., Beck, A. T., & Stolar, N. (2005). The negative symptoms of schizophrenia: A
cognitive perspective. Canadian Journal of Psychiatry, 50, 247–257.
Roder, V., Mueller, D., Mueser, K. T., & Brenner, H. D. (2006). Integrated psychological
therapy (IPT) for schizophrenia: Is it effective? Schizophrenia Bulletin, 32, 81–93.
Startup, M., Jackson, M. C., & Bendix, S. (2004). North Wales randomized controlled trial of
cognitive behaviour therapy for acute schizophrenia spectrum disorders: Outcomes at 6
and 12 months. Psychological Medicine, 34, 413–422.
Tarrier, N., Beckett, N., Harwood, S., Baker, A., Yusupoff, L., & Ugarteburu, I. (1993). A
trial of two cognitive-behavioural methods of treating drug-resistant residual symptoms
in schizophrenic patients: I. Outcome. British Journal of Psychiatry, 162, 524–532.
Tarrier, N., Yusopoff, L., Kinney, C., McCarthy, E., Gledhill, A., Haddock, G., &
Morris, J. (1998). RCT of intensive CBT for patients with chronic schizophrenia.
British Medical Journal, 317 , 303–307.
Thewissen, V., Bentall, R. P., Lecomte, T., van Os, J., & Myin-Germeys, I. (2008). Fluctuations
in self-esteem and paranoia in the context of daily life. Journal of Abnormal Psychology,
117 , 143–153.
Thewissen, V., Myin-Germeys, I., Bentall, R. P., de Graaf, R., Vollebergh, W., &
van Os, J. (2007). Instability in self-esteem and paranoia in a general population sample.
Social Psychiatry and Psychiatric Epidemiology, 42, 1–5.
Trower, P., Birchwood, M., Meaden, A., Byrne, S., Nelson, A., & Ross, K. (2004). Cognitive
therapy for command hallucinations: Randomised controlled trial. British Journal of
Psychosis 461
Turkington, D., Kingdon, D. G., & Turner, T. (2002). Effectiveness of a brief cognitive-
behavioural therapy intervention in the treatment of schizophrenia. British Journal of
van Os, J., Linscott, R. J., Myin-Germeys, I., Delespaul, P., & Krabbendam, L. (2009). A
systematic review and meta-analysis of the psychosis continuum: Evidence for a psychosis
proneness-persistence-impairment model of psychotic disorder. Psychological Medicine,
39, 179–195.
Waller, H., Freeman, D., Jolley, S., Dunn, G., & Garety, P. (2011). Targeting reasoning biases
in delusions: A pilot study of the Maudsley Review Training Programme for individuals
with persistent, high conviction delusions. Journal of Behavior Therapy and Experimental
Westermann, S., Kesting, M.-L., & Lincoln, T. M. (2012). Being deluded after being excluded?
How emotion regulation deficits in paranoia-prone individuals impact on state paranoia
during experimentally induced social stress. Behavior Therapy, 43, 329–340.
Wykes, T., Hayward, P., Thomas, N., Green, N., Surguladze, S., Fannon, D., & Landau, S.
(2005). What are the effects of group cognitive behaviour therapy for voices? A randomised
control trial. Schizophrenia Research, 77 , 201–210.
Wykes, T., Huddy, V., Cellard, C., McGurk, S. R., & Czobor, P. (2011). A meta-analysis of
cognitive remediation for schizophrenia: Methodology and effect sizes. American Journal
of Orthopsychiatry, 168, 472–485.
Wykes, T., Steel, C., Everitt, B., & Tarrier, N. (2008). Cognitive behavior therapy for
schizophrenia: Effect sizes, clinical models, and methodological rigor. Schizophrenia
Bulletin, 34, 523–537.
Young, J. E., Klosko, J. S., & Weishaar, M. E. (2003). Schema therapy: A practitioner guide.
Zimmermann, G., Favrod, J., Trieu, V. H., & Pomini, V. (2005). The effect of cognitive
behavioral treatment on the positive symptoms of schizophrenia spectrum disorders: A
meta-analysis. Schizophrenia Research, 77 , 1–9.
Zubin, J., & Spring, B. (1977). Vulnerability: a new view of schizophrenia. Journal of Abnormal
20
Chronic Pain
Stephen J. Morley
University of Leeds, United Kingdom
Johan W. S. Vlaeyen
University of Leuven, Belgium, and Maastricht University, The Netherlands
Interruption, Interference, and Identity: A Framework

for the Psychology of Pain
The literature on the psychology of pain is extensive but much of it can be subsumed
under three interlinked themes: interruption, interference, and identity (Morley,
2008; Morley & Eccleston, 2004). Interruption refers to the impact of pain on the
disruption of attention and its behavioral consequences on a moment-to-moment
basis (Eccleston & Crombez, 1999; Legrain et al., 2009). Continued disruption has
significant consequences for behavioral and cognitive performance (Dick & Rashiq,
2007; Grisart, Van der Linden, & Masquelier, 2002), resulting in interference in daily
life activities, so that a person either fails to complete tasks effectively or performs
them in a degraded manner that is unacceptable to them or members of their social
group. Repeated interference in key tasks impacts upon individuals’ sense of who
they are and, perhaps more importantly, who they might become by distorting their
vision of their future and reshaping their view of the past (Charmaz, 1999; Risdon,
Eccleston, Crombez, & McCracken, 2003). The importance of each theme varies
across people and the duration of pain. Brief laboratory pain has interruptive effects
but is unlikely to produce interference or impact on identity. Acute clinical pain
has both interruptive and temporary interference effects but is unlikely to affect a
person’s identity. Chronic pain frequently has a profound effect on all three categories.
Repeated interference with tasks that are essential to achieving various life goals and
maintaining a person’s status in society impact on the person’s sense of self and
future plans (Morley, Davies, & Barton, 2005; Sutherland & Morley, 2008). This
brief analysis illustrates the breadth of disruption that pain may have on normal
psychological processes. The range of treatment procedures developed within the
cognitive behavioral framework represents considered attempts to relieve elements of
suffering at each level of interruption, interference, and identity.

DOI: 10.1002/9781118528563.wbcbt20
The Emergence of Contemporary Psychological

Approaches to Pain
Until the early 1960s, chronic pain problems were approached as a symptom of
an underlying biomedical pathology. Pain was implicitly assumed to be related in a
1:1 ratio to the severity of the underlying pathology. According to this perspective,
the treatment of pain basically consisted of two operations: (a) localization of the
underlying pathology, and (b) removal of the pathology with appropriate remedy. In
the absence of bodily damage, the mind was assumed to be at fault, and a psychological
pathology was inferred. The limitations of the biomedical model became apparent
during the late 1950s, and Melzack and Wall’s gate-control theory (Melzack &
Wall, 1965) provided a Kuhnian paradigm shift that figuratively opened the gate for
research on the role of psychological variables moderating and mediating pain. Cortical
processes were acknowledged to be intimately involved in the integration of both
sensory-discriminative and affective-motivational aspects of pain. One revolutionary
finding was that pain is not just the result of nociceptive information ascending from
the periphery, but is also profoundly moderated by descending pathways. It was not
long until psychological approaches that are now part of contemporary cognitive
behavioral therapy (CBT) emerged. CBT is the dominant force in contemporary
psychological treatments for chronic pain. To understand some of the key elements,
it is useful to see how the main strands have developed and where they have been
incorporated into the field of pain.
Table 20.1 uses a timeline to schematize major strands in contemporary CBT
for chronic pain beginning with the application of behavior analysis by Fordyce in
the 1960s (Fordyce, 1976) and ending with the introduction of acceptance and
commitment therapy (ACT) in the late 1990s and from 2000 onward (McCracken,
2005). Table 20.1 also indicates the origins of each of the strands. Fordyce’s
applications of operant principles and ACT both have their roots in the analysis of
respondent behavior originating with Skinner’s work in the 1930s. The next part of
this chapter briefly reviews each major approach. The details of how to implement the
approaches in clinical practice cannot be given here but we have noted publications
that provide such information. We then briefly review the current status of the evidence
for CBT, and as a result of this we suggest that making therapeutic advances in this
field requires better specification of the problem. We illustrate this with reference to
the application of the general fear-avoidance model to a particular problem that arises
in a proportion of people with chronic pain.
Operant Treatment
About 10 years after the publication of the gate-control theory, Wilbert Fordyce pro-
duced his influential book Behavioral Methods for Chronic Pain and Illness (Fordyce,
1976). His work stemmed from the obvious shortcomings of the attempts of tradi-
tional health care to resolve chronic pain problems. Fordyce was the first to apply
the principles of operant conditioning to problems of chronic pain. Central was his
Table 20.1 Timeline Outlining the Development of Cognitive Behavioral Therapy as Applied to the Treatment of Chronic Pain
1940 1950 1960 1970 1980 1990 2000
Operant behavior Operant

analysis
Operant behavior Biofeedback
analysis
1. Cognitive Stress
theory of stress management
2. Behavioral
analysis of
self- control
Clinical Cognitive
observations therapy
Buddhism Mindfulness-
(1000 based stress
BCE) reduction
Mower-Miller 2- Fear
process theory avoidance
Operant behavior Behavior Acceptance and
analysis analysis of commitment
language therapy
Note. From Morley (2011), p. S100. With permission of the International Association for the Study of Pain® (IASP).
idea that pain behavior—that is, the observable signs of pain and suffering—should
be the focus of treatment. At least two assumptions underlie this approach. First, the
factors that maintain the pain problem can be different from those that have initiated
it. Pain behaviors may be subject to a graded shift from structural/mechanical to
functional/environmental control. Second, biomedical findings do not eliminate the
possibility that psychological or social factors contribute to the level of disability
associated with pain. Fordyce also authored what is probably the first empirical CBT
study in patients with chronic pain.
Behavior analysis established that much behavior is a function of two significant
classes of external factors. The first class, reinforcement, refers to consequences that
determine the future probability of a specific behavior. The second class, antecedents,
refers to the context in which behavior occurs and includes the presence of discrim-
inative stimuli, which signal the availability of reinforcement. Fordyce’s insight was
to recognize that although pain is essentially a private experience there are publicly
observable expressions of pain (pain behavior) that are subject to the influences of
reinforcement and the context. As a consequence, pain behavior may be modified
in unhelpful ways. Similarly, it could be changed using the same principles of rein-
forcement modifying the context. The aim of behavioral treatment, in contrast to
interventions stemming from the biomedical model, is not to diminish the pain
experience, but rather to increase functioning despite the pain. To achieve this goal,
behavioral therapists attempt to decrease the frequency of pain behaviors and increase
the frequency of healthy behaviors by a contingency management procedure.
In a typical operant treatment, baseline levels of activities and pain behaviors are reg-
istered using a pain–rest contingency principle (Sanders, 2002). Patients are asked to
engage in activities until pain or other physical discomfort prevents them from contin-
uing. Subsequently, a treatment contract is made with the patient including concrete
goals and incremental performance quota. Treatment starts when the patient agrees
to follow the quota according to the activity–rest contingency principle. Patients are
positively reinforced for increased activity tolerance levels and develop a daily activity
schedule to be used at home. This procedure is also known as graded activity when
operant procedures are used to increase activity levels. Usually, the operant treatment
includes the involvement of the family, or at least the spouse, who are taught to
differentiate between pain and healthy behaviors, to identify their own responses to
these behaviors, and to socially reinforce healthy behaviors rather than pain behaviors.
Medication use is managed in a time-contingent fashion (White & Sanders, 1985).
In severely disabled patients who lack sufficient healthy behaviors to reinforce, the
generation of new healthy behaviors can be facilitated by the use of shaping, otherwise
called reinforcement of successive approximations. These are behaviors that progres-
sively approach a final target behavior. While reinforcement is initially contingent
on simple behaviors, it is gradually shifted toward more complex behavior patterns,
leading to the exhibition of the target behavior. Vlaeyen et al. (1989) successfully
used such a shaping procedure in a chronic pain patient with standing and sitting
intolerance. Specifically, they divided the higher goals of standing and sitting into
a hierarchy of smaller steps, and provided reinforcement each time one of them was
achieved. The patient progressively moved along this hierarchy of sub-goals, reaching
Chronic Pain 467
a significant increase in standing and sitting tolerance that was still visible at a 6-month
follow-up assessment, despite the fact that no changes in pain intensity were reported.
Activity Pacing
Another therapeutic approach that has its roots in the operant tradition is what is
currently called activity pacing (AP). AP is breaking down an activity into smaller parts
and alternating it with breaks. According to several authors, AP involves changing
the contingency of the breaks from pain or fatigue to a specific time point or
the completion of a part of the activity. However, a clear consensus regarding the
definition of AP is lacking. From the operant perspective, the rationale for AP is that
the continued performance of an activity to tolerance level exacerbates pain intensity,
leaving the patient in need of prolonged rest before being active again. The increase
in pain then functions as a punisher of activity, whereas rest is being negatively
reinforced by pain reduction. After a while, the patient might again be active until
pain becomes intolerable to make up for the lost time. Patients are then trapped in an
overactivity/underactivity cycle. To help patients to take breaks in response to cues
other than pain, the baseline level for the target activity is first established in a way
similar to that described earlier. Patients can use a timer as a reminder to interrupt or
resume an activity, and a daily activity diary, which captures the time spent on target
activities and rest, to obtain feedback regarding their progress in relation to the goals
initially set. Unfortunately, AP has not yet been systematically investigated (Gatzounis,
Schrooten, Crombez, & Vlaeyen, 2012; Nielson, Jensen, Karsdorp, & Vlaeyen, 2013).
Biofeedback and Relaxation
By the beginning of the 1970s, biofeedback and relaxation were introduced into
treatment protocols. Biofeedback also had its roots in the analysis of learning. The
experimental studies were concerned with a particular distinction between classical
(Pavlovian) conditioning and respondent (operant) conditioning which hypothesized
that autonomic responses could not be operantly conditioned. Paradoxically, the
first applications of biofeedback to pain disorder appear to have been for chronic
headache which targeted striated muscle (Holroyd et al., 1984). Both biofeedback
and relaxation were incorporated into treatments for pain aimed at modifying the
hypothesized pain–tension–pain cycle (Arena & Blanchard, 2002) and biofeedback
directed at direct modification of musculoskeletal pathology is also occasionally used
(Flor & Birbaumer, 1993).
Coping Skills Training
The recognition that complaints might be construed as a stress response was also
developed in the 1970s. Elements of this analysis were drawn from the work of Lazarus
and colleagues (Folkman & Lazarus, 1980) in the preceding decade that sought to
elucidate factors that were responsible for the variation in responses to aversive
stimulation (stressors). This work established two crucial ideas in the pain field,
appraisal and coping, that are still current (e.g., catastrophizing and self-efficacy). Also
by the mid-1970s work on self-control, which also had its roots in behavior analysis
(Mahoney & Thoresen, 1974), was incorporated into the treatment armamentarium
and a definitive text, Pain and Behavioral Medicine: A Cognitive-Behavioral Perspective
(Turk, Meichenbaum, & Genest, 1983), was published in 1983. A recent update can
be found in Chronic Pain: An Integrated Biobehavioral Approach (Flor & Turk, 2011).
Perhaps the most extensive and consistent series of clinical trials of psychological
approaches to the treatment of pain is that by Keefe and colleagues (Keefe, Beaupré,
Gil, Rumble, & Aspnes, 2002). Keefe developed a coping skills training treatment
(CST) that has been trialed in patients with pain arising from a number of sources.
It is the exemplar of the general cognitive behavioral approach adopted by many pain
management programs. Treatment incorporates a significant education and induction
phase that uses the gate metaphor from Melzack and Wall’s theory to engage
patients with the concept of pain and the importance of psychological influences on
pain. Progressive relaxation training is taught and the skills learned are transferred
so that patients learn a brief relaxation technique that can be applied quickly in
situations where pain is problematic. The essential part of this is the application of
differential relaxation; the ability to remove unnecessary tension while still maintaining
appropriate muscle tension necessary to engage in activity. While relaxation skills are
being mastered patients are introduced to the principles of rest–activity cycling (AP)
using the principles developed by Fordyce with the aim of shifting the control of
activity from a pain contingency to a time contingency. Throughout the program
particular attention is given to the implementation of skills at home and outside
the clinical setting. For example, applying rest–activity cycling will require the
patient to explain and negotiate the change in his or her behavioral pattern with
family and friends. To facilitate this change the protocol suggests that patients role
play and rehearse their expected interactions. The next element in the protocol
is the development of attention-diversion strategies, especially the use of pleasant
imagery and the development of “focal point distraction” to be used at times when
pain becomes particularly intense, perhaps during exercise (Morley, 2010; Morley,
Shapiro, & Biggs, 2004). Attention management strategies are taught after basic
relaxation skills have been acquired. Coping skills training may appear to be rather
light with regard to specific cognitive interventions but the group format in which it
is usually delivered gives considerable scope for patients to voice their fears, emotional
distress, and expectations. These issues are not avoided and Keefe et al. provide an
overview of the general strategy they adopt (Keefe, Crisson, Urban, & Williams,
1990). Finally, coping skills training has also been developed to involve the patient’s
spouse in assisting with the implementation of the protocol (Keefe et al., 2004).
Cognitive Treatment
At the turn of the 1970s, Beck published a text on the treatment of depression by
cognitive therapy (Beck, Rush, Shaw, & Greenberg, 1979). The significance of this
Chronic Pain 469
was that a substantive claim was made that a disorder that had previously been difficult
to treat using psychological methods was treatable. Beck (1970) and Ellis (1980)
had developed separate versions of what became known as cognitive therapy in the
previous two decades. Cognitive therapy emphasized the critical meditational role
played by idiosyncratic interpretations of events in determining a person’s emotional
and behavioral responses to events. The model included a structural analysis of
dysfunctional thinking and hypothesized the development of underlying schema and
modes of information processing also referred to as cognitive errors. Typical errors are
catastrophizing, overgeneralization, all-or-nothing thinking, jumping to conclusions,
selective attention, and mindreading. Perhaps because of the marked overlap between
pain and depression (Lefebvre, 1981; Smith, Follick, Ahern, & Adams, 1986),
elements of Beck’s therapy were incorporated into pain treatments and the model
was adapted to the treatment of chronic pain (Thorn, 2004). Researchers also
developed measures of a range of beliefs and attitudes in pain populations (Turk &
Melzack, 2001), many of which attempt to identify cognitive representations that
are specific to pain. Notwithstanding that there have been few trials of what one
might regard as pure cognitive therapy in which specific “core beliefs” have been
targeted (Turner & Jensen, 1993). Nevertheless, the central elements and practice of
cognitive therapy have been incorporated into many general therapy protocols. Thorn
(2004) provides specific guidance on applying cognitive therapy principles to chronic
pain.
Mindfulness
A second strand of treatment without roots in experimental psychology is mindfulness,

which was introduced in the mid-1980s. Kabat-Zinn (1982) reported uncontrolled
evaluations of the application of mindfulness training derived from Buddhist teaching
and 3,000 years of practice. Although Kabat-Zinn reported studies on pain patients,
it was not until his work was taken up by a group of researchers looking for a method
to prevent relapse after treatment for depression that mindfulness was incorporated
more generally into CBT (Bishop et al., 2004; Teasdale, Segal, & Williams, 1995).
Kabat-Zinn defines mindfulness as “attending to relevant aspects of experience in a
nonjudgmental manner.” The goal of mindfulness is “to maintain awareness moment
by moment, disengaging oneself from strong attachment to beliefs, thoughts, or
emotions, thereby developing a greater sense of emotional balance and well-being”
(Ludwig & Kabat-Zinn, 2008, p. 1350). Learning mindfulness may include different
types of formal meditation practice, yoga, and exercising mindfulness in everyday life.
It is suggested that mindfulness may be particularly useful in influencing susceptibility
to and recovery from disability and disease in general. A crucial component is perhaps
the phenomenon known as decentering, described as “the capacity to take a present-
focused, non-judgmental stance in regard to thoughts and feelings and accept them”
(Fresco, Segal, Buis, & Kennedy, 2007, p. 448). This aspect of mindfulness is also
central to ACT (McCracken, Keogh, McCracken, & Keogh, 2009). In addition to
Kabat-Zinn’s early application, there have been controlled trials of a mindfulness
protocol but it does not appear to be significantly superior to other treatments
(Morone, Greco, & Weiner, 2008; Schmidt et al., 2011). However, evidence is
emerging that mindfulness processes may play a significant role in mediating responses
to pain (Cassidy, Atherton, Robertson, Walsh, & Gillett, 2012; Schutze, Rees, Preece,
& Schutze, 2010).
ACT is also grounded in the experimental analysis of behavior, in particular the radical
behavioral analysis of the function of language and rule-governed behavior (Hayes,
Barnes-Holmes, & Roche, 2001). The complexity of ACT is harder to grasp than
Fordyce’s earlier implementation but the aims are essentially the same: to change
the control over behavior that pain exerts by altering the context. ACT targets
ineffective control strategies and experiential avoidance (Dahl, Wilson, Luciano, &
Hayes, 2005; McCracken, 2005). People learn to stay in contact with unpleasant
emotions, sensations, and thoughts rather than avoiding them. Negative thoughts
associated with pain are used as targets for exposure, rather than attempts being made
to change their content. ACT further focuses on value clarification, and the client’s
ability to commit to his or her personal values in daily life, and to engage in activities
that match these life goals. The results of a recent systematic review suggest that
ACT is not superior to more traditional CBT for chronic pain, but that it provides a
good alternative for a number of patients (Veehof, Oskam, Schreurs, & Bohlmeijer,
2011).
Exposure In Vivo
The final strand of current CBT is the application of the generalized fear-avoidance
model to chronic pain. The modern experimental and clinical analysis of fear and
avoidance has a long history dating back to the work of Masserman, Miller, and
Mowrer in the 1940s. This work shaped the development of behavioral treatments of
phobias. Fordyce noted the importance of fear learning and avoidance, but the analysis
and application to chronic pain is more recent (Vlaeyen & Linton, 2000). In contrast
to other approaches the fear-avoidance model is relatively specific and in its primary
instantiation it applies to a subgroup of patients who express fears that engaging in
specified movements will result in catastrophic consequences. Treatment proceeds by
having patients test the validity of their appraisals by engaging in the very behavior
of which they are frightened. In many regards the fear-avoidance model captures the
essence of CBT: collaborative engagement with the client; careful development of a
formulation of an individual’s problem; clarification of the problem and treatment
(education); development of a treatment strategy, based on known psychological
principles, that is devised to test an individual’s assumptions and alternative ways
of responding via individualized behavioral experiments; and reflective observations
on progress in treatment and careful monitoring. Results of exposure treatments are
summarized by Vlaeyen, Morley, Linton, Boersma, and de Jong (2012), and are
discussed later in this chapter.
Chronic Pain 471
The Evidence Base for Cognitive Behavioral Treatment

for Chronic Pain
The efficacy of CBT procedures has consistently been subjected to empirical testing
(Eccleston, Williams, & Morley, 2009; Hoffman, Papas, Chatkoff, & Kerns, 2007;
Williams, Eccleston, & Morley, 2012). There is evidence for the absolute efficacy of
CBT procedures (i.e., CBT is superior to no treatment) and some suggestion of their
relative efficacy (i.e., CBT may be marginally superior on some measures compared
with other treatments). This overall conclusion should be placed in the context of
the nature of the trials. Arguably we can have most confidence in the results of a
meta-analysis when all the key parameters (samples, diagnoses, interventions, control
arms, outcome measures, etc.) are homogeneous. This is not the case with respect to
CBT for chronic pain, as there is marked heterogeneity across all parameters which
then have to be aggregated (Higgins & Green, 2008). While this is not ideal it does
reflect the reality of this complex field and it is reasonable to conclude that there
is evidence for a class effect of CBT procedures for a range of conditions where
chronic pain is the significant feature. Most outcome measures in these studies are
continuous rather than categorical or binary, and the computed effect size is the
standardized mean difference between the treatment and control arms (Cohen’s d or
Hedge’s g) (Rosenthal, 1994); estimates of absolute efficacy range from d = 0.2 to
0.5 (Eccleston et al., 2009; Hoffman et al., 2007; Morley, Eccleston, & Williams,
1999; Williams et al., 2012). In summary, “average CBT has on average an effect for
the average patient, on general outcomes” (Morley, Williams, & Eccleston, in press).
The complexity of chronic pain is mirrored by the complexity of treatment. Many
of the trials entered into meta-analyses are pragmatic mixes of treatment content
and this makes it difficult to discern which, if any, of the components of treatment
contribute to specific changes. There are relatively few studies of change process
studies (Morley & Keefe, 2007) given the volume of trials, but several recent ones
(Litt, Shafer, Ibanez, Kreutzer, & Tawfik-Yonkers, 2010; Smeets, Vlaeyen, Kester, &
Knottnerus, 2006; Spinhoven et al., 2004; Turner, Holtzman, & Mancl, 2007) and
cohort studies (Burns, Kubilus, Bruehl, Harden, & Lofland, 2003) have begun to
explore this issue. The advent of daily diary methodology, including electronic diaries
and automated telephone contact (Naylor, Keefe, Brigidi, Naud, & Helzer, 2008),
and the development of suitable statistical analysis (multilevel modeling) provide a
suite of tools that may help advance our understanding of change. Possible indicators
of good outcomes include changes in catastrophizing, self-efficacy, and control beliefs,
all of which can be measured with relative ease.
We suggest that treatment for chronic pain by psychological methods is at a critical
juncture. Although treatment is effective the average impact is not large, but that
is not to deny that some patients may respond extremely well, and the delivery of
multicomponent therapies in randomized controlled trials means that it is not possible
to determine the functional relationships between intervention, process, and outcome.
On the other hand, clinicians and researchers might adopt the “old” technology of
single case experimentation to test the efficacy of specific treatment components
(Barlow, Nock, & Hersen, 2009; McMillan & Morley, 2010). Fordyce’s early studies
were dependent on this methodology, and more recently Vlaeyen and his colleagues
(de Jong et al., 2008; Vlaeyen, de Jong, Geilen, Heuts, & van Breukelen, 2001) have
used replicated single cases to establish the therapeutic potential of the fear-avoidance
model. The cardinal feature of behaviorally informed single case methodology is
that the target outcome measure may also be the process measure (Sidman, 1960).
These methods are readily implementable and in the rest of the chapter we outline
the development of a specific version of CBT with a strong theoretical foundation
(exposure in vivo for pain-related fear) that we have developed and tested with both
single case experiments and randomized controlled trials (Vlaeyen et al., 2012).
Application of Fear Avoidance to Chronic Pain
Acquisition and Maintenance of Pain-Related Fear

By virtue of its biological significance, pain is an important motivator in learning.
Indeed, pain informs the individual that there is imminent or actual threat of body
damage. Therefore, pain is considered an unconditioned stimulus (US) that activates
an immediate fearful defensive system. Research supporting the role of fear in chronic
pain stems from prospective studies in acute pain (Gheldof et al., 2010; M. P. Jensen,
Wang, Potts, & Gould, 2013; Swinkels-Meewisse, Roelofs, Oostendorp, Verbeek, &
Vlaeyen, 2006) and studies using structural equation modeling (Crombez et al.,
2002; Goubert, Crombez, & Van Damme, 2004; Trost, France, & Thomas, 2008;
Wideman, Adams, & Sullivan, 2009). One of the unanswered questions, however, is
how pain-related fear occurs in the first place. What kinds of stimuli are involved in such
learning, and what are the potential sources of information leading to propositional
knowledge between neutral and to-be-conditioned stimuli (CS) and unconditioned
stimuli? There is accumulating evidence that (persistent) fear of pain can be acquired
by verbal instruction (Bailey, Carleton, Vlaeyen, & Asmundson, 2010), observation
(Helsen, Goubert, Peters, & Vlaeyen, 2011), and direct experience (Meulders,
Vansteenwegen, & Vlaeyen, 2011; Trost et al., 2008). For example, the threat value
of pain can be manipulated by telling participants performing a cold pressor task
“when feeling tingling sensation in your hand, this may be the first signs of frostbite”
(Bailey et al., 2010) or warning patients that “lifting weights may cause back injury”
(Houben et al., 2005), without actually experiencing these associations. But there is
also a nonverbal pathway, during which the mere observation of another person in
pain can be sufficient to instill fear of that particular stimulus. In one study, participants
observed human models who performed a cold pressor task, in which the color of the
water (orange or pink) was associated with painful or neutral facial expressions. When
tested themselves, the observers’ fear and pain scores show that they had learned the
CS–pain associations they had observed in the model, despite the equal temperatures
of both cold pressor tests (Helsen et al., 2011). Proprioceptive fear conditioning
is particularly relevant in patients with pain in the musculoskeletal system. A recent
study employed joystick movements of which the direction predicted painful shock
to the hand (e.g., moving upwards as CS+ and moving downwards as CS–). As
compared with a condition in which both movements were explicitly unpaired with
Chronic Pain 473
painful shock, the CS+ movement elicited increased fear of movement-related pain,
larger eyeblink startle amplitudes, and slower movement latency responses than the
CS–, validating the acquisition of fear of movement-related pain in healthy individuals
(Meulders et al., 2011). An intriguing but as yet untested idea is that interactions
among these pathways may facilitate learning. For example, previous observational
learning may enhance subsequent experiential learning of pain-related fear during the
actual encounter of a similar CS–pain pairing.
Extinction of Pain-Related Fear

Extinction is the reduction of conditioned fear responses as a result of repeated
exposure to the CS in absence of the US. In pain-related fear, patients are exposed to
movements and activities without the feared consequences in terms of pain, harm, or
(re)injury. Using the joystick movement paradigm mentioned above, Meulders and
Vlaeyen (2012) showed that fear ratings for the CS+ movement were extinguished
when it was no longer followed by pain. Generally, there is a marked asymmetry
between the ease by which acquisition of fear occurs compared to the difficulty by
which extinction takes place. For example, learning that bending the back results
in a shooting pain and accompanied by thoughts about being handicapped can
be established with only one exposure to a CS–US association. Extinction of this
association has shown to be more difficult. There is now growing consensus that
extinction does not result in simple unlearning or forgetting the association between
CS and US. Rather, there is evidence showing that a new form of learning occurs
that modifies the CS–US contingency in such a way that the CS no longer signals
an aversive event and thereby inhibits the expression of the fear response. Exposure
to the CS without the US creates an exception to the rule and competes with the
previously learned knowledge, namely that the US follows the CS. Extinction can
be viewed as additional (inhibitory) learning that in a particular context the CS–US
association does not exist. Therefore, it is difficult to generalize the extinction of fear
to dissimilar contexts, making relapse likely to occur (Crombez et al., 2002; Trost
et al., 2008). Phenomena such as spontaneous recovery, reinstatement, renewal, and
rapid reacquisition show that the formerly learned association is still a weak spot after
successful extinction.
Exposure In Vivo in Patients with Chronic Pain
Education and Preparing a Formulation

Helping patients to engage in exposure sessions therefore begins with an educational
phase during which the therapist presents an individualized formulation of the pain
problem. The goal here is to help patients reframe their pain experience and to correct
any misconceptions that have occurred early on during the development of the pain-
related fear. Ideally, their experience is reframed as a common condition that can be
self-managed, rather than as some serious disease that needs careful protection. The
other major goal of the educational phase is to increase the willingness of the patient
to engage in valued activities that have been avoided for a long time. Ideally, both the
psychologist and a medical specialist provide an educational session. This combination
of professionals generally increases the credibility of the new information provided to
the patient. In cases where the pain-related fear appears to be related to the patient’s
previous experiences of diagnostic tests (X-ray, magnetic resonance imaging), it may
be useful to review these tests together with a medical specialist. The purpose of
this consultation is to explain to patients that they have probably overestimated the
value of these tests, and that in symptom-free people similar abnormalities can also
be found. In this context, informing patients about the findings of studies which
reveal that individuals with and without back pain have similar magnetic resonance
imaging scans, suggests that the relevance of these imaging techniques in people with
chronic pain is rather limited (M. C. Jensen et al., 1994). Additionally, the therapist
can advise the patient to read one of the existing patient-centered books or leaflets
(Burton, Waddell, Tillotson, & Summerton, 1999). Generally, education is a useful
treatment component, but not always a sufficient one in order to inhibit avoidance
and more subtle safety behaviors.
One of the key elements of the educational session for patients with pain-related
fear is to provide an alternative explanation for the symptoms, which is credible and
integrates the idiosyncrasies of the patient’s pain problem. The general point of the
explanation is that the patient’s safety behaviors are a normal defensive response to
pain, which may have been adaptive in acute pain but have lost their efficacy as
pain has persisted. Over time the defensive avoidance behavior will interfere with
the performance of valued activities of daily life, which in turn may increase distress
and aggravate the pain. The educational session is not meant to convince patients of
the alternative explanation, but to help them prepare for treatment, and to increase
their willingness to engage in the exposure sessions (see Box 20.1 and Box 20.2). In
our experience, the education works best when a medical specialist, who can explain
that medical findings are absent or at least not indicative of serious pathology that
requires prolonged caution (such as medication, rest, or supportive devices), is part of
the treatment team. Sometimes, patients who have already consulted many specialists
are quite skeptical about the possible outcome of any new treatment proposed. The
graphical presentation of the fear-avoidance model is a usual way to help patients
understand that their own defensive behavior paradoxically may worsen the problem.
In an interactive way the therapist tries to map out beliefs, feelings, and behavior, and
their consequences. If patients accept that there may be alternatives to a biomedical
explanation of their pain problem, the educational session usually is a springboard to
the first exposure session.
Determining Treatment Goals

After the provision of an alternative framework aimed at helping the patient better
understand how beliefs, feelings, and behavior may maintain the chronic pain problem,
there are several reasons why the clinician may also spend some time determining
treatment goals (Bovend’Eerdt, Botell, & Wade, 2009). First, cognitive behavioral
treatments for pain, including exposure in vivo, never aim at the reduction of pain
but at the restoration of functional abilities despite pain. It helps to make this general
Chronic Pain 475
Box 20.1 Therapist informing a patient about exposure

treatment
THERAPIST: You just talked to the physician about the medical tests that
were carried out a week ago. Can you tell me more about that?
PATIENT: Well, we both looked at the scans, and they appeared less
alarming than I thought. Apparently there are no fractures, and no
trapped nerves. The doctor said that the scans show some wear and tear,
but that this is not unusual for a person of my age.
THERAPIST: How was it for you to hear this information?
PATIENT: Well, some relief because there is nothing dangerous going on.
At the same time, difficult to understand … because why is it that I have so
much pain and cannot walk or lift properly? There must be some reason.
THERAPIST: In people suffering from chronic pain such as yourself, it is not
unusual to see that the medical diagnostics are quite normal and that there
are no signs of physical damage.
PATIENT: Are you suggesting that my pain is all imagined?
THERAPIST: The physician told you that there is nothing medically wrong
with your back and that in principle, you may do whatever you wish. This
sounds like a positive message, perhaps sufficient to resolve the limitations
in your daily life that you experience. Have you been more active since the
meeting with the physician?
PATIENT: Of course not, because my pain has not diminished.
THERAPIST: Right. The pain is an obstacle for you to do the things that
you want to do, even though you have been reassured that your back is
not damaged. Let’s have a closer look at your pain problem. It is very
common for people with chronic pain to adapt and adjust their behavior,
as a natural way to protect the body against further pain. Sometimes,
however, this protective behavior may go astray and become
counterproductive. We believe that this may be the case in your situation.
Given what we know about your condition, we believe that you will be
capable of doing significantly more than you are doing right now and that
you are suffering more than needed.
PATIENT: I have seen a lot of doctors, and so far none of them have been
able to help me. Nobody could take away my pain.
THERAPIST: I understand, and this must be quite frustrating. How about
taking another perspective and looking at other ways of improving your
current life situation?
PATIENT: What do you mean?
THERAPIST: Well, we think there may be a way of becoming more active
by not trying to reduce pain first, but by analyzing what your activity
pattern is first. Suppose you could be more active with the same level of
pain, would that be an improvement?
PATIENT: I suppose so.
Box 20.2 Education session

THERAPIST: Let’s try to draw your own way of protecting against pain on
the white board. To start with, what have you learned to do so far when in
pain?
PATIENT: Well, when my pain is really bad, I should keep still because
otherwise a nerve may rupture.
THERAPIST: I understand, so pain tells you something is wrong, and that
you need to be still. You mentioned earlier that a week ago, while cleaning
the house, you experienced a sudden pain increase, right? How did you
feel?
PATIENT: I felt helpless, I couldn’t move any more, and I was scared that I
was going to become paralyzed.
THERAPIST: I can imagine that if you think that pain signals bodily damage
and that when cleaning your back pain increases, then you become quite
concerned. What did you do after feeling scared?
PATIENT: I stopped cleaning and lay down for a while.
THERAPIST: Did the pain go away?
PATIENT: Not really. It went down a bit, but it came back later. The pain
did not go away.
THERAPIST: May I conclude that the “solution” of stopping activities
when pain increases is not working well?
PATIENT: Well, it helps for a while, but it does not solve the problem.
THERAPIST: The advantage of taking rests is that it eases the pain for a
while. Are there also disadvantages of stopping activities?
PATIENT: I don’t know … but I do not feel happy with doing so little.
THERAPIST: Yes, it is quite possible that not doing activities that are
important to you can be frustrating and may get you down.
PATIENT: I used to be an active person, working for my family. Now I feel
worthless.
THERAPIST: There also might be physical effects as well. What do you
think are the effects of inactivity on your physical condition?
PATIENT: It hasn’t got any better … I’ve also gained weight.
goal explicit, and both patient and therapist should agree on one or more realistic and
specific goals that are formulated in positive terms. If reduction of pain is the only
or the most important goal, then exposure treatment may not be the right choice.
Typical examples of suitable treatment goals are: lifting a child, lifting a shopping bag,
using a bicycle, walking to the supermarket alone, and resuming swimming. More
general life goals, such as returning to work, taking up household chores, or going
on holiday, are best broken down into sub-goals or smaller activities that can each
be a subject for an exposure in vivo session. Goals are best formulated according to
popular SMART guidelines; the acronym refers to goals being specific, measurable,
attainable, relevant, and time-bound. The key question always remains: Why does
Chronic Pain 477
the patient consider such a life goal not achievable at the moment? There might be
specific movements involved which the patient is convinced are harmful, or there may
be other obstacles that may lead to additional behavioral experiments. Second, setting
goals also helps to structure the treatment and to design the hierarchy of stimuli
that will be introduced during the actual exposure in vivo sessions. For example, if a
patient wishes to resume his or her sports activities, than the therapist will make sure
that aspects of these will be included in the graded exposure activities. Third, setting
functional goals also redirects the focus of attention from pain and physical symptoms
toward daily life activities with the emphasis on the possibility of change away from
the disability status. Finally, as the patient is invited to formulate his or her own goals,
goal setting inadvertently reinforces the notion that active participation is an essential
part of the treatment.
Establishing a Fear Hierarchy

The goal of this session is not only to identify the activities that the patient is
avoiding, but also to decide which activities will be selected for the subsequent
exposure sessions. Using the Photograph Series of Daily Activities (PHODA; Leeuw,
Goossens, van Breukelen, Boersma, & Vlaeyen, 2007), patients sort photos of various
daily life activities on a “harm” thermometer ranging from 0 (this is not harmful
at all) to 100 (this is extremely harmful) (see Figure 20.1). Note that patients are
explicitly asked not to judge photos on the degree of anticipated painfulness, but on
the expected harmfulness of the activity. This is quite relevant as painfulness is more
difficult to challenge during the exposure sessions, while in most patients there is an
overestimation of harm that can be challenged.
Graded Exposure In Vivo with Behavioral Experiments

Current treatments of excessive fears and anxiety are based on Wolpe’s (1958)
work on systematic desensitization. The essence of this treatment method is that
individuals progress through increasingly anxiety-provoking encounters with phobic
stimuli while using relaxation to inhibit their rising anxiety. Because relaxation was
intended to compete with the anxiety response, a graded format was chosen to
keep anxiety levels as weak as possible. Later studies revealed that the exposure to
the feared stimuli appeared to be the most essential component of the systematic
desensitization, and it could be applied without relaxation to produce a comparable
effect. For fearful patients first-hand evidence of experiencing themselves behaving
differently is far more convincing than rational argument. The essential step consists
of graded exposure to the situations the patient has identified as “dangerous” or
“threatening.” Subsequently, individually tailored practice tasks are developed based
on the graded hierarchy of fear-eliciting situations and the general principles for
exposure are followed in which the patient agrees to perform certain activities or
movements that he or she used to avoid. Each activity or movement is first modeled
by the therapist, thereby demonstrating that it is a safe thing to do. The presence of
the therapist, who may serve as an initial safety signal to promote more exposures,
is gradually withdrawn to facilitate independence, and to create contexts that mimic
Extremely harmful
100
90
80
70
60
50
How harmful do you think this activity is to

your back?
40
30
20
28 29 30 31 32 33 3
10
0 FINISH
Not harmful at all
Figure 20.1 A screen shot of the computerized version of the Photograph Series of Daily
Activities (PHODA-SeV). From Vlaeyen, Morley, Linton, Boersma, & De Jong (2012), with
permission of the International Association for the Study of Pain® (IASP).
those outside of treatment. Patients are also encouraged to engage in these fearful
activities as much as possible until disconfirmation has occurred and anxiety levels
have decreased. This can be monitored by asking the patient to report his subjective
units of distress on a scale from 0 to 10 and repeat the exposure task until the level of
distress has substantially decreased.
Exposure in vivo often takes the form of a behavioral experiment. It is sometimes
mistakenly assumed that cognitive errors can be corrected simply through conscious
reasoning. In fact, behavioral experiments are an essential part of therapy. The essence
of a behavioral experiment is that the patient performs an activity to challenge
the validity of his or her catastrophic assumptions and misinterpretations. These
assumptions take the form of “if P then Q” statements, and are empirically tested
during a behavioral experiment (see Box 20.3). Three steps can be distinguished.
First, the patient formulates a hypothesis with the guidance of the therapist. For
example, “If I jump down off a stair, then I will inevitably experience nerve damage
in the spine and excruciating pain.” Second, a one session experiment is designed.
For example, if the patient is convinced that jumping down is harmful, the therapist
can further inquire about the minimal height that the patient considers necessary to
Chronic Pain 479
Box 20.3 Dialogue between a patient and his therapist during a

behavioral experiment
THERAPIST: OK, today we’ll start with the next activity. Why don’t we try
lifting this empty crate. What do you think?
PATIENT: [Sighs] I don’t think I can manage that.
THERAPIST: What do you think might happen?
PATIENT: I’m sure I’ll get more pain. The disks in my back can’t take such
pressure. It may further damage the nerves there.
THERAPIST: How would you notice this?
PATIENT: My back will collapse, I won’t be able to stand, and I may
become paralyzed.
THERAPIST: How likely is it that this will happen when lifting this crate, on
a scale of 0 (not likely) to 100 (very likely)?
PATIENT: I am not sure: around 70.
THERAPIST: OK, well, why don’t we try it and see what happens? I’ll do it
first, and then it’s your turn.
At this point the therapist models the lifting task and invites the patient to do
the same, and while he is holding the crate, the therapist continues to inquire
about what is happening.
THERAPIST: Good. You’re doing very well. How did it go?
PATIENT: OK, I guess. It did hurt somewhat, but my back could hold it
quite well. It didn’t collapse.
THERAPIST: Right, despite the pain, you managed to lift this crate, right?
Suppose we do this again, how would you rate the chances of your
becoming paralyzed?
PATIENT: Well, I would say a 40, but there wasn’t a crack.
THERAPIST: Would the situation be different if you had felt a crack?
PATIENT: Oh yes, definitely.
THERAPIST: How could we induce such a crack?
PATIENT: When I was still working, I usually carried heavier weights than
the one I just lifted.
THERAPIST: Shall we make this one a bit heavier?
PATIENT: [Laughs nervously] OK then.
cause nerve injury. Finally, the experiment is carried out and evaluated. After having
modeled the activity, the therapist invites the patient to jump off the stair and
the experienced consequences are evaluated. In practice, behavioral experiments are
difficult to separate from mere exposure, and they can best be used simultaneously.
So in addition to monitoring changes in distress, as in exposure, the evaluation of
each behavioral experiment determines changes in the beliefs that the patient holds
about particular activities. For example, these can be monitored by asking patients
to predict the occurrence of harm prior to the experiment, and repeating the same
question after exposure to that activity: “How would you rate the probability (0–100)
that you will be unable to move after doing this activity?” When the rating has decreased
substantially the therapist may consider moving on to the next item of the hierarchy.
Other Forms of Exposure

The in vivo form of graded exposure described earlier was specifically developed for
patients with chronic non-specific musculoskeletal pain, and back pain in particular,
who are severely disabled and who report substantial pain-related fear. Nevertheless,
one has to bear in mind that there are several variations in the way exposure treatment
can be conducted, most of which have not been systematically evaluated. One could
for example consider imagined exposure or exposure using virtual reality instead of
in vivo (Meyerbroker & Emmelkamp, 2010; Morris, Grimmer-Somers, Spottiswoode,
& Louw, 2011). Rather than approaching the fearful stimuli in a graded fashion,
an interesting question would be to what extent the process of change would be
accelerated by directly exposing patients to the most intensely feared stimuli (Craske
et al., 2008). So far, this has not been tested, and of course an obvious condition would
be the willingness of the patient to engage in such an activity. Besides exposure to
painful movements, interoceptive exposure has been developed, when the conditioned
stimulus is considered to be within the body. Interoceptive exposure has been applied
in people with panic disorder and posttraumatic stress disorder (Wald, Taylor, Chiri,
& Sica, 2010) and the first results in chronic pain patients are encouraging (Craske
et al., 2011; De Peuter, Van Diest, Vansteenwegen, Van den Bergh, & Vlaeyen, 2011;
Flink, Nicholas, Boersma, & Linton, 2009). Finally, the treatment would be made
more accessible to a larger group of patients if self-exposure, with a manual, were to
be as effective as the therapist-guided exposure we described here. The reason we have
chosen graded exposure with the aid of the therapist is that, based on our experience,
we felt that it would provide the most credible, safe, and effective treatment approach.
Outcome Studies of Exposure In Vivo for Pain-Related Fear
A recent review of treatments available to address fear-avoidance beliefs in patients with

chronic musculoskeletal pain suggests that both graded exposure and acceptance and
commitment therapy result in the best outcomes for treating patients with increased
pain-related fear (Bailey et al., 2010). So far, the published randomized controlled
trials on the effectiveness of graded exposure in chronic low back pain have produced
mixed results. Woods and Asmundson (2008) randomly assigned 44 patients to
graded exposure, graded activity, or a wait-list condition. In comparison with the
graded activity condition, patients in the graded exposure condition demonstrated
significantly larger improvements on measures of fear of pain/movement, fear-
avoidance beliefs, and pain-related anxiety, but only trend differences for pain-related
disability and pain self-efficacy. When graded exposure was compared to the wait-
list control group, graded exposure showed significantly greater improvements on
measures of fear-avoidance beliefs, fear of pain/movement, pain-related anxiety, pain
catastrophizing, pain experience, anxiety, and depression. Over a 3-month follow-
up, the graded exposure condition maintained improvements. Linton et al. (2008)
Chronic Pain 481
randomized 46 participants to either a graded exposure plus usual treatment or a

wait-list control plus usual treatment group. After the waiting period, the control
group crossed over and received graded exposure. The exposure group scored better
on functioning, but not on fear nor on pain, and the effect sizes were modest. When
the control group crossed over to treatment, significant treatment effects were noted
for fear and function. Compared to a group receiving usual treatment and waiting
for exposure, graded exposure demonstrated a significantly larger improvement on
function. Overall, graded exposure had moderate effects on function, fear, and pain
intensity. The authors conclude that graded exposure may be important in treatment,
but that it is not recommended as a stand-alone intervention that is added to usual
care. A multicenter trial included 85 patients in either a graded exposure or a graded
activity program (Leeuw et al., 2008). It was demonstrated that graded exposure,
despite excelling in diminishing pain catastrophizing and perceived harmfulness of
activities, was equally effective as graded activity in improving functional disability and
main complaints, although the group difference almost reached statistical significance
in favoring exposure. Treatment conditions did not differ in changing pain intensity
and daily activity levels, nor was graded exposure superior to graded activity in the
subgroup of highly fearful patients. Irrespective of treatment, approximately half the
patients reported clinically relevant improvements in main complaints and functional
disability, although for the latter outcome the group difference was almost significant
in favoring graded exposure. This study demonstrates that up to 6 months after
treatment exposure is an effective treatment, but not more effective than graded
activity, in moderately to highly fearful patients, although its superiority in altering
pain catastrophizing and perceived harmfulness of activities is clearly established.
An interesting additional finding of this study is that the differential effects of
both treatments on disability are mediated by changes in the perceived harmfulness
of physical activities. All the abovementioned studies have included patients with
chronic low back pain. Single case studies have shown that graded exposure can also
be successfully applied to other chronic pain conditions as complex regional pain
syndrome type I (CRPS-I; de Jong et al., 2005), posttraumatic neck pain (de Jong
et al., 2008), work-related upper extremity pain (de Jong, Vlaeyen, van Eijsden, Loo,
& Onghena, 2012), and vaginismus (ter Kuile et al., 2009).
References
Arena, J. G., & Blanchard, E. B. (2002). Biofeedback training for chronic pain disorders.
In D. C. Turk & R. J. Gatchel (Eds.), Psychological approaches to pain management: A
practitioner’s handbook (2nd ed., pp. 138–158). New York, NY: Guilford Press.
Bailey, K. M., Carleton, R. N., Vlaeyen, J. W., & Asmundson, G. J. (2010). Treatments
addressing pain-related fear and anxiety in patients with chronic musculoskeletal pain: A
preliminary review. Cognitive Behaviour Therapy, 39, 46–63.
Barlow, D. H., Nock, M., & Hersen, M. (2009). Single case experimental designs: Strategies for
studying behavior change (3rd ed.). New York, NY: Pearson.
Beck, A. T. (1970). Cognitive therapy: Nature and relation to behavior therapy. Behavior
Therapy, 1, 184–200.
Beck, A. T., Rush, A. J., Shaw, B. F., & Greenberg, R. L. (1979). Cognitive therapy of
depression. New York, NY: Guilford Press.
Bishop, S. R., Lau, M., Shapiro, S., Carlson, L., Anderson, N. D., & Carmody, J. (2004).
Mindfulness: A proposed operational definition. Clinical Psychology Science & Practice,
11, 230–241.
Bovend’Eerdt, T. J., Botell, R. E., & Wade, D. T. (2009). Writing SMART rehabilitation
goals and achieving goal attainment scaling: A practical guide. Clinical Rehabilitation,
23, 352–361.
Burns, J. W., Kubilus, A., Bruehl, S., Harden, R. N., & Lofland, K. (2003). Do changes
in cognitive factors influence outcome following multidisciplinary treatment for chronic
pain? A cross-lagged panel analysis. Journal of Consulting & Clinical Psychology, 71,
81–91.
Burton, A. K., Waddell, G., Tillotson, K. M., & Summerton, N. (1999). Information and
advice to patients with back pain can have a positive effect: A randomized controlled trial
of a novel educational booklet in primary care. Spine, 24, 2484–2491.
Cassidy, E. L., Atherton, R. J., Robertson, N., Walsh, D. A., & Gillett, R. (2012). Mindfulness,
functioning and catastrophizing after multidisciplinary pain management for chronic low
back pain. Pain, 153, 644–650.
Charmaz, K. (1999). From the “sick role” to stories of self: Understanding the self in illness.
In R. J. Contrada & R. D. Ashmore (Eds.), Self, social identity, and physical health (1st
ed., Vol. 2, pp. 209–239). Oxford, England: Oxford University Press.
Craske, M. G., Kircanski, K., Zelikowsky, M., Mystkowski, J., Chowdhury, N., & Baker, A.
(2008). Optimizing inhibitory learning during exposure therapy. Behaviour Research and
Therapy, 46(1), 5–27.
Craske, M. G., Wolitzky-Taylor, K. B., Labus, J., Wu, S., Frese, M., & Mayer, E. A. (2011). A
cognitive-behavioral treatment for irritable bowel syndrome using interoceptive exposure
to visceral sensations. Behaviour Research & Therapy, 49, 413–421.
Crombez, G., Eccleston, C., Vlaeyen, J. W., Vansteenwegen, D., Lysens, R., & Eelen, P.
(2002). Exposure to physical movements in low back pain patients: Restricted effects of
generalization. Health Psychology, 21, 573–578.
Dahl, J. C., Wilson, K. G., Luciano, C., & Hayes, S. C. (2005). Acceptance and commitment
therapy for chronic pain. Reno, NV: Context Press.
de Jong, J. R., Vangronsveld, K., Peters, M. L., Goossens, M. E., Onghena, P., &
Bulte, I. (2008). Reduction of pain-related fear and disability in post-traumatic neck
pain: A replicated single-case experimental study of exposure in vivo. Journal of Pain, 9,
1123–1134.
de Jong, J. R., Vlaeyen, J. W., Onghena, P., Cuypers, C., den Hollander, M., & Ruijgrok, J.
(2005). Reduction of pain-related fear in complex regional pain syndrome type I: The
application of graded exposure in vivo. Pain, 116, 264–275.
de Jong, J. R., Vlaeyen, J. W., van Eijsden, M., Loo, C., & Onghena, P. (2012). Reduction of
pain-related fear and increased function and participation in work-related upper extremity
pain (WRUEP): Effects of exposure in vivo. Pain, 153, 2109–2118.
De Peuter, S., Van Diest, I., Vansteenwegen, D., Van den Bergh, O., & Vlaeyen, J. W. (2011).
Understanding fear of pain in chronic pain: Interoceptive fear conditioning as a novel
approach. European Journal of Pain, 15, 889–894. doi:10.1016/j.ejpain.2011.03.002
Dick, B. D., & Rashiq, S. (2007). Disruption of attention and working memory traces in
individuals with chronic pain. Anesthesia and Analgesia, 104, 1223–1229.
Eccleston, C., & Crombez, G. (1999). Pain demands attention: A cognitive-affective model of
the interruptive function of pain. Psychological Bulletin, 125, 356–366.
Chronic Pain 483
Eccleston, C., Williams, A. C. de C., & Morley, S. (2009). Psychological therapies for
the management of chronic pain (excluding headache) in adults. Cochrane Database of
Systematic Reviews, 15. doi:10.1002/14651858
Ellis, A. (1980). Psychotherapy and atheistic values: A response to A. E. Bergin’s “Psychotherapy
and religious values.” Journal of Consulting and Clinical Psychology, 48, 635–639.
Flink, I. K., Nicholas, M. K., Boersma, K., & Linton, S. J. (2009). Reducing the threat value of
chronic pain: A preliminary replicated single-case study of interoceptive exposure versus
distraction in six individuals with chronic back pain. Behaviour Research & Therapy, 47 ,
721–728.
Flor, H., & Birbaumer, N. (1993). Comparison of the efficacy of electromyographic biofeed-
back, cognitive-behavioral therapy, and conservative medical interventions in the treatment
of chronic musculoskeletal pain. Journal of Consulting & Clinical Psychology, 61, 653–658.
Flor, H., & Turk, D. C. (2011). Chronic pain: An integrated biobehavioral approach. Seattle,
WA: IASP Press.
Folkman, S., & Lazarus, R. S. (1980). An analysis of coping in a middle-aged community
sample. Journal of Health and Social Behavior, 21, 219–239.
Fordyce, W. E. (1976). Behavioral methods for chronic pain and illness. St Louis, MO: Mosby.
Fresco, D. M., Segal, Z. V., Buis, T., & Kennedy, S. (2007). Relationship of posttreatment
decentering and cognitive reactivity to relapse in major depression. Journal of Consulting
Gatzounis, R., Schrooten, M. G., Crombez, G., & Vlaeyen, J. W. (2012). Operant learning
theory in pain and chronic pain rehabilitation. Current Pain and Headache Reports, 16,
117–126. doi:10.1007/s11916-012-0247-1
Gheldof, E. L., Crombez, G., Van den Bussche, E., Vinck, J., Van Nieuwenhuyse, A., &
Moens, G. (2010). Pain-related fear predicts disability, but not pain severity: A path
analytic approach of the fear-avoidance model. European Journal of Pain, 14, 870e1–9.
Goubert, L., Crombez, G., & Van Damme, S. (2004). The role of neuroticism, pain catastro-
phizing and pain-related fear in vigilance to pain: A structural equations approach. Pain,
107 , 234–241.
Grisart, J., Van der Linden, M., & Masquelier, E. (2002). Controlled processes and automaticity
in memory functioning in fibromyalgia patients: Relation with emotional distress and
hypervigilance. Journal of Clinical and Experimental Neuropsychology, 24, 994–1009.
Hayes, S. C., Barnes-Holmes, D., & Roche, B. (2001). Relational frame theory: A post-
Skinnerian account of human language and cognition. New York, NY: Kluwer.
Helsen, K., Goubert, L., Peters, M. L., & Vlaeyen, J. W. (2011). Observational learning and
pain-related fear: An experimental study with colored cold pressor tasks. Journal of Pain,
12, 1230–1239.
Higgins, J. P. T., & Green, S. (2008). Cochrane Handbook for Systematic Reviews of Interven-
tions. Chichester, England: John Wiley and Sons, Ltd.
Hoffman, B. M., Papas, R. K., Chatkoff, D. K., & Kerns, R. D. (2007). Meta-analysis of
psychological interventions for chronic low back pain. Health Psychology, 26, 1–9.
Holroyd, K. A., Penzien, D. B., Hursey, K. G., Tobin, D. L., Rogers, L., & Holm, J. E.
(1984). Change mechanisms in EMG biofeedback training: Cognitive changes underlying
improvements in tension headache. Journal of Consulting & Clinical Psychology, 52,
1039–1053.
Houben, R. M., Ostelo, R. W., Vlaeyen, J. W., Wolters, P. M., Peters, M., & Stomp-van den
Berg, S. G. (2005). Health care providers’ orientations towards common low back pain
predict perceived harmfulness of physical activities and recommendations regarding return
to normal activity. European Journal of Pain, 9, 173–183.
Jensen, M. C., Brant-Zawadzki, M. N., Obuchowski, N., Modic, M. T., Malkasian, D., &
Ross, J. S. (1994). Magnetic resonance imaging of the lumbar spine in people without
back pain. New England Journal of Medicine, 331, 69–73.
Jensen, M. P., Wang, W., Potts, S. L., & Gould, E. M. (2013). The meaning of global outcome
measures in pain clinical trials: More than just change in pain intensity. Clinical Journal
of Pain, 29, 289–295.
preliminary results. General Hospital Psychiatry, 4, 443–447.
Keefe, F. J., Beaupré, P. M., Gil, K. M., Rumble, M. E., & Aspnes, A. K. (2002). Group
therapy with patients with chronic pain. In D. C. Turk & R. J. Gatchel (Eds.), Psychological
approaches to pain management: A practitioner’s handbook (2nd ed., pp. 234–255). New
Keefe, F. J., Blumenthal, J., Baucom, D., Affleck, G., Waugh, R., & Caldwell, D. S. (2004).
Effects of spouse-assisted coping skills training and exercise training in patients with
osteoarthritic knee pain: A randomized controlled study. Pain, 110, 539–549.
Keefe, F. J., Crisson, J., Urban, B. J., & Williams, D. A. (1990). Analyzing chronic low back
pain: The relative contribution of pain coping strategies. Pain, 40, 293–301.
Leeuw, M., Goossens, M. E., van Breukelen, G. J., Boersma, K., & Vlaeyen, J. W. (2007).
Measuring perceived harmfulness of physical activities in patients with chronic low back
pain: The Photograph Series of Daily Activities—Short electronic version. Journal of
Pain, 8, 840–849.
Leeuw, M., Goossens, M. E., van Breukelen, G. J., de Jong, J. R., Heuts, P. H., & Smeets,
R. J. (2008). Exposure in vivo versus operant graded activity in chronic low back pain
patients: Results of a randomized controlled trial. Pain, 138, 192–207.
Lefebvre, M. F. (1981). Cognitive distortion and cognitive errors in depressed psychiatric and
low back pain patients. Journal of Consulting and Clinical Psychology, 49, 517–525.
Legrain, V., Damme, S. V., Eccleston, C., Davis, K. D., Seminowicz, D. A., & Crombez, G.
(2009). A neurocognitive model of attention to pain: Behavioral and neuroimaging
evidence. Pain, 144, 230–232.
Linton, S. J., Boersma, K., Jansson, M., Overmeer, T., Lindblom, K., & Vlaeyen, J. W. (2008).
A randomized controlled trial of exposure in vivo for patients with spinal pain reporting
fear of work-related activities. European Journal of Pain, 12, 722–730.
Litt, M. D., Shafer, D. M., Ibanez, C. R., Kreutzer, D. L., & Tawfik-Yonkers, Z. (2010).
Momentary pain and coping in temporomandibular disorder pain: Exploring mechanisms
of cognitive behavioral treatment for chronic pain. Pain, 151, 110–116.
Ludwig, D. S., & Kabat-Zinn, J. (2008). Mindfulness in medicine. JAMA, 300, 1350–1352.
doi:10.1001/jama.300.11.1350
Mahoney, M. J., & Thoresen, C. E. (1974). Self-control: Power to the person. Monterey, CA:
Brooks/Cole.
McCracken, L. M. (2005). Contextual cognitive-behavioral therapy for chronic pain (Progress
in Pain Research and Management, Vol. 33). Seattle, WA: IASP Press.
McCracken, L. M., Keogh, E., McCracken, L. M., & Keogh, E. (2009). Acceptance, mindful-
ness, and values-based action may counteract fear and avoidance of emotions in chronic
pain: An analysis of anxiety sensitivity. Journal of Pain, 10, 408–415.
McMillan, D., & Morley, S. (2010). Single-case quantitative methods. In M. Barkham & G.
E. Hardy (Eds.), A core approach to delivering practice-based evidence (pp. 109–138).
Chichester, England: John Wiley & Sons, Ltd.
Melzack, R., & Wall, P. D. (1965). Pain mechanisms: A new theory. Science, 150, 971–979.
Chronic Pain 485
Meulders, A., Vansteenwegen, D., & Vlaeyen, J. W. (2011). The acquisition of fear of
movement-related pain and associative learning: A novel pain-relevant human fear condi-
tioning paradigm. Pain, 152, 2460–2469.
Meulders, A., & Vlaeyen, J. W. (2012). Reduction of fear of movement-related pain and pain-
related anxiety: An associative learning approach using a voluntary movement paradigm.
Pain, 153, 1504–1513.
Meyerbroker, K., & Emmelkamp, P. M. (2010). Virtual reality exposure therapy in anxiety
disorders: A systematic review of process-and-outcome studies. Depression and Anxiety,
27 , 933–944.
Morley, S. (2008). Psychology of pain. British Journal of Anaesthesia, 101, 25–31. doi:aen123
[pii] 10.1093/bja/aen123
Morley, S. (2010). Attention management. In R. Bell, E. Kalso, J. Plaice, & O. Soyannwo
(Eds.), A global problem: Cancer pain from the laboratory to the bedside (pp. 246–265).
Seattle, WA: IASP Press.
Morley, S., Davies, C., & Barton, S. (2005). Possible selves in chronic pain: Self-pain
enmeshment, adjustment and acceptance. Pain, 115, 84–94.
Morley, S., & Eccleston, C. (2004). The object of fear in pain. In G. J. Asmundson, J. Vlaeyen,
& G. Crombez (Eds.), Understanding and treating fear of pain (pp. 163–188). Oxford,
England: Oxford University Press.
Morley, S., Eccleston, C., & Williams, A. (1999). Systematic review and meta-analysis of
randomized controlled trials of cognitive behaviour therapy and behaviour therapy for
chronic pain in adults, excluding headache. Pain, 80, 1–13.
Morley, S., & Keefe, F. J. (2007). Editorial: Getting a handle on process and change in CBT
for chronic pain. Pain, 127 , 197–198.
Morley, S., Shapiro, D. A., & Biggs, J. (2004). Developing a treatment manual for attention
management in chronic pain. Cognitive Behaviour Therapy, 33, 1–11.
Morley, S., Williams, A., & Eccleston, C. (in press). Examining the evidence about psychological
treatments for chronic pain: time for a paradigm shift?. Pain. doi: 10.1016/j.pain.
2013.05.049
Morone, N. E., Greco, C. M., & Weiner, D. K. (2008). Mindfulness meditation for the
treatment of chronic low back pain in older adults: A randomized controlled pilot study.
Pain, 134, 310–319.
Morris, L. D., Grimmer-Somers, K. A., Spottiswoode, B., & Louw, Q. A. (2011). Virtual
reality exposure therapy as treatment for pain catastrophizing in fibromyalgia patients:
Proof-of-concept study (Study Protocol). BMC Musculoskeletal Disorders, 12, 85.
Naylor, M. R., Keefe, F. J., Brigidi, B., Naud, S., & Helzer, J. E. (2008). Therapeutic
Interactive Voice Response for chronic pain reduction and relapse prevention. Pain, 134,
335–345. doi:S0304-3959(07)00651-3 [pii] 10.1016/j.pain.2007.11.001
Nielson, W. R., Jensen, M. P., Karsdorp, P. A., & Vlaeyen, J. W. (2013). Activity pacing in
chronic pain: Concepts, evidence, and future directions. Clinical Journal of Pain, 29,
461–468.
Risdon, A., Eccleston, C., Crombez, G., & McCracken, L. (2003). How can we learn to live
with pain? A Q-methodological analysis of the diverse understandings of acceptance of
chronic pain. Social Science & Medicine, 56, 375–386.
Rosenthal, R. (1994). Parametric measures of effect size. In H. Cooper & L. V. Hedges
(Eds.), The handbook of research synthesis (pp. 231–244). New York, NY: Russell Sage
Foundation.
Sanders, S. H. (2002). Operant conditioning with chronic pain: Back to basics. In D. C. Turk
& R. J. Gatchel (Eds.), Psychological approaches to pain management: A practitioner’s
handbook (2nd ed., pp. 128–137). New York, NY: Guilford Press.
Schmidt, S., Grossman, P., Schwarzer, B., Jena, S., Naumann, J., & Walach, H. (2011).
Treating fibromyalgia with mindfulness-based stress reduction: Results from a 3-armed
randomized controlled trial. Pain, 152, 361–369.
Schutze, R., Rees, C., Preece, M., & Schutze, M. (2010). Low mindfulness predicts pain
catastrophizing in a fear-avoidance model of chronic pain. Pain, 148, 120–127.
Sidman, M. (1960). The tactics of scientific research. New York, NY: Basic Books.
Smeets, R. J. E. M., Vlaeyen, J. W. S., Kester, A. D. M., & Knottnerus, J. A. (2006). Reduction
of pain catastrophizing mediates the outcome of both physical and cognitive-behavioral
treatment in chronic low back pain. Journal of Pain, 7 , 261–271.
Smith, T. W., Follick, M. J., Ahern, D. K., & Adams, A. (1986). Cognitive distortion and
disability in chronic low back pain. Cognitive Therapy & Research, 10, 201–210.
Spinhoven, P., ter Kuile, M., Kole-Snijders, A. M., Hutten Mansfeld, M., den Ouden, D. J.,
& Vlaeyen, J. W. (2004). Catastrophizing and internal pain control as mediators of
outcome in the multidisciplinary treatment of chronic low back pain. European Journal of
Pain, 8, 211–219.
Sutherland, R., & Morley, S. (2008). Self-pain enmeshment: Future possible selves, sociotropy,
autonomy and adjustment to chronic pain. Pain, 137 , 366–377.
Swinkels-Meewisse, I. E., Roelofs, J., Oostendorp, R. A., Verbeek, A. L., & Vlaeyen, J. W.
(2006). Acute low back pain: Pain-related fear and pain catastrophizing influence physical
performance and perceived disability. Pain, 120, 36–43.
Teasdale, J. D., Segal, Z., & Williams, J. M. G. (1995). How does cognitive therapy
prevent depressive relapse and why should attentional control (mindfulness) training
help? Behaviour Research & Therapy, 33, 25–39.
ter Kuile, M. M., Bulté, I., Weijenborg, P. T. M., Beekman, A., Melles, R., & Onghena, P.
(2009). Therapist-aided exposure for women with lifelong vaginismus: A replicated
single-case design. Journal of Consulting and Clinical Psychology, 77 , 149–159.
Thorn, B. E. (2004). Cognitive therapy for chronic pain. New York, NY: Guilford Press.
Trost, Z., France, C. R., & Thomas, J. S. (2008). Exposure to movement in chronic back pain:
Evidence of successful generalization across a reaching task. Pain, 137 , 26–33.
Turk, D. C., Meichenbaum, D., & Genest, M. (1983). Pain and behavioral medicine: A
cognitive-behavioral perspective. New York, NY: Guilford Press.
Turk, D. C., & Melzack, R. (Eds.). (2001). Handbook of pain assessment (2nd ed.). New York,
NY: Guilford Press.
Turner, J. A., Holtzman, S., & Mancl, L. (2007). Mediators, moderators, and predictors of
therapeutic change in cognitive-behavioral therapy for chronic pain. Pain, 127 , 276–286.
Turner, J. A., & Jensen, M. P. (1993). Efficacy of cognitive therapy for chronic low back pain.
Pain, 52, 169–177.
Veehof, M. M., Oskam, M.-J., Schreurs, K. M. G., & Bohlmeijer, E. T. (2011). Acceptance-
based interventions for the treatment of chronic pain: A systematic review and meta-
analysis. Pain, 152, 533–542.
Vlaeyen, J. W., de Jong, J., Geilen, M., Heuts, P. H., & van Breukelen, G. (2001). Graded
exposure in vivo in the treatment of pain-related fear: A replicated single-case experimental
design in four patients with chronic low back pain. Behaviour Research & Therapy, 39,
151–166.
Vlaeyen, J. W., Groenman, N. H., Thomassen, J., Schuerman, J. A., van Eek, H., Snijders,
A. M., & van Houtem, J. (1989). A behavioral treatment for sitting and standing
intolerance in a patient with chronic low back pain. Clinical Journal of Pain, 5, 233–237.
Vlaeyen, J. W., & Linton, S. J. (2000). Fear-avoidance and its consequences in chronic
musculoskeletal pain: A state of the art. Pain, 85, 317–332.
Chronic Pain 487
Vlaeyen, J. W. S., Morley, S., Linton, S., Boersma, K., & de Jong, J. (2012). Pain-related fear:
Exposure-based treatment of chronic pain. Seattle, WA: IASP Press.
Wald, J., Taylor, S., Chiri, L. R., & Sica, C. (2010). Posttraumatic stress disorder and
chronic pain arising from motor vehicle accidents: Efficacy of interoceptive exposure plus
trauma-related exposure therapy. Cognitive Behaviour Therapy, 39, 104–113.
White, B., & Sanders, S. H. (1985). Differential effects on pain and mood in chronic pain
patients with time- versus pain-contingent medication delivery. Behavior Therapy, 16,
28–38.
Wideman, T. H., Adams, H., & Sullivan, M. J. (2009). A prospective sequential analysis of the
fear-avoidance model of pain. Pain, 145, 45–51.
Williams, A. C. de C., Eccleston, C., & Morley, S. (2012). Psychological therapies for
the management of chronic pain (excluding headache) in adults. Cochrane Database of
Systematic Reviews, 15.
Press.
Woods, M. P., & Asmundson, G. J. (2008). Evaluating the efficacy of graded in vivo exposure
for the treatment of fear in patients with chronic back pain: A randomized controlled
clinical trial. Pain, 136, 271–280.
21
Hypochondriasis
Gordon J. G. Asmundson, Daniel L. Peluso,
and Michel A. Thibodeau
University of Regina, Canada
Steven Taylor
University of British Columbia, Canada
Introduction
Bodily sensations and changes—such as the discovery of a new or unusual bump on

the inside of the thigh, repeated headaches, or shooting muscle pain—often lead a
person to experience concern and anxiety about his or her health. This often prompts
the person to seek medical advice. If the source of concern is deemed innocuous, or
if advised courses of action reduce or eliminate the concerning bodily sensation or
change, the perception of health threat typically abates and anxiety resolves. In some
cases, however, anxiety about one’s health may persist even after assurance from a
medical professional that there is no medical basis for concern. When health anxiety is
out of proportion to actual medical threat, and if associated with disproportionate and
persistent impairment or distress, a diagnosis of hypochondriasis may be warranted.
The purposes of this chapter are the following. First, we define health anxiety, a
construct that is closely tied to hypochondriasis and related diagnoses proposed for
the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5).
Second, we outline the classification of hypochondriasis and related diagnoses, along
with details pertaining to epidemiology, course, and prognosis. Third, we describe
factors implicated in the etiology and maintenance of hypochondriasis, including
important cognitive and behavioral factors. Finally, assessment and treatment options
and innovations are described.
Health Anxiety Defined
Anxiety about health is a ubiquitous experience that occurs when perceived bodily
sensations or changes are interpreted as symptoms of a serious disease. As several

DOI: 10.1002/9781118528563.wbcbt21
theorists (e.g., Salkovskis & Warwick, 1986; Taylor & Asmundson, 2004) have
suggested, health anxiety comprises core cognitive and behavioral features and,
collectively, these appear to range in magnitude along a continuum from mild to
severe. The core cognitive feature is disease conviction; that is, bodily sensations and
changes are perceived as being indicative of disease processes as opposed to benign
bodily perturbations, symptoms of minor ailments, or autonomic nervous system
arousal. A range of dysfunctional beliefs (e.g., the doctor has missed something
critical, the lab test must be wrong) may accompany disease conviction. These
cognitive factors, together with disease-related preoccupation and worry, motivate
several characteristic maladaptive coping behaviors, including reassurance seeking and
recurrent checking behaviors. These maladaptive coping behaviors, while providing
transient relief from health-related distress (Haenen, de Jong, Schmidt, Stevens, &
Visser, 2000), perpetuate dysfunctional beliefs, maladaptive coping behaviors, and
associated distress and functional limitations (Warwick & Salkovskis, 1990).
Whether health anxiety is a construct that varies between people in degree along
a continuum, as opposed to existing as nonpathological versus pathological classes
or taxa, might influence the nature of research and treatment. Three recent studies
using relatively large samples have empirically tested the conceptualization of health
anxiety as continuous. Both Ferguson (2009) and Longley et al. (2010) utilized
taxometric analyses to demonstrate that the health anxiety construct, measured using
data from a variety of measures, was best explained by a continuous as opposed to
taxonic (i.e., comprising qualitatively distinct normal and maladaptive forms) model.
A more recent study (Asmundson, Taylor, Carleton, Weeks, & Hadjstavropoulos,
2012) utilized factor mixture modeling to demonstrate that health anxiety might
best be conceptualized as taxonic; specifically, findings indicated a taxon comprising
a larger health “anxious” class and a smaller “nonanxious” class with few, if any,
concerns regarding health. While additional research regarding this putative nonanx-
ious health anxiety class is warranted, the findings appear to converge regarding the
conceptualization of health anxiety along a continuum ranging from moderate to
severe anxiety. It is the latter expression of health anxiety that is particularly germane
to hypochondriasis and related conditions.
Classification
Expressions of severe health anxiety are not circumscribed to any single mental dis-
order. Rather, severe health anxiety is an intrinsic feature of three mental disorders
outlined in the Diagnostic and Statistical Manual of Mental Disorders (4th ed., text
rev.; DSM-IV-TR; American Psychiatric Association [APA], 2000)—hypochondriasis,
specific phobia (other type; i.e., disease phobia), and delusional disorder (somatic
type). Disease phobia and delusional disorder (somatic type), respectively character-
ized by the fear of acquiring or catching a disease (e.g., HIV, cancer) and implausible
health-related fears (e.g., that the body is emitting a foul odor despite reassurance to
the contrary), are discussed in greater detail elsewhere (Taylor & Asmundson, 2004).
Hypochondriasis is classified as a somatoform disorder in the DSM-IV-TR. Somato-
form disorders are defined by medically unexplained physical symptoms that are not
Hypochondriasis 491
due to another mental disorder or due to the effects of substance use. In order to
meet DSM-IV-TR criteria for hypochondriasis, an individual must be significantly
concerned about having a serious medical condition based on the misinterpretation
of benign bodily sensations (criterion A). Concern ranges from highly specific (e.g.,
“This cough is so bad. I must have chronic obstructive pulmonary disease”) to vague
and diffuse (e.g., “I’m so clumsy lately. Why? Could it be multiple sclerosis? A brain
tumor? What about Parkinson’s disease?”). The concern must endure despite assur-
ance from medical professionals that there is no medical threat (criterion B) and must
not be of intensity reflecting a delusional disorder nor restricted to concerns about
physical appearance (such as in body dysmorphic disorder; criterion C). Health-related
preoccupation must cause significant distress and impairment (criterion D) and last
at least 6 months (criterion E). Hypochondriasis with poor insight may be assigned
in cases where an individual does not recognize that his or her preoccupations are
excessive.
Hypochondriasis overlaps in many ways with several anxiety disorders, which raises
the question of whether it should be classified as an anxiety disorder (Collimore,
Asmundson, Taylor, & Abramowitz, 2009; Olatunji, Deacon, & Abramowitz,
2009). Hypochondriasis and panic disorder are similar with respect to somatic
focus, somatization, and beliefs that arousal-related somatic sensations are indicative
of a serious medical condition (e.g., heart attack, stroke; Deacon & Abramowitz,
2008; Hiller, Leibbrand, Rief, & Fichter, 2005). Hypochondriasis and obsessive-
compulsive disorder are similar in repetitive checking behaviors and reassurance
seeking. Hypochondriasis differs from these disorders in that it is characterized by
more severe health anxiety and stronger health-related dysfunctional beliefs (Deacon
& Abramowitz, 2008).
The classification of hypochondriasis is likely to change considerably with the pub-
lication of the DSM-5 (http://dsm5.org). Hypochondriasis, somatization disorder,
and pain disorder will no longer be independent diagnoses and will likely be sub-
sumed within a new diagnosis called somatic symptom disorder. This new diagnosis
is characterized by at least 6 months of (a) one or more distressing somatic symp-
toms, (b) health-related dysfunctional beliefs (e.g., excessive worry), (c) excessive
health anxiety, and (d) maladaptive behaviors (e.g., unnecessary reassurance seeking).
The symptoms are not necessarily medically unexplained, but must be associated
with disproportionate concern. An optional specifier of predominant pain (previously
pain disorder) will also likely become applicable to a diagnosis of somatic symptom
disorder.
A new diagnosis—illness anxiety disorder—is also expected in the DSM-5. This
diagnosis, also called hypochondriasis without somatic symptoms, applies to individuals
who experience severe health anxiety without any salient bodily features or sensations.
Two subtypes have been proposed, including a care-seeking subtype (associated with
elevated health care usage) and a care-avoidant subtype (medical care is avoided as
diagnostic procedures elevate one’s anxiety). An individual who experiences significant
fear and anxiety regarding contracting an illness would meet criteria for illness
anxiety disorder. Consequently, the diagnosis of specific phobia (other type) will
likely no longer be relevant as a diagnosis for severe health anxiety under DSM-5
classification.
Epidemiology
The lifetime prevalence rate of hypochondriasis is approximately 1 to 5% (APA,

2000). It has point and 12-month prevalence rates of approximately 0.4% and 4.5%,
respectively, in the general population (Bleichhardt & Hiller, 2007; Faravelli et al.,
1997; Looper & Kirmayer, 2001). Not surprisingly, the prevalence is greater in health
care settings (Escobar et al., 1998; Gureje, Ustun, & Simon, 1997; Noyes et al.,
1993). Specific phobia (other type) has a lifetime prevalence of 3–4%. Delusional
disorder (somatic type) is comparatively rare, with a lifetime prevalence of less than
0.05% (Agras, Sylvester, & Oliveau, 1969; APA, 2000; Malis, Hartz, Doebbeling, &
Noyes, 2002).
Course and Prognosis
Severe health anxiety is typically chronic and usually develops in early adulthood,
although it can develop at any age (APA, 2000). Onset typically occurs during
or after illness, after the loss of a family member, or after exposure to illness-
related information (e.g., via the media or anecdotally from a friend; Barsky &
Klerman, 1983). Whether health anxiety increases with age is not well under-
stood. Prognosis of severe health anxiety is difficult to predict because of the
heterogeneity of presentation and substantial comorbidity with other disorders
(e.g., anxiety disorders, somatization disorders; Barsky, Wyshak, & Klerman, 1992;
Noyes et al., 1994). Certain prognostic indicators have been associated with a
good outcome, such as short duration of health anxiety, mild symptoms, fewer
stressful life events, absence of strongly held health-related beliefs and dysfunc-
tional cognitions related to bodily functioning, lack of medical conditions, and
absence of secondary gains that reinforce illness behavior (APA, 2000; Barsky, 1996;
Fallon, Klein, & Liebowitz, 1993; Hiller, Leibbrand, Rief, & Fichter, 2002; Noyes
et al., 1993; Pilowsky, 1968; Speckens, Spinhoven, van Hermert, Bolk, & Hawton,
1997).
Etiology and Maintenance
We find it useful to separate the etiological factors from maintenance factors of

severe health anxiety. Understanding which factors (e.g., biological predispositions,
traumatic events) contribute to initial development is crucial to theoretical concep-
tualization of health anxiety and these factors can often be considered as targets in
relapse prevention (e.g., identifying what factors could lead to severe health anxiety
in the future). Factors that maintain health anxiety (e.g., environmental factors, cog-
nitive distortions, maladaptive behaviors), on the other hand, are often direct targets
of treatment.
Hypochondriasis 493
Etiology
Behavioral-genetic (twin) research indicates that the core facets of severe health
anxiety (i.e., disease conviction, checking behavior) are shaped by a combination
of genetic and environmental factors (Taylor, Thordarson, Jang, & Asmundson,
2006). This suggests that severe presentations of health anxiety may, at least in
part, be heritable. However, environmental factors as well as gene by environment
interactions appear important as well. Adverse childhood experiences, such as physical
abuse, are associated with numerous mental disorders in adulthood (Paris, 1998; Stein
et al., 1996), including hypochondriasis (Barsky, Wool, Barnett, & Cleary, 1994).
Retrospective studies suggest parental style (e.g., being overprotective, reinforcing
illness behaviors) may impact the expression of hypochondriasis (Baker & Merskey,
1982; Parker & Lipscombe, 1980; Schwartz, Gramling, & Mancini, 1994; Whitehead
et al., 1994). The problem with these studies is that they fail to take genetic factors
into consideration. Twin research indicates that parenting style and other forms of
family environment play a minor role, if any, in health anxiety and hypochondriasis
(Taylor & Asmundson, 2012; Taylor et al., 2006). More important are environmental
factors that are not shared by members of a twin pair, such as severe illness or
hospitalizations, in addition to genetic factors (Taylor & Asmundson, 2012; Taylor
et al., 2006).
Little is known about the genes associated with hypochondriasis. As with other dis-
orders, such as obsessive-compulsive disorder (e.g., Taylor, in press), hypochondriasis
is likely to be influenced by numerous genes, with each making a small, incremental
contribution to a person’s risk of developing the disorder. Little is also known about
nonshared environmental factors and individual difference factors that may increase
vulnerability. In addition to periods of significant stress, experiencing serious illness
or hospitalization, or loss of a family member, recent evidence suggests that learning
of the health struggles of strangers may also play a role in the development of
severe health anxiety (Karademas, 2009). A number of putative vulnerability factors,
including anxiety sensitivity (i.e., the fear of arousal-related bodily sensations based
on the belief that they might be harmful) and propensity toward disgust, have also
been implicated in the etiology of severe health anxiety (for a review, see Asmundson,
Abramowitz, Richter, & Whedon, 2010). Additional research on genes and non-
shared environmental factors involved in severe health anxiety and hypochondriasis is
clearly warranted.
Maintenance
Cognitive behavioral formulations (Abramowitz, Schwartz, & Whiteside, 2002;
Taylor & Asmundson, 2004; Warwick & Salkovskis, 1990) highlight how mal-
adaptive health beliefs, interacting with bodily changes or sensations, begin the
cycle that maintains severe health anxiety (see Figure 21.1). Maladaptive health
beliefs are typically centered on personal health, the meaning of illness, and the
meaning of bodily sensations or changes. Individuals with severe health anxiety fre-
quently overestimate the likelihood of being ill and erroneously perceive themselves
as being more likely than others to suffer an illness (Barsky, Cleary, & Klerman,
Environmental factors influencing the Biological factors influencing the

detection of bodily changes or sensations occurrence of somatosensory
(e.g., unstimulating environment) stimulation (e.g., autonomic arousal)
Detection of benign bodily

changes or sensations
Dysfunctional beliefs Increased

about disease focus on body
Sensations misinterpreted
in light of dysfunctional beliefs.
Focus of apprehension:
(1) I might have a serious disease,
or (2) I am at high risk for acquiring
a serious disease
Negative thoughts about Health Attention to relevant

consequences; anxiety (e.g., disease-related)
worry about lack of control over information
these worries; selective recall in environment
of disease-related information
Behavioral consequences (coping responses such as

checking, reassurance-seeking, avoidance, and seeing
many doctors for second, third, etc. opinions) and their
complications (i.e., exposure to terrifying information,
increased focus on health threats, and increased feelings
of vulnerability and dependency).
Figure 21.1 Factors involved in precipitating and perpetuating episodes of excessive health
anxiety. Adapted from Taylor & Asmundson (2004), p. 21. Copyright The Guildford Press.
Reprinted with permission of The Guilford Press.
1992; Barsky, Ettner, Horsky, & Bates, 2001; Hollifield, Paine, Tuttle, & Kellner,
1999). Similarly, individuals with severe health anxiety typically overestimate the costs
of illness and overestimate the consequences of becoming ill (Ditto, Jemmott, &
Darley, 1988; Easterling & Leventhal, 1989; Marcus & Church, 2003). Individuals
with severe health anxiety, compared to controls, are more likely to misinterpret
normal bodily sensations (e.g., transient pain, flushing of the skin) and changes
(e.g., changes in fat distribution due to aging, benign skin imperfections) as indi-
cators of poor health or serious disease rather than normal “bodily noise” (Barsky,
Coeytaux, Sarnie, & Cleary, 1993; Barsky & Wyshak, 1989; Haenen, Schmidt,
Schoenmakers, & van den Hout, 1997). People with severe health anxiety are also
Hypochondriasis 495
more likely to believe that bodily changes do not occur in healthy individuals (Barsky
et al., 1993). Together, these beliefs contribute to the perceived notion and con-
viction that one’s health is in danger (e.g., “The tingling in my arm means I must
be having a heart attack and that I am going to die”), which result in elevated
anxiety.
In order to reduce distress resulting from maladaptive beliefs, individuals with
severe health anxiety often seek reassurance that they are healthy or avoid certain
cues or situations that would exacerbate their anxiety. Seeking reassurance typically
involves consulting a medical professional and requesting medical testing, with the
hope that the results will disprove any health-related fears (e.g., having HIV). For
people without severe health anxiety, assurance from a medical professional is enough
to attenuate their health concerns. This is typically not the case for people with severe
health anxiety. Their reassurance seeking reduces anxiety only for a short time (e.g.,
24 hours; Haenen et al., 2000), which drives the need to seek repeated medical
consultations and testing.
Medical professionals are not the only sources of reassurance. People with severe
health anxiety often seek reassurance from friends and family, and also attempt to
reassure themselves by checking their body for signs of disease or by searching libraries
or the Internet for reassuring medical information. For example, a woman with a
fear of having breast cancer may repeatedly palpate her breast to reassure herself that
she does not have breast cancer, and may also read Internet articles about breast
cancer to find evidence that her symptoms are not actually indicative of breast cancer.
These two forms of reassurance seeking, similar to seeking medical consultations, are
rarely beneficial. Bodily checking leads to the identification of previously unnoticed
and harmless bodily changes (e.g., temporary skin reddening) and the abundance of
health-related information (and misinformation) on the Internet often leads to the
discovery of alarming information about highly rare, lethal disease. This increases
perceived health threat.
Some people with severe health anxiety avoid health-related cues, such as hospitals,
doctors, and bodily checking, as well as television and Internet material pertaining
to health and disease. Activities that induce bodily sensations, such as physical
exertion, may also be feared and avoided. Although reassurance seeking and avoidance
seem contradictory, it is not uncommon for people with severe health anxiety
to use a mix of avoidance and reassurance-seeking as methods for coping with
health anxiety (Taylor & Asmundson, 2004). To illustrate, a woman who fears
having a stroke may avoid cues or situations associated with strokes and increases
in blood pressure (e.g., aspirin commercials, health documentaries), but may also
frequently request medical testing and do independent research on the detriments of
hypertension.
Treatment
The treatments discussed in this section focus primarily on cognitive behavioral

therapy (CBT) approaches to treating severe health anxiety. While other treatments
are available (e.g., pharmacotherapy, psychodynamic), CBT and related therapies
are generally accepted as the front-line treatment for individuals presenting with
severe health anxiety and hypochondriasis (Abramowitz & Braddock, 2011; Taylor
& Asmundson, 2004). Asmundson et al. (2010) provide a recent overview of
pharmacotherapy for severe presentations of health anxiety, as well as evidence
indicating a marked patient preference for CBT.
Treatment always begins with comprehensive assessment, the details of which are
described elsewhere (Taylor & Asmundson, 2004). To summarize, critical steps in
assessment include ruling out medical conditions that may be responsible for present-
ing concerns, establishing that the presenting disease-based concerns are associated
with severe health anxiety, and gathering information pertinent to understanding the
presenting concerns (e.g., personal history, reasons for seeking treatment). People
with severe health anxiety are often unwilling or reluctant to accept that their concerns
are caused by anything other than disease. This poses a considerable challenge to the
cognitive behavioral therapist—how to engage the reluctant patient in psychother-
apy. A combination of validating statements (e.g., “I understand that what you are
experiencing is real”) and motivational interviewing (“You’ve tried many other things
that haven’t provided relief. If these other things haven’t helped, isn’t this at least
worth a try?”) are often helpful in this regard, establishing trust and initiating the
treatment process.
The general goal of CBT for severe health anxiety is not to reduce bodily sensations
or changes (although it often does so); instead, the goal is to help the person discover
explanations for his or her concerns that are not rooted in disease. For example, a
person might discover that the heavy limbs and clumsiness he or she thought likely
to be multiple sclerosis are consequences of recent increases in stress and fatigue.
Psychoeducation, behavioral stress management, exposure and response prevention,
and cognitive therapy are particularly effective in reducing disease conviction and
checking behavior while improving overall functioning and quality of life (Taylor &
Asmundson, 2004); however, meta-analytic findings indicate that the largest effect
sizes are for treatments that combine cognitive and behavioral strategies (Taylor,
Asmundson, & Coons, 2005). The rest of this section discusses the main cognitive
and behavioral strategies.
Psychoeducation
Psychoeducation-based treatments emphasize the dissemination of correct and clear
information to patients about their disorder. Psychoeducation discusses the nature
and function of anxiety in relation to health, focusing on the adaptiveness of these
thoughts and feelings. Importantly, the cognitive behavioral model of health anxiety is
emphasized and the patient is encouraged to conceptualize how the model applies to
his or her specific presentation. Information about safety behaviors, bodily sensations
and changes, and the role of these elements in maintaining and exacerbating anxiety
are discussed. Psychoeducation can be delivered via lectures, demonstrations, focused
group discussions, brief exercises, and homework assignments (Taylor & Asmundson,
2004). Treatments based on psychoeducation have produced reductions in health
Hypochondriasis 497
anxiety, medical consultations, time spent worrying, and physical complaints (Avia
et al., 1996; Buwalda, Bouman, & van Duijn, 2007; Lidbeck, 1997).
Cognitive Therapy
As described earlier, the contemporary cognitive behavioral models of health anxiety
suggest that catastrophic interpretations of bodily sensations/changes and health
information contribute to distressing emotions and maladaptive behaviors that main-
tain anxiety. Cognitive therapy seeks to identify dysfunctional beliefs and replace them
with more adaptive ways of thinking about health. A central technique is cognitive
restructuring, whereby patients learn to gather objective evidence in order to test
faulty beliefs about health and illness (Beck, 1976). The goal is to identify beliefs
and consider alternative interpretations in the service of forming a more accurate or
realistic belief. Additional components of cognitive therapy may include attentional
modification, building tolerance for uncertainty, and worry management (Taylor &
Asmundson, 2004; Warwick & Salkovskis, 2001). Cognitive therapy techniques have
been demonstrated to be effective in reducing maladaptive health-related beliefs, dis-
ease conviction, and somatic arousal (Avia et al., 1996). Generally, treatment studies
using cognitive therapy include a mix of both cognitive and behavioral strategies
(e.g., Clark et al., 1998; Warwick, Clark, Cobb, & Salkovskis, 1996), thereby making
it difficult to discern whether cognitive or behavioral techniques are more effective.
The few dismantling studies that have directly compared cognitive and exposure
therapies as stand-alone treatments (e.g., Bouman & Visser, 1998; Visser & Bouman,
2001) reveal that both techniques are equally effective in reducing severe health
anxiety.
Exposure and Response Prevention

Based on the conceptualization that health anxiety is maintained by preoccupation
with bodily sensations or changes, exposure and response prevention (ERP) is
employed in the treatment of health anxiety. In ERP, the task is for the patient to
confront anxiety-provoking stimuli in order to habituate to the anxiety response and
to notice the dissipation of this arousal. The exposure task also serves as an experiment
to test out the validity of the patient’s fears. Response prevention strategies are
introduced after the exposure, as the patient is discouraged from performing safety
behaviors (e.g., reassurance seeking, bodily checking). In vivo or situational exposure
typically involves exposing the patient to disease-related stimuli that are harmless
(e.g., walking into a hospital). Interoceptive exposure involves exposing the patient
to feared but harmless bodily sensations. Through repeated exposure the patient
learns that the feared sensations are discomforting but innocuous. Imaginal exposure
involves creating fear-evoking thoughts or images involving health-related situations
(e.g., picturing having HIV). This type of exposure can be particularly useful when
situational triggers are logistically impossible (e.g., the patient’s fears center around
being dead and decaying) or when the therapist seeks to augment a situational
exposure (e.g., after visiting a cancer ward in a hospital the patient imagines they are
dying of cancer; Abramowitz, Deacon, & Whiteside, 2011). Though a limited number
of controlled trials exist, preliminary evidence strongly suggests ERP is effective for
reducing severe health anxiety (Abramowitz & Moore, 2007; Bouman & Visser,
1998; Taylor et al., 2005; Visser & Bouman, 2001).
Cognitive Behavioral Therapy

In this integrated approach, the educational, cognitive, and behavioral techniques
described above are integrated. Significant reductions in symptoms have been reported
in uncontrolled and controlled trials of integrated CBT for severe health anxiety
(Asmundson et al., 2010; Taylor et al., 2005). Results from uncontrolled trials have
demonstrated the effectiveness of CBT in reducing dysfunctional beliefs, maladaptive
behaviors, and symptoms of anxiety and depression (Buwalda et al., 2007; Furer et al.,
2001; Martinez & Botella, 2005), with gains maintained at follow-ups of at least 6
months. The majority of these uncontrolled trials have occurred in academic settings,
although equally promising findings have come from trials conducted in nonacademic
health care settings (e.g., Wattar et al., 2005).
In the first controlled trial, Warwick et al. (1996) found CBT produced greater
reductions in health anxiety than did a wait-list control condition. Similar results have
been observed in other controlled trials. For example, Clark et al. (1998) found that
CBT was more effective than wait-list control in reducing disease fears and medical
consultation at posttreatment. While gains in the CBT condition were maintained at
1-year follow-up, they were comparable to 1-year posttreatment gains observed for a
second control condition—behavioral stress management. Barsky and Ahern (2004)
reported that CBT was more effective in reducing disease fears and health anxiety
symptoms compared to routine primary medical care. Again, treatment gains were
maintained at 6-month and 1-year follow-up in this study. Seivewright et al. (2008)
conducted a randomized controlled trial at a genitourinary clinic wait-list. Participants
in the CBT group showed greater reduction in health anxiety symptoms, generalized
anxiety, depression, social function, and health service consultations than did those
randomized to wait-list.
More recently, Sørensen, Birket-Smith, Wattar, Buemann, and Salkovskis (2011)
conducted a randomized controlled trial based on a health anxiety treatment protocol
developed by Salkovskis, Warwick, and Deale (2003). This particular study compared
the relative efficacy of CBT, short-term psychodynamic psychotherapy, and a wait-
list control group. The CBT protocol—eight individual sessions (45 minutes each)
followed by eight group sessions—included an explanation of the cognitive behavioral
model for health anxiety, behavioral experiments, mindfulness training, and other core
CBT interventions. Short-term psychodynamic therapy involved 16 weekly sessions
(50 minutes each) focusing on the influence of the unconscious, the therapeutic
relationship, and interpersonal interactions. Participants in the CBT group showed
greater improvement on all measures compared to the wait-list group and greater
improvement on health anxiety and depression measures compared to the short-term
psychodynamic psychotherapy group.
The aforementioned controlled trials provide evidence that CBT produces sig-
nificant improvement in core facets of severe health anxiety and reduced medical
care visits. Moreover, treatment gains appear to be maintained over 6 months to 1
Hypochondriasis 499
year, depending on the study and population. CBT also consistently outperforms
other therapies (e.g., psychodynamic) and wait-list control conditions. The efficacy
of CBT for presentations of severe health anxiety with co-occurring diagnoses is also
encouraging, with some studies reporting diffuse symptom reduction as a result of
treatment. Warwick et al. (1996) observed significant reductions in both generalized
anxiety and depression among 32 health anxiety patients. Similarly, patients receiving
treatment for hypochondriasis with comorbid somatization showed 1-year reduc-
tions in intolerance of bodily complaints, frequency of medical consulting, general
psychopathology, and life satisfaction (Bleichhardt, Timmer, & Rief, 2005). These
results suggest that gains observed from CBT interventions may indeed extend to
other areas of concern.
Innovative Cognitive Behavioral Therapy-Based Applications

There have been several recent innovative adaptations of CBT for severe health
anxiety. Mindfulness-based CBT (Kabat-Zinn, 1994) for health anxiety extends
acceptance to health-related thoughts and bodily sensations. To illustrate, a patient
may be asked to consider how worried attention (e.g., “This tingling in my chest
must mean I am having a heart attack”) and mindful attention (e.g., “The tingling
in my chest is interesting and feels warm”) can lead to differences in magnification
of bodily sensations or changes. Only one pilot study has been conducted to test the
effectiveness of mindfulness-based CBT for health anxiety (Lovas & Barsky, 2010),
with promising results. Similarly, Internet-based CBT protocols, proven effective for
depression and some anxiety disorders (Andersson, Cuijpers, Carlbring, & Lindefors,
2007; Spek et al., 2007), have been adapted for severe health anxiety. Findings of a
recent randomized controlled trial (Hedman et al., 2011) indicate that participants
in the Internet-based CBT group had significant and large decreases in their health
anxiety symptoms compared to those participating only in an online discussion
forum on health anxiety. Finally, guided self-help treatments have been extended to
severe health anxiety, with two clinical trials demonstrating effectiveness (Buwalda &
Bouman, 2009). Although promising, more research is needed on these and other
innovative adaptations of CBT for severe health anxiety.
Conclusions
Throughout its history hypochondriasis has been understood in several different ways,
be it a stress response, a personality disturbance, the result of psychic conflict, or a
problem secondary to other psychiatric diagnoses (e.g., depression). Current con-
ceptualizations of hypochondriasis, however, see it as an anxiety-based psychological
disorder with a characteristic set of cognitions and action tendencies. Advances in
empirical and conceptual understanding of severe health anxiety point to its develop-
ment and maintenance as being the result of a complex interaction of psychological
and biological processes. Cumulative research has established a strong evidence base
for a cognitive behavioral conceptualization and treatment of severe health anxiety. By
addressing dysfunctional thoughts about disease and reducing maladaptive behaviors
such as avoidance, reassurance seeking, and checking, CBT has proven to be an

effective means of reducing symptoms and improving functioning and quality of life.
References
Abramowitz, J. S., & Braddock, A. E. (2011). Hypochondriasis and health anxiety. Cambridge,
MA: Hogrefe.
Abramowitz, J. S., Deacon, B. J., & Whiteside, S. P. H. (2011). Exposure therapy for anxiety:
Principles and practice. New York, NY: Guilford Press.
Abramowitz, J. S., & Moore, E. L. (2007). An experimental analysis of hypochondriasis.
Abramowitz, J. S., Schwartz, S. A., & Whiteside, S. P. (2002). A contemporary conceptual
model of hypochondriasis. Mayo Clinic Proceedings, 77 , 1323–1330.
Agras, S., Sylvester, D., & Oliveau, D. (1969). The epidemiology of common fears and phobias.
Comprehensive Psychiatry, 10, 151–156.
Andersson, G., Cuijpers, P., Carlbring, P., & Lindefors, N. (2007). Effects of internet-
delivered cognitive behaviour therapy for anxiety and mood disorders. Helix Review
Series: Psychiatry, 2, 9–14.
Asmundson, G. J. G., Abramowitz, J. S., Richter, A. A., & Whedon, M. (2010). Health anxiety:
Current perspectives and future directions. Current Psychiatry Reports, 12, 306–312.
Asmundson, G. J. G., Taylor, S., Carleton, R. N., Weeks, J. W., & Hadjstavropoulos, H. D.
(2012). Should health anxiety be carved at the joint? A look at the health anxiety construct
using factor mixture modeling in a non-clinical sample. Journal of Anxiety Disorders, 26,
246–251.
Avia, M. D., Ruiz, M. A., Olivares, M. E., Crespo, M., Guisado, A. B., Sanchez, A., & Varela,
A. (1996). The meaning of psychological symptoms: Effectiveness of a group intervention
with hypochondriacal patients. Behaviour Research and Therapy, 34, 23–31.
Baker, B., & Merskey, H. (1982). Parental representations of hypochondriacal patients from a
psychiatric hospital. British Journal of Psychiatry, 141, 233–238.
Barsky, A. J. (1996). Hypochondriasis: Medical management and psychiatric treatment. Psy-
chosomatics, 37 , 48–56.
Barsky, A. J., & Ahern, D. K. (2004). Cognitive behavior therapy for hypochondriasis: A
randomized controlled trial. JAMA, 291, 1464–1470.
Barsky, A. J., Cleary, P. D., & Klerman, G. L. (1992). Determinants of perceived health status
of medical outpatients. Social Science & Medicine, 34, 1147–1154.
Barsky, A. J., Coeytaux, R. R., Sarnie, M. K., & Cleary, P. D. (1993). Hypochondriacal
patients’ beliefs about good health. American Journal of Psychiatry, 150, 1085–1089.
Barsky, A. J., Ettner, S. L., Horsky, J., & Bates, D. W. (2001). Resource utilization of patients
with hypochondriacal health anxiety and somatization. Medical Care, 39, 705–715.
Barsky, A. J., & Klerman, G. L. (1983). Overview: Hypochondriasis, bodily complaints, and
somatic styles. American Journal of Psychiatry, 140, 273–283.
Barsky, A. J., Wool, C., Barnett, M. C., & Cleary, P. D. (1994). Histories of childhood trauma
in adult hypochondriacal patients. American Journal of Psychiatry, 151, 397–401.
Barsky, A. J., & Wyshak, G. (1989). Hypochondriasis and related health attitudes. Psychoso-
matics, 30, 412–420.
Barsky, A. J., Wyshak, G., & Klerman, G. L. (1992). Psychiatric comorbidity in DSM-III-R
hypochondriasis. Archives of General Psychiatry, 49, 101–108.
Hypochondriasis 501
Beck, A. T. (1976). Cognitive therapy and the emotional disorders. New York, NY: International
Universities Press.
Bleichhardt, G., & Hiller, W. (2007). Hypochondriasis and health anxiety in the German
population. British Journal of Health Psychology, 12, 511–523.
Bleichhardt, G., Timmer, B., & Rief, W. (2005). Hypochondriasis among patients with multiple
somatoform symptoms: Psychopathology and outcome of a cognitive-behavioral therapy.
Journal of Contemporary Psychotherapy, 35, 239–249.
Bouman, T. K., & Visser, S. (1998). Cognitive and behavioural treatment of hypochondriasis.
Psychotherapy and Psychosomatics, 67 , 214–221.
Buwalda, F. M., & Bouman, T. K. (2009). Cognitive-behavioural bibliotherapy for hypochon-
driasis: A pilot study. Behavioural and Cognitive Psychotherapy, 37 , 335–340.
Buwalda, F. M., Bouman, T. K., & van Duijn, M. A. (2007). Psychoeducation for hypochondri-
asis: A comparison of a cognitive-behavioural approach and a problem-solving approach.
Clark, D. M., Salkovskis, P. M., Hackmann, A., Wells, A., Fennell, M., Ludgate, J., … Gelder,
M. (1998). Two psychological treatments for hypochondriasis: A randomised controlled
trial. British Journal of Psychiatry, 173, 218–225.
Collimore, K. C., Asmundson, G. J. G., Taylor, S., & Abramowitz, J. S. (2009). Classification
of hypochondriasis and other somatoform disorders. In D. McKay, J. S. Abramowitz,
S. Taylor, & G. J. G. Asmundson (Eds.), Current perspectives on the anxiety disorders:
Implications for DSM-V and beyond (pp. 431–447). New York, NY: Springer.
Deacon, B., & Abramowitz, J. S. (2008). Is hypochondriasis related to obsessive-compulsive dis-
order, panic disorder, or both? An empirical evaluation. Journal of Cognitive Psychotherapy:
An International Quarterly, 22, 115–127.
Ditto, P. H., Jemmott, J. B., III, & Darley, J. M. (1988). Appraising the threat of illness: A
mental representational approach. Health Psychology, 7 , 183–201.
Easterling, D. V., & Leventhal, H. (1989). Contribution of concrete cognition to emotion:
Neutral symptoms as elicitors of worry about cancer. Journal of Applied Psychology, 74,
787–796.
Escobar, J. I., Gara, M., Waitzkin, H., Silver, R. C., Holman, A., & Compton, W. (1998).
DSM-IV hypochondriasis in primary care. General Hospital Psychiatry, 20, 155–159.
Fallon, B. A., Klein, B. W., & Liebowitz, M. R. (1993). Hypochondriasis: Treatment strategies.
Psychiatric Annals, 23, 374–381.
Faravelli, C., Salvatori, S., Galassi, F., Aiazzi, L., Drei, C., & Cabras, P. (1997). Epidemiology of
somatoform disorders: A community survey in Florence. Social Psychiatry and Psychiatric
Epidemiology, 32, 24–29.
Ferguson, E. (2009). A taxometric analysis of health anxiety. Psychological Medicine, 39,
277–285.
Furer, P., Walker, J. R., & Freeston, M. H. (2001). Integrated approach to cognitive-behavioral
therapy for intense illness worries. In G. J. G. Asmundson, S. Taylor, & B. J. Cox (Eds.),
Health anxiety: Hypochondriasis and related disorders (pp. 161–192). Chichester, England:
John Wiley & Sons, Ltd.
Gureje, O., Ustun, T. B., & Simon, G. E. (1997). The syndrome of hypochondriasis: A
cross-national study in primary care. Psychological Medicine, 27 , 1001–1010.
Haenen, M. A., de Jong, P. J., Schmidt, A. J., Stevens, S., & Visser, L. (2000). Hypochondriacs’
estimation of negative outcomes: Domain-specificity and responsiveness to reassuring and
alarming information. Behaviour Research and Therapy, 38, 819–833.
Haenen, M. A., Schmidt, A. J. M., Schoenmakers, M., & van den Hout, M. A. (1997). Tactual
sensitivity in hypochondriasis. Psychotherapy and Psychosomatics, 66, 128–132.
Hedman, E., Andersson, G., Andersson, E., Ljotsson, B., Ruck, C., Asmundson, G. J., …
Lindefors, N. (2011). Internet-based cognitive-behavioural therapy for severe health
anxiety: Randomised controlled trial. British Journal of Psychiatry, 198, 230–236.
Hiller, W., Leibbrand, R., Rief, W., & Fichter, M. M. (2002). Predictors of course and outcome
in hypochondriasis after cognitive-behavioral treatment. Psychotherapy and Psychosomatics,
71, 318–325.
Hiller, W., Leibbrand, R., Rief, W., & Fichter, M. M. (2005). Differentiating hypochondriasis
from panic disorder. Journal of Anxiety Disorders, 19, 29–49.
Hollifield, M., Paine, S., Tuttle, L., & Kellner, R. (1999). Hypochondriasis, somatization, and
perceived health and utilization of health care services. Psychosomatics, 40, 380–386.
Kabat-Zinn, J. (1994). Wherever you go there you are: Mindfulness meditation in everyday life.
Karademas, E. C. (2009). Effects of exposure to the suffering of unknown persons on
health-related cognitions, and the role of mood. Health, 13, 491–504.
Lidbeck, J. (1997). Group therapy for somatization disorders in general practice: Effectiveness
of a short cognitive-behavioural treatment model. Acta Psychiatrica Scandinavica, 96,
14–24.
Longley, S. L., Broman-Fulks, J. J., Calamari, J. E., Noyes, R., Wade, M., & Orlando, C.
M. (2010). A taxometric study of hypochondriasis symptoms. Behavior Therapy, 41,
505–514.
Looper, K. J., & Kirmayer, L. J. (2001). Hypochondriacal concerns in a community population.
Lovas, D. A., & Barsky, A. J. (2010). Mindfulness-based cognitive therapy for hypochondriasis,
or severe health anxiety: A pilot study. Journal of Anxiety Disorders, 24, 931–935.
Malis, R. W., Hartz, A. J., Doebbeling, C. C., & Noyes, R. (2002). Specific phobia of illness
in the community. General Hospital Psychiatry, 24, 135–139.
Marcus, D. K., & Church, S. E. (2003). Are dysfunctional beliefs about illness unique to
hypochondriasis? Journal of Psychosomatic Research, 54, 543–547.
Martinez, M. P., & Botella, C. (2005). An exploratory study of the efficacy of a cognitive-
behavioral treatment for hypochondriasis using different measures of change. Psychotherapy
Research, 14, 392–408.
Noyes, R. Jr., Kathol, R. G., Fisher, M. M., Phillips, B. M., Suelzer, M. T., & Holt, C. S.
(1993). The validity of DSM-III-R hypochondriasis. Archives of General Psychiatry, 50,
961–970.
Noyes, R. Jr., Kathol, R. G., Fisher, M. M., Phillips, B. M., Suelzer, M. T., & Woodman, C. L.
(1994). Psychiatric comorbidity among patients with hypochondriasis. General Hospital
Olatunji, B. O., Deacon, B. J., & Abramowitz, J. S. (2009). Is hypochondriasis an anxiety
disorder? British Journal of Psychiatry, 194, 481–482.
Paris, J. (1998). Does childhood trauma cause personality disorders in adults? Canadian
Parker, G., & Lipscombe, P. (1980). The relevance of early parental experiences to adult
dependency, hypochondriasis and utilization of primary physicians. British Journal of
Medical Psychology, 53, 355–363.
Pilowsky, I. (1968). The response to treatment in hypochondriacal disorders. Australian and
New Zealand Journal of Psychiatry, 2, 88–94.
Salkovskis, P. M., & Warwick, H. M. (1986). Morbid preoccupations, health anxiety and
reassurance: A cognitive-behavioural approach to hypochondriasis. Behaviour Research
Hypochondriasis 503
Salkovskis, P. M., Warwick, H. M. C., & Deale, A. C. (2003). Cognitive-behavioral treatment

for severe and persistent health anxiety (hypochondriasis). Brief Treatment and Crisis
Intervention, 3, 353–368.
Schwartz, S. M., Gramling, S. E., & Mancini, T. (1994). The influence of life stress, personality,
and learning history on illness behavior. Journal of Behavior Therapy and Experimental
Seivewright, H., Green, J., Salkovskis, P., Barrett, B., Nur, U., & Tyrer, P. (2008). Cognitive-
behavioural therapy for health anxiety in a genitourinary medicine clinic: Randomised
controlled trial. British Journal of Psychiatry, 193, 332–337.
Sørensen, P., Birket-Smith, M., Wattar, U., Buemann, I., & Salkovskis, P. (2011). A ran-
domized clinical trial of cognitive behavioral therapy versus short-term psychodynamic
psychotherapy versus no intervention for patients with hypochondriasis. Psychological
Medicine, 41, 431–441.
Speckens, A. E. M., Spinhoven, P., van Hermert, A. M., Bolk, J. H., & Hawton, K. E. (1997).
Cognitive behavioural therapy for unexplained physical symptoms: Process and prognostic
factors. Behavioural and Cognitive Psychotherapy, 25, 291–294.
Spek, V., Cuijpers, P., Nyklicek, I., Riper, H., Keyzer, J., & Pop, V. (2007). Internet-based
cognitive behaviour therapy for symptoms of depression and anxiety: A meta-analysis.
Psychological Medicine, 37 , 319–328.
Stein, M. B., Walker, J. R., Anderson, G., Hazen, A. L., Ross, C. A., Eldridge, G., … Forde,
D. R. (1996). Childhood physical and sexual abuse in patients with anxiety disorders and
in a community sample. American Journal of Psychiatry, 153, 275–277.
Taylor, S. (in press). Molecular genetics of obsessive-compulsive disorder: A comprehensive
meta-analysis of genetic association studies. Molecular Psychiatry, 18, 799–805.
Taylor, S., & Asmundson, G. J. G. (2004). Treating health anxiety: A cognitive-behavioral
approach. New York, NY: Guilford Press.
Taylor, S., & Asmundson, G. J. G. (2012). Etiology of hypochondriasis: A behavioral-genetic
investigation. International Journal of Genetics and Gene Therapy, 2, 1–5.
Taylor, S., Asmundson, G. J. G., & Coons, M. J. (2005). Current directions in the treatment
of hypochondriasis. Journal of Cognitive Psychotherapy, 19, 285–304.
Taylor, S., Thordarson, D. S., Jang, K. L., & Asmundson, G. J. G. (2006). Genetic and
environmental origins of health anxiety: A twin study. World Psychiatry, 5, 47–50.
Visser, S., & Bouman, T. K. (2001). The treatment of hypochondriasis: Exposure plus response
prevention vs cognitive therapy. Behaviour Research and Therapy, 39, 423–442.
Warwick, H. M. C., Clark, D. M., Cobb, A. M., & Salkovskis, P. M. (1996). A controlled trial
of cognitive-behavioural treatment of hypochondriasis. British Journal of Psychiatry, 169,
189–195.
Warwick, H. M. C., & Salkovskis, P. M. (1990). Hypochondriasis. Behaviour Research and
Therapy, 28, 105–117.
Warwick, H. M. C., & Salkovskis, P. M. (2001). Cognitive-behavioral treatment of hypochon-
driasis. In V. Starcevic & D. R. Lipsitt (Eds.), Hypochondriasis: Modern perspectives on an
ancient malady. New York, NY: Oxford University Press.
Wattar, U., Sørensen, P., Buemann, I., Birket-Smith, M., Salkovskis, P. M., Albertsen, M.,
… Strange, S. (2005). Outcome of cognitive-behavioural treatment for health anxiety
(hypochondriasis) in a routine clinical setting. Behavioural and Cognitive Psychotherapy,
33, 165–175.
Whitehead, W. E., Crowell, M. D., Heller, B. R., Robinson, J. C., Schuster, M. M., & Horn,
S. (1994). Modeling and reinforcement of the sick role during childhood predicts adult
illness behavior. Psychosomatic Medicine, 56, 541–550.
22
Somatization and Conversion
Disorders
Lesley A. Allen
University of Medicine and Dentistry of New Jersey–Robert Wood Johnson Medical
School, United States
Robert L. Woolfolk
Rutgers University and Princeton University, United States
Somatization disorder and conversion disorder are characterized by physical symp-

toms that suggest a medical condition but are not fully explained by a medical
condition (American Psychiatric Association [APA], 1994). Patients presenting with
somatization and conversion disorders represent a formidable challenge to the
health care system. These patients tend to overuse medical services, derive little
benefit from treatment, and experience substantial functional impairment (Reuber,
Fernandez, Bauer, Helmstaedter, & Elger, 2002; Smith, Monson, & Ray, 1986a).
Patients with somatization often become dissatisfied with the medical services they
receive and repeatedly change physicians (Lin et al., 1991). Meanwhile, physi-
cians of these patients often feel frustrated by patients’ frequent complaints and
dissatisfaction with treatment (Hahn, 2001; Lin et al., 1991). Because standard
medical care has been relatively unsuccessful in treating somatization and conver-
sion disorders, alternative treatments have been developed. Cognitive behavioral
therapy (CBT) has been the most widely studied alternative treatment for these
disorders.
This chapter provides a review of research on CBT for somatization and conversion
disorders. A brief history of the disorders is provided, along with a framework in
which to conceptualize these disorders. Also summarized is the research on the
demographic and clinical characteristics of these patients. Future directions for
treatment are discussed.

DOI: 10.1002/9781118528563.wbcbt22
Historical Background
The history of somatization and conversion disorders begins with hysteria, first
described 4,000 years ago by the Egyptians and later elaborated and named by
the Greeks. Cases typically involved somatic symptoms in the absence of injury or
illness. The Egyptians hypothesized that a “wandering” uterus moved about the body
and produced somatic symptoms from various regions. Greek physicians described a
similar set of psychosomatic symptoms and essentially retained the Egyptian theory.
The Greeks gave us the word hysteria, from the Greek hystera, meaning womb.
The Greco-Egyptian formulation reveals that the disorder was primarily observed in
females and that there was something thought to be essentially female about the
disorder.
The ancient terminology and conceptualization remained essentially unchanged
until modern times. Foucault (1965) suggests that by the end of the eighteenth
century hysteria was beginning to be viewed as a disease “of the nerves” akin to
such recognized mental disorders as melancholia. Due to the heterogeneous nature
of hysterical symptoms and the hypothesized connection with the emotions, some
physicians began to allege that these symptoms were feigned or imagined. The
unsympathetic attitudes of contemporary health care workers toward somatizers and
the tendency to regard them as malingerers can be traced to this period in the history
of medicine.
Our current conception of somatization and conversion disorders derives directly
from Pierre Briquet’s (1859) monograph, Traité Clinique et Thérapeutique de
l’Hystérie. Briquet’s meticulous and exhaustive listing of the symptomatology of
hysteria remains unsurpassed. Briquet described three related syndromes: conversion
phenomena, hysterical personality, and multiple chronic unexplained somatic symp-
toms (Dongier, 1983; Mai & Merskey, 1980). These three syndromes overlapped in
symptomatology somewhat and they often were observed to co-occur.
Sigmund Freud and Pierre Janet began expanding theoretical conceptualizations
of hysteria by the end of the nineteenth century. Both men had studied with and
observed the world’s leading authority, Jean-Martin Charcot, as he used hypnosis
to remove hysterical symptoms. Janet (1907) asserted that hysterical symptoms were
produced when patients dissociated. Freud, on the other hand, proposed the process of
“conversion” whereby intrapsychic activity putatively brings about somatic symptoms
(Breuer & Freud, 1974). Janet’s and Freud’s work on hysteria provided a blueprint
for and harbinger of later theoretical efforts. Here the ideas of early emotional trauma
or intrapsychic conflict as the cause of physical symptoms began to take shape. This
work also introduced the notion of a physical symptom as an unconscious form of
communication, as a device for securing secondary gain, or a means for avoiding
emotional pain.
The notion of the transduction of psychological conflict into bodily symptoms was
widely disseminated as psychoanalysis began to dominate psychiatry. Stekel (1924)
coined the term somatization (somatisieren) during the early 1920s and defined it as
“the conversion of emotional states into physical symptoms” (p. 341). That is, Stekel
Somatization and Conversion Disorders 507
regarded somatization as equivalent to the mechanism of conversion, which Freud had

used to explain the development of sensory or voluntary motor symptoms in hysteria.
The father of modern American psychosomatic medicine, Franz Alexander, dis-
tinguished between two types of psychosomatic symptoms: (a) those cases in which
psychological conflict was “converted” and communicated symbolically through phys-
ical symptoms, and (b) those cases in which the somatic symptoms resulted from
the direct and indirect physiological effects of emotional arousal (Alexander, 1950).
This second kind of psychosomatic mechanism required few, if any, psychoanalytic
assumptions and was quite compatible with mainstream scientific research, especially
the work of Cannon, Seyle, and others on psychosocial stress.
Diagnostic Criteria
Although medicine has long recognized the existence of a group of patients with
medically unexplained physical symptoms, there has been and continues to be dis-
agreement over the diagnostic criteria and terminology for what were once labeled
hysterical symptoms. In the first and second editions of the Diagnostic and Statis-
tical Manual of Mental Disorders, “conversion reaction” and “hysterical neurosis,
conversion type” were employed, respectively (1st ed., DSM-I; APA, 1952; 2nd ed.,
DSM-II; APA, 1968). Conversion symptoms were defined as those that affected
voluntary motor or sensory function and were psychogenic in origin. Also included
in DSM-I and DSM-II were psychophysiologic disorders which were characterized by
physical symptoms attributable to emotional factors (APA, 1952, 1968).
In DSM-III the hysterical neuroses and psychophysiologic disorders were replaced
with two new groupings of mental disorders: somatoform disorders and psychological
factors affecting physical condition (APA, 1980). Somatoform disorders were charac-
terized by physical symptoms that suggested a medical condition for which there
were no organic pathology or physiological mechanisms. Specific somatoform disor-
ders listed in DSM-III were conversion disorder, somatization disorder, psychogenic
pain disorder, hypochondriasis, and a residual category for other related symptom
presentations (APA, 1980). Briquet’s (1859) work on medically unexplained somatic
symptoms served as the foundation for DSM-III’s somatization disorder, which was
distinguished from conversion disorder (APA, 1980). Patients diagnosed with soma-
tization disorder complained of multiple medically unexplained symptoms, typically
both neurological and nonneurological symptoms. Conversion disorder, on the other
hand, was reserved for purely pseudoneurological symptom presentations. The sepa-
rate category of psychological factors affecting physical condition was used to describe
physical symptoms with either a demonstrable organic pathology or a known patho-
physiological process that also appeared to be affected by psychological factors (APA,
1980).
The criteria required for the diagnosis of the different somatoform disorders as well
as for psychological factors affecting physical condition have been revised in each of
the manual’s subsequent versions (DSM-III-R; APA, 1987; DSM-IV; APA, 1994).
Future editions of the DSM are likely to see more changes as well (the DSM-5 will be
discussed later in this chapter).
According to the current edition of the DSM (DSM-IV; APA, 1994), somatization
disorder is characterized by a lifetime history of at least four unexplained pain
complaints (e.g., in the back, chest, joints), two unexplained nonpain gastrointestinal
complaints (e.g., nausea, bloating), one unexplained sexual symptom (e.g., sexual
dysfunction, irregular menstruation), and one pseudoneurological symptom (e.g.,
seizures, paralysis, numbness). For a symptom to be counted toward the diagnosis
of somatization disorder, its presence must be medically unexplained or its degree of
severity be substantially in excess of the associated medical pathology. Somatization
symptoms are not intentionally produced or feigned. Also, symptoms counted toward
the diagnosis must either prompt the seeking of medical care or interfere with
the patient’s functioning. In addition, some of the somatization symptoms must
have occurred prior to the patient’s 30th birthday (APA, 1994). The course of
somatization disorder tends to be characterized by symptoms that wax and wane,
remitting only to return later and/or be replaced by new unexplained physical
symptoms. Thus, somatization disorder is a chronic, polysymptomatic disorder whose
requisite symptoms need not be manifested concurrently.
Although somatization disorder is classified as a distinct disorder in the DSM-IV,
it has been argued that somatization disorder represents the extreme end of a
somatization continuum (Escobar, Burnam, Karno, Forsythe, & Golding, 1987;
Kroenke et al., 1997). The number of unexplained physical symptoms reported
correlates positively with the patient’s degree of emotional distress and functional
impairment (Katon et al., 1991). A broadening of the somatization construct has
been advocated by those wishing to emphasize the many patients encumbered by
unexplained symptoms that are not numerous or diverse enough to meet criteria for
full somatization disorder (Escobar et al., 1987; Katon et al., 1991; Kroenke et al.,
1997).
The DSM-IV includes a residual diagnostic category for subthreshold somatization
cases. Undifferentiated somatoform disorder is a diagnosis characterized by one or
more medically unexplained physical symptom(s) lasting for at least 6 months (APA,
1994). Long considered a category that is too broad because it includes patients with
only one unexplained symptom as well as those with many unexplained symptoms,
undifferentiated somatoform disorder has never been well validated or widely applied
(Kroenke, Sharpe, & Sykes, 2007).
As an alternative to the wide-ranging category of undifferentiated somatoform dis-
order, two groups of researchers have suggested alternative categories for subthreshold
somatization using criteria less restrictive and requiring less extensive symptomatol-
ogy than the standards for the DSM-IV’s full somatization disorder. Escobar et al.
(1987) proposed the label abridged somatization, to be applied to men experiencing
four or more unexplained physical symptoms or to women experiencing six or more
unexplained physical symptoms. Kroenke et al. (1997) suggested the category of
multisomatoform disorder to describe men or women currently experiencing at least
three unexplained physical symptoms and reporting a 2-year history of somatization.
When the clinical presentation consists of purely pseudoneurological symptoms and
no history of medically unexplained pain or gastrointestinal or sexual symptoms, a
diagnosis of conversion disorder is considered. The DSM-IV’s conversion disorder is
characterized by the presence of one or more symptoms affecting voluntary motor
or sensory function that are associated with psychological stressor(s) or conflict(s).

The symptom(s) are not intentionally produced and must cause significant distress or
dysfunction (APA, 1994). The diagnosis of conversion disorder requires a thorough
psychiatric evaluation as well as a physical examination in order to rule out organic
neurological illness. Patients presenting with conversion symptoms typically have
normal reflexes and normal muscle tone.
The course of conversion disorder appears to be different from that of somatization
disorder, which tends to be chronic (Kent, Tomasson, & Coryell, 1995). The onset
and course of conversion disorder often take the form of an acute episode. Symptoms
may remit within a few weeks of an initial episode and they may recur in the future.
Some research indicates that a brief duration of symptoms prior to treatment is
associated with a better prognosis (Crimlisk et al., 1998; Hafeiz, 1980; Ron, 2001).
A number of changes have been proposed for DSM-5 by the DSM-5 Somatic
Symptom Disorders Work Group (APA, 2011). The somatoform disorders category
will be renamed somatic symptom disorders. The specific disorders within that group
will include psychological factors affecting medical condition and most of the somato-
form diagnostic categories in revised forms. Changes to somatization disorder and
conversion disorder are detailed below.
A new diagnostic category, somatic symptom disorder, has been proposed for DSM-5
to replace and subsume somatization disorder, undifferentiated somatoform disorder,
pain disorder, and most cases of hypochondriasis. The rationale for grouping together
these disorders is that their “similarities outweigh their differences” (Dimsdale et al.,
2009, p. 474). Somatic symptom disorder, as currently proposed, is characterized
by a history of one or more somatic symptoms that are distressing and/or disrupt
daily life for at least 6 months. In an attempt to remove the mind–body dualism
implied by previous versions of the DSM, the DSM-5 Somatic Symptom Work
Group has recommended eliminating the requirement that somatic symptoms be
medically unexplained or in excess of related organic pathology. Thus, any somatic
symptom that is distressing and disruptive for at least 6 months could potentially be
considered toward the diagnosis of somatic symptom disorder. An additional criterion
for the diagnosis of somatic symptom disorder is that patients report at least one
of the following: (a) health anxiety, (b) disproportionate and persistent concerns
about the seriousness of their somatic symptom(s), or (c) excessive time and energy
devoted to health concerns (APA, 2011). In other words, the diagnosis requires not
only distressing somatic symptoms, but also the association of these symptoms with
dysfunctional health behaviors, beliefs, and anxiety.
The proposal for conversion disorder in the DSM-5 is to retain this diagnostic
category with slight alterations. DSM-IV’s requirement that the symptom(s) not
be intentionally produced or feigned by the patient will be eliminated, given the
difficulty clinicians have making such determinations. Also no longer required will
be the judgment that psychological factors are associated with the symptom(s).
Conversion disorder is the one somatic symptom disorder category that will retain
the dualistic diagnostic criterion of the symptom(s) being medically unexplained.
The DSM-5 Somatic Symptom Disorders Work Group cites the recent evidence
that neurologists can reliably make the distinction between organic and conversion
symptoms (Stone et al., 2009).
We have very little empirical research on the new somatic symptom disorder
categories proposed for DSM-5. One recent study supports the validity of somatic
symptom disorder (Rief, Mewes, Martin, Glaesmer, & Brahler, 2011), while research
on the older diagnostic categories is summarized in this chapter.
Epidemiology and Clinical Characteristics
Prevalence
Epidemiological research suggests that somatization disorder is relatively rare. The
prevalence of somatization disorder in the general population has been estimated to
be 0.1–0.7% (Faravelli et al., 1997; Robins & Reiger, 1991; Weissman, Myers, &
Harding, 1978). When patients in primary care, specialty medical, and psychiatric
settings are assessed, the rate of somatization is higher than in the general popu-
lation, with estimates ranging from 1.0 to 5.0% (Altamura et al., 1998; Fabrega,
Mezzich, Jacob, & Ulrich, 1988; Fink, Steen Hansen, & Søndergaard, 2005; Gureje,
Simon, Ustun, & Goldberg, 1997; Kirmayer & Robbins, 1991; Peveler, Kilkenny, &
Kinmonth, 1997).
The prevalence of subthreshold somatization categories appears to be significantly
higher than is that for somatization disorder as defined by the DSM-IV. Abridged
somatization has been observed in 4% of community samples (Escobar et al., 1987) and
16–22% of primary care samples (Escobar, Waitzkin, Silver, Gara, & Holman, 1998;
Gureje et al., 1997; Kirmayer & Robbins, 1991). The occurrence of multisomatoform
disorder has been estimated at 8% of primary care patients (Jackson & Kroenke, 2008;
Kroenke et al., 1997).
Estimates of the prevalence of conversion disorder have varied widely, ranging
from 0.01 to 0.3% in the community (Faravelli et al., 1997; Stefansson, Messina, &
Meyerowitz, 1979). As is the case with somatization disorder, conversion disorder is
much more common in medical and psychiatric practices than in community samples
(Folks, Ford, & Regan, 1984). As many as 25% of neurology clinic patients may
present for treatment of a medically unexplained neurological symptom (Creed, Firth,
Timol, Metcalfe, & Pollock, 1990; Perkin, 1989).
Demographics
Gender is the demographic variable that most consistently has been associated with
somatization disorder, subthreshold somatization, and conversion disorder. In the
Epidemiological Catchment Area (ECA) study, the ratio of women to men who met
criteria for somatization disorder was 10 to 1 (Swartz, Landermann, George, Blazer,
& Escobar, 1991). Higher rates of occurrence in women, though not as extreme, also
have been found in studies examining subthreshold somatization categories, such as
Escobar’s abridged somatization or Kroenke’s multisomatoform disorder (Escobar,
Rubio-Stipec, Canino, & Karno, 1989; Kroenke et al., 1997), and conversion disorder
(Deveci et al., 2007; Faravelli et al., 1997).
Ethnicity, race, and education have been associated with somatization disorder,
subthreshold somatization, and conversion disorder. Epidemiological research has
shown patients with somatization or conversion disorders to be more likely to be
nonwhite and less educated than patients with medically explained symptoms (Gureje
et al., 1997; Robins & Reiger, 1991; Stefansson et al., 1979). Findings on ethnicity
have been less consistent across studies. In the ECA study, Hispanics were no more
likely to meet criteria for somatization disorder than were non-Hispanics (Robins &
Reiger, 1991). A World Health Organization study, conducted in 14 different
countries, revealed a higher incidence of somatization in Latin American countries
than in the United States (Gureje et al., 1997).
Clinical Characteristics
Much attention has focused on the illness behavior of patients with somatization or
conversion disorder. These patients disproportionately use and misuse health care
services. When standard diagnostic evaluations fail to uncover organic pathology,
patients with somatization or conversion disorders may seek additional medical pro-
cedures, often from several different physicians. Patients may even subject themselves
to unnecessary hospitalizations and surgeries, which introduce the risk of iatrogenic
illness (Fink, 1992). One study found that somatization disorder patients, on aver-
age, incurred nine times the U.S. per capita health care cost (Smith et al., 1986a).
Abridged somatization, multisomatoform disorder, and conversion disorder also have
been associated with significant health care utilization (Barsky, Orav, & Bates, 2005;
Escobar, Golding, et al., 1987; Kroenke et al., 1997; Mace & Trimble, 1996; Martin,
Bell, Hermann, & Mennemeyer, 2003).
The abnormal illness behavior of patients with somatization or conversion disorder
extends beyond medical offices and hospitals to patients’ workplaces and households.
These patients withdraw from both productive and pleasurable activities because of
discomfort, fatigue, and/or fears of exacerbating their symptoms. In a study assessing
the efficacy of cognitive behavioral therapy for somatization disorder, we found 19% of
patients meeting DSM-IV criteria for somatization disorder to be receiving disability
payments from either their employers or the government (Allen, Woolfolk, Escobar,
Gara, & Hamer, 2006). Estimates of unemployment among somatization disorder
patients range from 36 to 83% (Allen et al., 2006; Smith et al., 1986a; Yutzy et al.,
1995). Whether working outside their homes or not, these patients report substantial
functional impairment. Some investigators have found that somatization disorder
patients report being bedridden for 2 to 7 days per month (Katon et al., 1991; Smith
et al., 1986a). Likewise, high levels of functional impairment have been associated with
subthreshold somatization and conversion disorder (Allen, Gara, Escobar, Waitzkin,
& Cohen-Silver, 2001; Binzer, Andersen, & Kullgren, 1997; Escobar, Golding, et al.,
1987; Gureje et al., 1997; Jackson & Kroenke, 2008; Kroenke et al., 1997).
Comorbid psychiatric distress in patients with somatization or conversion disorder
is high. As many as 80% of patients meeting criteria for somatization disorder or
subthreshold somatization meet DSM criteria for another lifetime Axis I disorder,
usually an anxiety or mood disorder (Smith et al., 1986a; Swartz, Blazer, George, &
Landerman, 1986). When investigators consider only current psychiatric diagnoses,
rates of Axis I psychiatric comorbidity associated with somatization are closer to

50% (Allen et al., 2001; Simon & Von Korff, 1991). Studies on conversion disorder
have suggested that 30–90% of patients seeking treatment for pseudoneurological
symptoms also meet criteria for at least one other psychiatric disorder, typically
somatoform disorders, affective disorders, anxiety disorders, or personality disorders
(Binzer et al., 1997; Crimlisk et al., 1998; Mokleby et al., 2002; Sar et al., 2004). Rates
of Axis II psychiatric comorbidity also are high in somatization disorder, subthreshold
somatization, and conversion disorder (Garcia-Campayo, Alda, Sobradiel, Olivan,
& Pascual, 2007; Rost, Akins, Brown, & Smith, 1992). Also, overall severity of
psychological distress, defined as the number of psychological symptoms reported,
correlates positively with the number of functional somatic symptoms reported (Katon
et al., 1991; Simon & Von Korff, 1991).
Conceptualization
The biopsychosocial concept of illness, proposed by George Engel (1977), suggests

that illness is a complex entity involving the interplay of biological, psychological, and
social factors. A biopsychosocial conceptualization of medically unexplained somatic
symptoms emphasizes the interaction among biology, cognition, emotion, behavior,
and environment (Brown, 2004; Sharpe, Peveler, & Mayou, 1992).
There is a growing body of research that supports key features of the biopsychosocial
model of medically unexplained somatic symptoms. Genetic and early environmental
factors may predispose individuals to experiencing somatic symptomatology (Rief,
Hennings, Riemer, & Euteneuer, 2010). Patients presenting with somatization have
higher levels of physiological arousal and are less likely to habituate to a stressful task
than control subjects (Rief, Shaw, & Fichter, 1998). These predisposing factors may
be compounded by dysfunctional attentional and cognitive tendencies. The more
attention one focuses upon one’s body, the more likely one is to report somatic
symptoms (Pennebaker, 1982; Schmidt, Wolfs-Takens, Oosterlaan, & van den Hout,
1994). Barsky (1992) suggested patients with unexplained physical symptoms have
a tendency to amplify somatosensory information; that is, they are hypersensitive to
bodily sensations which are experienced as intense, noxious, and disturbing. Other
researchers have shown that somatization patients form negative cognitive appraisals
of their physical sensations, thinking catastrophically about their symptoms (Rief,
Hiller, & Margraf, 1998) and/or overestimating the medical severity of symptoms
after a medical evaluation (Rief, Heitmüller, Reisberg, & Rüddel, 2006).
Dysfunctional cognitions may elicit negative emotions, or be elicited by negative
emotions (Teasdale, 1983). This cognition–emotion cycle may interact in a complex
fashion with maladaptive behaviors. For example, thoughts of possible illness give
rise to feelings of anxiety, dysphoria, and frustration, which are likely to generate and
maintain physiological arousal and physical symptomatology. Intending to prevent
injury or exacerbation of symptoms, somatoform patients typically withdraw from
their normal activities (Katon et al., 1991; Smith et al., 1986a). Such time away from
activities provides opportunities for additional attention to be focused upon one’s
physical health. Furthermore, patients suffering from these physical symptoms, dis-
torted cognitions, and negative affect may seek repeated contact with physicians and
request medical tests. Pain catastrophizing has been associated with medical utiliza-
tion and disability (Severeijns, Vlaeyen, & van den Hout, 2004). Physicians, in turn,
attempting to conduct thorough evaluations and avoid malpractice suits, may encour-
age somatizing behavior by ordering unnecessary diagnostic procedures. Chronic
medical testing may ingrain patients in the “sick role” and reinforce somatizers’
maladaptive belief that any physical symptom indicates organic pathology. Also,
unnecessary medical procedures, if implemented, may result in iatrogenic illness.
A biopsychosocial model of medically unexplained symptoms leads to specific psy-
chosocial treatment strategies that include behavioral, cognitive, and interpersonal
interventions. Relaxation training may be employed to teach patients to use pro-
gressive muscle relaxation and/or diaphragmatic breathing to reduce physiologic
arousal. Behavioral activation/activity regulation promotes increases in pleasurable
and meaningful activities to modify the tendency of these patients to withdraw from
important aspects of their lives. Also, activity pacing is taught so that patients will
increase their activity levels gradually without exhausting or injuring themselves. The
cognitive restructuring component aims to help patients combat dysfunctional cog-
nitive tendencies. Communication skills, especially assertiveness training, are taught
to address the social disability that has been reported by somatizers (Zoccolillo
& Cloninger, 1986). Finally, patients’ environments are examined for factors that
reinforce their physical symptoms. Those factors are targeted for change. In some
treatment protocols the patient’s spouse/partner is invited to participate in treatment
sessions. Given the important role that spouses play in reinforcing patients’ expression
of pain and pain behavior (Kerns & Weiss, 1994), spousal behaviors that reinforce
patients’ symptoms may be modified.
Cognitive Behavioral Therapy for Somatization

A number of studies have been conducted examining the efficacy of CBT for
somatization disorder or for subthreshold somatization. Two studies enrolled patients
with at least one somatization symptom. Two other studies enrolled patients with
multiple medically unexplained symptoms. Only one study enrolled patients meeting
DSM-IV criteria for somatization disorder, the most severely disturbed somatizing
patients. Various different approaches to integrating CBT into primary care have also
been investigated.
The earliest randomized controlled trials of CBT for somatization included patients
presenting with relatively mild levels of somatization, those presenting with at
least one psychosomatic symptom. The treatment protocols included identifying and
restructuring dysfunctional cognitions, behavioral activation, or reengaging patients in
avoided activities, problem solving, and relaxation training (Lidbeck, 1997; Speckens
et al., 1995). In the first study patients treated with six to 16 sessions of individually-
administered CBT showed significantly greater improvement in their psychosomatic
complaints than did patients treated with standard medical care (Speckens et al.,
1995). The other study found an eight-session group CBT superior to a wait-
list control condition in reducing physical symptoms and hypochondriacal beliefs
(Lidbeck, 1997). In both studies improvements were observed after treatment as well
as 6 months later (Lidbeck, 1997; Speckens et al., 1995). Both of these studies were
conducted in primary care offices, the setting where somatization is most likely to be
seen.
Two more recently published randomized controlled trials examined the efficacy of
CBT for somatization with patients presenting with more severe somatization than the
earlier trials. One study required that participants meet Escobar’s criteria of abridged
somatization. That is, men were required to experience at least four somatization
symptoms and women were required to experience at least six somatization symptoms
(Escobar et al., 2007). The other trial enrolled participants who complained of five
or more unexplained physical symptoms (Sumathipala, Hewege, Hanwella, & Mann,
2000). In both studies patients were identified and treated with CBT in primary
care. Treatment protocols were similar to those of Lidbeck (1997) and Speckens
et al. (1995), with the addition of involving the patient’s spouse or another family
member in treatment (Escobar et al., 2007; Sumathipala et al., 2000). Spouses
are included to provide additional information regarding patients’ functioning, to
facilitate patients’ engagement in and compliance with treatment, and to help reduce
reinforcement of illness behavior. Findings from both trials show individual CBT
coincided with greater reductions in somatic complaints than did standard medical
care (Escobar et al., 2007; Sumathipala et al., 2000). CBT was associated with
a reduction in the number of physician visits in one study (Sumathipala et al.,
2000).
We are the only group of researchers who have published a randomized controlled
trial on the efficacy of CBT for DSM-IV full somatization disorder (Allen et al.,
2006). In the study 84 patients meeting DSM-IV criteria for somatization disorder
were randomly assigned to one of two conditions: (a) standard medical care, or (b) a
10-session manualized individually-administered CBT in combination with standard
medical care (see Table 22.1). The treatment protocol included relaxation training,
activity regulation, facilitation of emotional awareness, cognitive restructuring, and
interpersonal communication. As many as three of the 10 sessions were administered
conjointly with the patient’s spouse or significant other. An outline of the treatment
components and the sessions in which they were addressed is provided in Table
22.1. Although the elicitation and exploration of affect is an approach rarely used in
CBT, we have found this component to be a powerful clinical tool with patients who
cannot or do not willingly access and experience emotion. We have described our
treatment in detail elsewhere (Woolfolk & Allen, 2007). Participants’ symptomatology
and functioning were assessed with clinician-administered instruments, self-report
questionnaires, and medical records before randomization as well as 3 months, 9
months, and 15 months after randomization. Just after the completion of treatment,
as well as one year later—that is, at the 15-month follow-up assessment—patients
who received CBT experienced a greater reduction in somatization and functional
impairment. Substantially more participants who received CBT than the control
treatment were rated as either “very much improved” or “much improved” by a
Table 22.1 Woolfolk and Allen 10-Session Cognitive Behavioral Treatment for Somatization
Topics discussed in individual sessions Session no.
Treatment rationale 1–10

Symptom monitoring forms 1–10
Diaphragmatic breathing 1–10
Behavioral activation 2–10
Activity pacing 2–10
Differential relaxation 4–10
Sleep hygiene/stimulus control techniques (if appropriate) 4–10
Distraction 4–10
Emotional awareness/focusing 5–10
Cognitive restructuring 5–10
Abbreviated progressive muscle relaxation 7–10
Advantages and disadvantages of the sick role 8
Assertiveness 8–10
Termination and plan for additional treatment, as needed 10
Topics discussed in conjoint sessions Session no.
Treatment rationale 3, 6, 9
Couple’s pleasurable activities 3, 6, 9
Couple’s communication about physical symptoms 3, 6, 9
Significant other’s reinforcement of patient’s illness behavior 6, 9
clinician who was blind to participants’ treatment condition (40% vs. 5%, respectively).
Also, for the 68% of the sample for whom complete medical records were reviewed,
CBT was associated with a reduction in health care costs and physician visits (Allen
et al., 2006). Thus, the study suggests CBT can result in long-term improvements
in symptomatology, functioning, and health care utilization of the most severely
disturbed somatizing patients.
Integrating Cognitive Behavioral Therapy for Somatization

into Primary Care
Because somatization is so prevalent in primary care practices (Escobar et al., 1998;
Gureje et al., 1997; Kirmayer & Robbins, 1991), some approaches to the treatment
of somatization have been focused on primary care physicians’ behavior. Smith,
Monson, and Ray (1986b) sent a psychiatric consultation letter to patients’ primary
care physicians, describing somatization disorder and providing recommendations
to guide primary care. The recommendations to physicians were straightforward:
(a) to schedule somatizers’ appointments every 4 to 6 weeks instead of as-needed
appointments, (b) to conduct a physical examination in the organ system or body part
relevant to the presenting complaint, (c) to avoid diagnostic procedures and surgeries
unless clearly indicated by underlying somatic pathology, and (d) to avoid making
disparaging statements, such as “your symptoms are all in your head.” Patients whose
primary physicians had received the consultation letter experienced better health
outcomes, such as physical functioning and cost of medical care, than those whose
physicians had not received the letter. The same group of investigators replicated these
results in three additional studies, one study using patients meeting criteria for full
somatization disorder (Rost, Kashner, & Smith, 1994) and two studies using patients
with subthreshold somatization (Dickinson et al., 2003; Smith, Rost, & Kashner,
1995).
Given the success of the consultation letter just described and the success of
CBT, some investigators have attempted to train primary care physicians to better
detect somatization and to incorporate cognitive and behavioral techniques into their
treatment of these patients. Five groups of investigators have reported controlled
clinical trials on the effects of such physician training (Arnold et al., 2009; Larish,
Schweickhardt, Wirsching, & Fritzsche, 2004; Morriss et al., 2007; Rief, Martin,
Rauh, Zech, & Bender, 2006; Rosendal et al., 2007). The two studies providing
the most extensive physician training (20–25 hours) resulted in no association
between physician training and patients’ symptomatology, functioning, or quality
of life (Arnold et al., 2009; Rosendal et al., 2007). Three other studies found less
intensive physician training programs—12 hours (Larish et al., 2004), 1 day (Rief,
Martin, et al., 2006), or 6 hours (Morriss et al., 2007)—to coincide with no clear
improvement in somatization symptomatology; however, Rief and colleagues did find
their training to result in fewer health care visits for the 6 months subsequent to
training (Rief, Martin, et al., 2006).
One other study examined the effect of training primary care clinicians to identify
and treat somatization using cognitive behavioral techniques and pharmacotherapy
(Smith et al., 2006). This study involved the most intensive such training program
studied, one entailing 84 hours over 10 weeks. Nurse practitioners were trained
to provide a year-long 12-session multidimensional intervention in primary care
that employed relaxation training, recommendations to exercise and to reduce the
use of controlled substances, medication management (i.e., antidepressants as well
as medications to treat comorbid organic disease), and physical therapy. Patients
who received treatment from these trained nurses reported modest improvements
on self-report scales of mental health as well as physical functioning. A post hoc
analysis was interpreted by the study’s investigators as suggesting that improvements
were attributable to more frequent and appropriate use of antidepressant medication
among patients of nurses who received the training (Smith et al., 2006).
A slightly different model for integrating CBT into primary care is a collaborative
care model of treatment, in which mental health professionals work together with
medical practitioners in the primary care setting (Katon et al., 1995; Von Korff,
Gruman, Schaefer, Curry, & Wagner, 1997). The one study investigating the efficacy
of such a model for the treatment of somatization had psychiatrists provide primary
care physicians and their staff with training on the diagnosis and treatment of
somatization and comorbid psychopathology (van der Feltz-Cornelis, van Oppen,
Ader, & van Dyck, 2006). Also, the psychiatrist provided case-specific consultations
to primary physicians regarding referrals for CBT and/or psychiatric treatment (van
der Feltz-Cornelis et al., 2006). A control comparison treatment included the same
training for primary care physicians and their staff by the psychiatrist without the case-
specific consultation. Six months after randomization, participants whose primary care
physician received psychiatric consultation reported a greater reduction in somatic
symptoms and in health care visits (van der Feltz-Cornelis et al., 2006).
Cognitive Behavioral Therapy for Conversion Disorder

We are aware of only one published randomized controlled trial investigating the
efficacy of CBT for conversion or functional neurological disorder. In the study
patients diagnosed by a neurologist as having psychogenic nonepileptic seizures
were randomly assigned to receive standard neuropsychiatry care alone or standard
neuropsychiatry care plus individual CBT (Goldstein et al., 2010). The 12-session
CBT was designed to help patients interrupt behavioral, physiological, and emotional
responses that occurred at the onset of seizures. Specifically, patients were encouraged
to engage in avoided activities, utilize relaxation methods, and restructure their
dysfunctional cognitions (Goldstein et al., 2010). At the conclusion of treatment,
patients who received CBT reported a significantly greater reduction in psychogenic
seizures than did the control group. At the 6-month follow-up assessment, the
difference between treatment and control groups was only marginally significant.
Health care utilization and social and work functioning did not change differentially
between the treatment groups (Goldstein et al., 2010).
Conclusions and Future Research
Although the literature on CBT for somatization and conversion disorders is relatively
small, a few global conclusions can be posited. The literature on the treatment of
somatization supports the use of six to 16 sessions of CBT administered by a mental
health professional. A recent meta-analysis indicated CBT is modestly effective in
reducing somatization symptomatology and minimally effective in improving physical
functioning (Kleinstäuber, Witthöft, & Hiller, 2011). To date there is no evidence that
CBT reduces health care services when the cost of CBT itself is considered. Researchers
have just begun to develop and examine the effectiveness of true collaboration of
cognitive behavioral therapists and primary care clinicians and integration of their
services. There are inadequate data on the treatment of conversion disorder and on
treatment of the new DSM-5 diagnostic categories to make any conclusion.
One hurdle in administering CBT to somatically-focused patients is that most
of these patients seek treatment in primary care (or, in the case of conversion
disorder, neurology clinics), not in psychiatric clinics. When patients with somatoform
symptoms are referred to mental health treatment, it is estimated that 50–90% of
these patients fail to complete the referral (Escobar et al., 1998; Regier et al., 1988).
Impediments to successful psychiatric referral of patients presenting with somatization
occur at both the professional institutional level (e.g., lack of collaboration between
primary care and mental health practitioners, lack of mental health training for primary
care physicians, inadequate mental health insurance) and the level of the individual
patient (e.g., concerns about the stigma of having a psychiatric disorder, resistance to
psychiatric diagnosis, health beliefs that lead to somatic presentations, pessimism, and
fatigue) (Freidl et al., 2007; Pincus, 2003). This literature highlights the importance of
conducting research on the effectiveness of CBT for somatization and for conversion
disorder in medical settings where the overwhelming majority of these patients are
seen. Also, as suggested by the research on somatization, an integration of mental
health providers into primary care and collaboration with primary care physicians and
staff would seem imperative in that it could increase the acceptability and availability
of CBT. Additional research is required to substantiate these recommendations.
As we move forward to refine the treatment of patients with somatic symptom
disorders, one direction for future research is to improve treatment outcome. As
a whole, cognitive and behavioral treatments have been shown to reduce physical
discomfort and functional limitations in these patients. Although even the most
severely and chronically disturbed patients have benefited from treatment, a majority
of the treated patients continued to suffer with significant symptomatology after
treatment ended (see Woolfolk & Allen, 2007, for a review). Also, there are few
data on the impact of treatment on health care utilization, especially when the cost
of a psychosocial intervention is factored in to the equation. The investigation of
longer-term treatments has been recommended for patients who are severely or
chronically disturbed (Woolfolk & Allen, 2007). Some researchers have argued for
studying a stepped-care approach in which all patients would receive low-intensity
targeted primary care management. Response to this initial phase of treatment would
guide the level of intensity of additional treatment and possible referral to mental
health specialists (Arnold et al., 2009; Fink & Rosendal, 2008).
References
Alexander, F. (1950). Psychosomatic medicine. New York, NY: Norton.
Allen, L. A., Gara, M. A., Escobar, J. I., Waitzkin, H., & Cohen-Silver, R. (2001). Somatization:
A debilitating syndrome in primary care. Psychosomatics, 42, 63–67.
Allen, L. A., Woolfolk, R. L., Escobar, J. I., Gara, M. A., & Hamer, R. M. (2006). Cognitive-
behavioral therapy for somatization disorder: A randomized controlled trial. Archives of
Internal Medicine, 166, 1512–1518.
Altamura, A. C., Carta, M. G., Tacchini, G., Musazzi, A., Pioli, M. R., & the Italian Collabo-
rative Group on Somatoform Disorders. (1998). Prevalence of somatoform disorders in a
psychiatric population: An Italian nationwide survey. European Archives of Psychiatry and
Clinical Neuroscience, 248, 267–271.
American Psychiatric Association (1952). Diagnostic and statistical manual of mental disorders.
Washington, DC: Author.
American Psychiatric Association (1968). Diagnostic and statistical manual of mental disorders
(2nd ed.). Washington, DC: Author.
(3rd ed.). Washington, DC: Author.
(3rd ed., rev.). Washington, DC: Author.
(4th ed.). Washington, DC: Author.
American Psychiatric Association (2011). DSM–5 development. Retrieved from
http://www.dsm5.org/proposedrevision/Pages/SomaticSymptomDisorders.aspx
Arnold, I. A., de Waal, M. W., Eekhof, J. A., Assendelft, W. J., Spinhoven, P., & van Hemert,
A. M. (2009). Medically unexplained physical symptoms in primary care: A controlled
study on the effectiveness of cognitive-behavioral treatment by the family physician.
Barsky, A. J. (1992). Amplification, somatization, and the somatoform disorders. Psychosomatics,
33, 28–34.
Barsky, A. J., Orav, E. J., & Bates, D. W. (2005). Somatization increases medical utilization
and cost independent of psychiatric and medical utilization. Archives of General Psychiatry,
62, 903–910.
Binzer, M., Andersen, P. M., & Kullgren, G. (1997). Clinical characteristics of patients with
motor disability due to conversion disorder: A prospective control group study. Journal
of Neurology, Neurosurgery and Psychiatry, 63, 83–88.
Breuer, J., & Freud, S. (1974). Studies on hysteria (J. Strachey & A. Strachey, Trans.).
Harmondsworth, England: Penguin. (Original work published 1895)
Briquet, P. (1859). Traité clinique et thérapeutique de l’hystérie. Paris, France Baillière.
Brown, R. (2004). Psychological mechanisms of medically unexplained symptoms: An integra-
tive conceptual model. Psychological Bulletin, 130, 793–812.
Creed, F., Firth, D., Timol, M., Metcalfe, R., & Pollock, S. (1990). Somatization and illness
behaviour in a neurology ward. Journal of Psychosomatic Research, 34, 427–437.
Crimlisk, H. L., Bhatia, K., Cope, H., David, A., Marsden, C. D., & Ron, M. A. (1998). Slater
revisited: 6-year follow-up study of patients with medically unexplained motor symptoms.
British Medical Journal, 316, 582–586.
Deveci, A., Taskin, O., Dinc, G., Yilmaz, H., Demet, M. M., Erbay-Dundar, P., … Ozmen, E.
(2007). Prevalence of pseudoneurological conversion disorder in an urban community in
Manisa, Turkey. Social Psychiatry and Psychiatric Epidemiology, 42, 857–864.
Dickinson, W. P., Dickinson, L. M., deGruy, F. V., Main, D. S., Candib, L. M., & Rost,
K. (2003). A randomized clinical trial of a care recommendation letter intervention for
somatization in primary care. Annals of Family Medicine, 1, 228–235.
Dimsdale, J., Creed, F., & DSM-V Workgroup on Somatic Symptom Disorders. (2009).
The proposed diagnosis of somatic symptom disorders in DSM-5 to replace somato-
form disorders in DSM-IV: A preliminary report. Journal of Psychosomatic Research, 66,
473–476.
Dongier, M. (1983). Briquet and Briquet’s syndrome viewed from France. Canadian Journal
Engel, G. L. (1977). The need for a new medical model: A challenge for biomedicine. Science,
196, 129–136.
Escobar, J. I., Burnam, A., Karno, M., Forsythe, A., & Golding, J. M. (1987). Somatization in
the community. Archives of General Psychiatry, 44, 713–718.
Escobar, J. I., Gara, M. I., Diaz-Martinez, A. M., Interian, A., Warman, M., Allen, L. A.,
… Rodgers, D. (2007). Effectiveness of a time-limited cognitive behavior therapy-type
intervention among primary care patients with medically unexplained symptoms. Annals
of Family Medicine, 5, 328–335.
Escobar, J. I., Golding, J. M., Hough, R. L., Karno, M., Burnam, M. A., & Wells, K. B.
(1987). Somatization in the community: Relationship to disability and use of services.
American Journal of Public Health, 77 , 837–840.
Escobar, J. I., Rubio-Stipec, M., Canino, G., & Karno, M. (1989). Somatic Symptom
Index (SSI): A new and abridged somatization construct. Prevalence and epidemiological
correlates in two large community samples. Journal of Nervous and Mental Disease, 177 ,
140–146.
Escobar, J. I., Waitzkin, H., Silver, R. C., Gara, M., & Holman, A. (1998). Abridged
somatization: A study in primary care. Psychosomatic Medicine, 60, 466–472.
Fabrega, H., Mezzich, J., Jacob, R., & Ulrich, R. (1988). Somatoform disorder in a psychiatric
setting: Systematic comparisons with depression and anxiety disorders. Journal of Nervous
and Mental Disease, 176, 431–439.
Faravelli, C., Salvatori, S., Galassi, F., Aiazzi, L., Drei, C., & Cabras, P. (1997). Epidemiology of
somatoform disorders: A community survey in Florence. Social Psychiatry and Psychiatric
Epidemiology, 32, 24–29.
Fink, P. (1992). Surgery and medical treatment in persistent somatizing patients. Journal of
Psychosomatic Research, 36, 439–447.
Fink, P., & Rosendal, M. (2008). Recent developments in the understanding and management
of functional somatic symptoms in primary care. Current Opinion in Psychiatry, 21,
182–188.
Fink, P., Steen Hansen, M., & Søndergaard, L. (2005). Somatoform disorders among first-time
referrals to a neurology service. Psychosomatics, 46, 540–548.
Folks, D. G., Ford, C. V., & Regan, W. M. (1984). Conversion symptoms in a general hospital.
Foucault, M. (1965). Madness and civilization: A history of insanity in the age of reason. (R.
Howard, Trans.). New York, NY: Pantheon. (Original work published 1961)
Freidl, M., Spitzl, S. P., Prause, W., Zimprich, F., Lehner-Baumgartner, E., Baumgartner, C.,
& Aigner, M. (2007). The stigma of mental illness: Anticipation and attitudes among
patients with epileptic, dissociative or somatoform pain disorder. International Review of
Psychiatry, 19, 123−129.
Garcia-Campayo, J., Alda, M., Sobradiel, N., Olivan, B., & Pascual, A. (2007). Personality
disorders in somatization disorder patients: A controlled study in Spain. Journal of
Goldstein, L. H., Chalder, T., Chigwedere, C., Khondoker, M. R., Moriarty, J., Toone, B.
K., & Mellers, J. D. (2010). Cognitive-behavioral therapy for psychogenic nonepileptic
seizures: A pilot RCT. Neurology, 74, 1986–1994.
Gureje, O., Simon, G. E., Ustun, T., & Goldberg, D. P. (1997). Somatization in cross-cultural
perspective: A World Health Organization study in primary care. American Journal of
Hafeiz, H. B. (1980). Hysterical conversion: A prognostic study. British Journal of Psychiatry,
136, 548–551.
Hahn, S. R. (2001). Physical symptoms and physician-experienced difficulty in the
physician–patient relationship. Annals of Internal Medicine, 134, 897–904.
Jackson, J. L., & Kroenke, K. (2008). Prevalence, impact, and prognosis of multisomatoform
disorder in primary care: A 5-year follow-up study. Psychosomatic Medicine, 70, 430–434.
Janet, P. (1907). The major symptoms of hysteria. New York, NY: Macmillan.
Katon, W., Lin, E., Von Korff, M., Russo, J., Lipscomb, P., & Bush, T. (1991). Somatization:
A spectrum of severity. American Journal of Psychiatry, 148, 34–40.
Katon, W., von Korff, M., Lin, E., Walker, E., Simon, G. E., Bush, T., … Russo, J. (1995).
Collaborative management to achieve treatment guidelines: Impact on depression in
primary care. Journal of the American Medical Association, 273, 1026–1031.
Kent, D. A., Tomasson, K., & Coryell, W. (1995). Course and outcome of conversion and
somatization disorder: A four-year follow-up. Psychosomatics, 36, 138–144.
Kerns, R. D., & Weiss, L. A. (1994). Family influences on the course of chronic illness: A
cognitive behavioral transactional model. Annals of Behavior Medicine, 16, 116–121.
Kirmayer, L. J., & Robbins, J. M. (1991). Three forms of somatization in primary care:
Prevalence, co-occurrence, and sociodemographic characteristics. Journal of Nervous and
Mental Disease, 179, 647–655.
Kleinstäuber, M., Witthöft, M., & Hiller, W. (2011). Efficacy of short-term psychotherapy for
multiple medically unexplained physical symptoms: A meta-analysis. Clinical Psychology
Review, 31, 146–160.
Kroenke, K., Sharpe, M., & Sykes, R. (2007). Revising the classification of somatoform
disorders: Key questions and preliminary recommendations. Psychosomatics, 48, 277–285.
Kroenke, K., Spitzer, R. L., deGruy, F. V., Hahn, S. R., Linzer, M., Williams, J. B., … Davies,
M. (1997). Multisomatoform disorder: An alternative to undifferentiated somatoform
disorder for the somatizing patient in primary care. Archives of General Psychiatry, 54,
352–358.
Larisch, A., Schweickhardt, A., Wirsching, M., & Fritzsche, K. (2004). Psychosocial interven-
tions for somatizing patients by the general practitioner: A randomized controlled trial.
Journal of Psychosomatic Research, 57 , 507–514.
Lidbeck, J. (1997). Group therapy for somatization disorders in general practice: Effectiveness
of a short cognitive-behavioural treatment model. Acta Psychiatrica Scandinavica, 96,
14–24.
Lin, E. H., Katon, W., Von Korff, M., Bush, T., Lipscomb, R., Russo, J., & Wagner, E. (1991).
Frustrating patients: Physician and patient perspectives among distressed high users of
medical services. Journal of General Internal Medicine, 6, 241–246.
Mace, C. J., & Trimble, M. R. (1996). Ten-year prognosis of conversion disorder. British
Mai, F. M., & Merskey, H. (1980). Briquet’s treatise on hysteria: A synopsis and commentary.
Archives of General Psychiatry, 37 , 1401–1405.
Martin, R., Bell, B., Hermann, B., & Mennemeyer, S. (2003). Non epileptic seizures and their
costs: The role of neuropsychology. In G. P. Pritigano & N. H. Pliskin (Eds.), Clinical
neuropsychology and cost outcome research: A beginning (pp. 235–258). New York, NY:
Psychology Press.
Mokleby, K., Blomhoff, S., Malt, U. F., Dahlström, A., Tauböll, E., & Gjerstad, L. (2002).
Psychiatric comorbidity and hostility in patients with psychogenic nonepileptic seizures
compared with somatoform disorders and healthy controls. Epilepsia, 43, 193–198.
Morriss, R., Dowrick, C., Salmon, P., Peters, S., Dunn, G., Rogers, A., … Gask, L. (2007).
Cluster randomised controlled trial of training practices in reattribution for medically
unexplained symptoms. British Journal of Psychiatry, 191, 536–542.
Pennebaker, J. W. (1982). The psychology of physical symptoms. New York, NY: Springer.
Perkin, G. D. (1989). An analysis of 7,836 successive new outpatient referrals. Journal of
Neurology, Neurosurgery, and Psychiatry, 52, 447–448.
Peveler, R., Kilkenny, L., and Kinmonth, A. L. (1997). Medically unexplained physical
symptoms in primary care: A comparison of self-report screening questionnaires and
clinical opinion. Journal of Psychosomatic Research, 42, 245–252.
Pincus, H. A. (2003). The future of behavioral health and primary care: Drowning in the
mainstream or left on the bank? Psychosomatics, 44, 1–11.
Regier, D., Boyd, J., Burke, J., Rae, D. S., Myers, J. K., Kramer, M., … Locke, B. Z. (1988).
One-month prevalence of mental disorders in the U.S.: Based on five epidemiological
catchment area sites. Archives of General Psychiatry, 45, 977–986.
Reuber, M., Fernandez, G., Bauer, J., Helmstaedter, C., & Elger, C. E. (2002). Diagnostic
delay in psychogenic nonepileptic seizures. Neurology, 58, 493–495.
Rief, W., Heitmüller, A. M., Reisberg, K., & Rüddel, H. (2006). Why reassurance fails
in patients with unexplained symptoms: An experimental investigation of remembered
probabilities. PLoS Medicine, 3, e269.
Rief, W., Hennings, A., Riemer, S., & Euteneuer, F. (2010). Psychobiological differences
between depression and somatization. Journal of Psychosomatic Research, 68, 495–502.
Rief, W., Hiller, W., & Margraf, J. (1998). Cognitive aspects of hypochondriasis and the
somatization syndrome. Journal of Abnormal Psychology, 107 , 587–595.
Rief, W., Martin, A., Rauh, E., Zech, T., & Bender, A. (2006b). Evaluation of general
practitioners’ training: How to manage patients with unexplained physical symptoms.
Psychosomatics, 47 , 304–311.
Rief, W., Mewes, R., Martin, A., Glaesmer, H., & Brahler, E. (2011). Evaluating new proposals
for the psychiatric classification of patients with multiple somatic symptoms. Psychosomatic
Medicine, 73, 760–768.
Rief, W., Shaw, R., & Fichter, M. M. (1998). Elevated levels of psychophysiological arousal and
cortisol in patients with somatization syndrome. Psychosomatic Medicine, 60, 198–203.
Robins, L. N., & Regier, D. (1991). Psychiatric disorders in America: The epidemiological
catchment area study. New York, NY: Free Press.
Ron, M. (2001). The prognosis of hysteria/somatization disorder: Contemporary approaches to the
study of hysteria. Oxford, England: Oxford University Press.
Rosendal, M., Olesen, F., Fink, P., Toft, T., Sokolowski, I., & Bro, F. (2007). A randomized
controlled trial of brief training in the assessment and treatment of somatization in primary
care: Effects on patient outcome. General Hospital Psychiatry, 29, 364–373.
Rost, K. M., Akins, R. N., Brown, F. W., & Smith, G. R. (1992). The comorbidity of DSM-
III-R personality disorders in somatization disorder. General Hospital Psychiatry, 14,
322–326.
Rost, K., Kashner, T. M., & Smith, G. R. (1994). Effectiveness of psychiatric intervention with
somatization disorder patients: Improved outcomes at reduced costs. General Hospital
Sar, V., Akyuz, G., Kundakci, T., Kiziltan, E., & Dogan, O. (2004). Childhood trauma,
dissociation, and psychiatric comorbidity in patients with conversion disorder. American
Schmidt, A. J. M., Wolfs-Takens, D. J., Oosterlaan, J., & van den Hout, M. A. (1994). Psy-
chological mechanisms in hypochondriasis: Attention-induced physical symptoms without
sensory stimulation. Psychotherapy & Psychosomatics, 61, 117−120.
Severeijns, R., Vlaeyen, J. W. S., & van den Hout, M. A. (2004). Pain catastrophizing is
associated with health indices in musculoskeletal pain: A cross-sectional study in the
Dutch community. Health Psychology, 23, 49−57.
Sharpe, M., Peveler, R., & Mayou, R. (1992). The psychological treatment of patients with
functional somatic symptoms: A practical guide. Journal of Psychosomatic Research, 36,
515–529.
Simon, G. E. & Von Korff, M. (1991). Somatization and psychiatric disorder in the NIMH
Epidemiologic Catchment Area Study. American Journal of Psychiatry, 148, 1494–1500.
Smith, G. R., Monson, R. A., & Ray, D. C. (1986a). Patients with multiple unexplained
symptoms: Their characteristics, functional health, and health care utilization. Archives of
Internal Medicine, 146, 69–72.
Smith, G. R., Monson, R. A., & Ray, D. C. (1986b). Psychiatric consultation letter in
somatization disorder. New England Journal of Medicine, 314, 1407–1413.
Smith, G. R., Rost, K., & Kashner, M. (1995). A trial of the effect of a standardized psychiatric
consultation on health outcomes and costs in somatizing patients. Archives of General
Smith, R. C., Lyles, J. S., Gardiner, J. C., Sirbu, C., Hodges, A., Collins, C., … Goddeeris,
J. (2006). Primary care clinicians treat patients with medically unexplained symptoms: A
randomized controlled trial. Journal of General Internal Medicine, 21, 671–677.
Speckens, A. E. M., van Hemert, A. M., Spinhoven, P., Hawton, K. E., Bolk, J. H., & Rooi-
jmans, G. M. (1995). Cognitive behavioural therapy for medically unexplained physical
symptoms: A randomised controlled trial. British Medical Journal, 311, 1328–1332.
Stefansson, J. G., Messina, J. A., & Meyerowitz, S. (1979). Hysterical neurosis, conversion
type: Clinical and epidemiological considerations. Acta Psychiatrica Scandinavica, 53,
119–138.
Stekel, W. (1924). Peculiarities of behaviour (Vols. 1–2). London, England: Williams and
Norgate.
Stone, J., Carson, A., Duncan, R., Coleman, R., Roberts, R., Warlow, C., … Sharpe, M. (2009).
Symptoms “unexplained by organic disease” in 1144 new neurology out-patients: How
often does the diagnosis change at follow-up? Brain, 132, 2878–2888.
Sumathipala, A., Hewege, S., Hanwella, R., & Mann, A. H. (2000). Randomized controlled
trial of cognitive behaviour therapy for repeated consultations for medically unexplained
complaints: A feasibility study in Sri Lanka. Psychological Medicine, 30, 747–757.
Swartz, M., Blazer, D., George, L., & Landerman, R. (1986). Somatization disorder in a
community population. American Journal of Psychiatry, 143, 1403–1408.
Swartz, M., Landermann, R., George, L., Blazer, D., & Escobar, J. (1991). Somatization.
In L. N. Robins & D. Reiger (Eds.), Psychiatric disorders in America (pp. 220–257).
New York, NY: Free Press.
Teasdale, J. D. (1983). Negative thinking in depression: Cause, effect or reciprocal relationship?
Advances in Behaviour Research and Therapy, 5, 3–25.
van der Feltz-Cornelis, C. M., van Oppen, P., Ader, H. J., & van Dyck, R. (2006). Randomised
controlled trial of a collaborative care model with psychiatric consultation for persistent
medically unexplained symptoms in general practice. Psychotherapy and Psychosomatics,
75, 282–289.
Von Korff, M., Gruman, J., Schaefer, J., Curry, S. J., & Wagner, E. H. (1997). Collaborative
management of chronic illness. Annals of Internal Medicine, 127 , 1097–1102.
Weissman, M. M., Myers, J. K., & Harding, P. S. (1978). Psychiatric disorders in a U.S. urban
community: 1975–1976. American Journal of Psychiatry, 135, 459–462.
Woolfolk, R. L., & Allen, L. A. (2007). Treating somatization: A cognitive-behavioral approach.
Yutzy, S. H., Cloninger, R., Guze, S. B., Pribor, E. F., Martin, R. L., Kathol, R. G., …
Strain, J. J. (1995). DSM-IV field trial: Testing a new proposal for somatization disorder.
Zoccolillo, M., & Cloninger, C. R. (1986). Somatization disorder: Psychological symptoms,
social disability, and diagnosis. Comprehensive Psychiatry, 27 , 65–73.
23
Chronic Fatigue Syndrome
Trudie Chalder
King’s College London, United Kingdom
Introduction, Definitions, and Prevalence
Fatigue is a very common complaint but it is typically transient, self-limiting, or

explained by other circumstances. Chronic fatigue syndrome (CFS) is characterized
by persistent or relapsing unexplained fatigue of new or definite onset lasting for
at least 6 months. It is not a new condition and corresponds very clearly to an
illness called neurasthenia, commonly seen in Europe around the turn of the twen-
tieth century. The terms “myalgic encephalomyelitis” (ME) and “postviral fatigue
syndrome” have also been used to describe CFS but are misleading and unsat-
isfactory: ME implies the occurrence of a distinct pathological process whereas
postviral fatigue syndrome wrongly suggests that all cases are preceded by a viral
illness.
Operational criteria developed for research purposes by the U.S. Centers for
Disease Control and Prevention (CDC) (Fukuda et al., 1994) and by researchers
in Oxford, United Kingdom (Sharpe et al., 1991), are now widely used to
define CFS (see Box 23.1 for a summary of the criteria). The CDC criteria
require at least 6 months of persistent fatigue causing substantial functional
impairment and at least four somatic symptoms (from a list of eight) occurring
with the fatigue in a 6-month period. The presence of medical disorders that
explain prolonged fatigue excludes a patient from a diagnosis of CFS, as do a
number of psychiatric diagnoses. Although the British definition is similar, it
differs by requiring both physical and mental fatigue but no physical symptoms.
By including a requirement for several physical symptoms, the CDC defini-
tion reflects the belief that an infective or immune process may underlie the
syndrome.

DOI: 10.1002/9781118528563.wbcbt23
Box 23.1 Summary of Oxford criteria for chronic fatigue

syndrome
Characterized by fatigue as the principal symptom.
Of definite onset that is not lifelong.
Fatigue is severe, disabling, and affects physical and mental functioning.
Fatigue should have been present for a minimum of 6 months for more than
50% of the time.
Other symptoms may be present, particularly myalgia, and mood and sleep
disturbance.
Certain patients should be excluded from the definition. They include:
(a) patients with established medical conditions known to produce chronic

fatigue (e.g., severe anemia, hypothyroidism) whether the medical condi-
tion is diagnosed at presentation or only subsequently;
(b) patients with a current diagnosis of schizophrenia, manic depressive illness,
substance abuse, eating disorder, or proven organic brain disease.
Other psychiatric disorders (including depressive illness, anxiety disorders,

and hyperventilation syndrome) are not necessarily reasons for exclusion.
All patients should have a history and physical examination performed by a
competent physician.
(Adapted from Sharpe et al., 1991)
The prevalence of CFS has been reported as 0.1–2.6% in community and

primary-care-based studies, depending on the criteria used (Wessely, Chalder, Hirsch,
Wallace, & Wright, 1997). Women are at higher risk than men (relative risk 1.3–1.7)
(Wessely, 1995).
Diagnosis
There are no unequivocal diagnostic signs or symptoms of CFS. The clinical evaluation
of chronically fatigued patients is aimed at excluding underlying medical or psychiatric
causes of fatigue. In individuals with fatigue of more than 6 months’ duration, a
thorough history, physical examination, routine laboratory tests (full blood count,
erythrocyte sedimentation rate, renal, liver, and thyroid function, and urinary protein
and glucose), and mental state examination are sufficient to reach a diagnosis of
CFS in most cases. Where abnormalities are revealed on physical or laboratory
investigation, further investigations can be helpful (serological tests for Epstein–Barr
virus, cytomegalovirus, Q fever, toxoplasmosis, and HIV; chest X-ray, rheumatoid
factor, and antinuclear factor) but should otherwise be limited to avoid the risk of
iatrogenic harm. Specialist referral should be limited to situations where there is an
increased probability of an alternative diagnosis.
Chronic Fatigue Syndrome 527
The relationship between CFS and psychiatric illness is more complex. Fatigue
is a common symptom in mental illness, and where an individual’s fatigue is fully
explained by a specific psychiatric disorder, a diagnosis of CFS should not be made.
However, psychiatric comorbidity (particularly with depressive, somatoform, and
anxiety disorders) is also common and when present should be diagnosed and treated
in addition to the symptoms of CFS. This does not mean that psychiatric disorders
are the cause of CFS and indeed a substantial minority of patients do not fulfill criteria
for any psychiatric diagnosis (Wessely, Hotopf, & Sharpe 1998).
Predisposing, Precipitating, and Perpetuating Factors
In relation to etiology, a number of different biological, social, and psychological

factors are thought to work together to predispose an individual to CFS and to
precipitate and perpetuate the illness (Afari & Buchwald, 2003).
Several studies have investigated childhood experiences in relation to a diagnosis of
CFS in later life. Fisher and Chalder (2003) used a retrospective case–control design
to compare early illness experience (up to the age of 16) between 30 adults with CFS
and 30 patients attending a fracture clinic. No differences were found between the
two groups on any self-reported childhood illness category, but they found increased
levels of childhood maternal overprotection in those with CFS compared with the ill
controls.
In the only prospective study, higher emotional instability and self-reported stress
in the premorbid period were associated with higher risk for CFS-like illness 25
years later (Kato, Sullivan, Evengard, & Pedersen, 2006). In two retrospective
population-based studies of adult CFS patients and nonfatigued control participants,
CFS patients reported significantly higher levels of childhood trauma compared
with controls (Heim et al., 2006; Heim et al., 2009). Both studies used a self-
report Childhood Trauma Questionnaire with moderate to severe cut-off scores. The
Heim et al. (2009) study also showed that adults with CFS who had experienced
childhood trauma had flattened cortisol awakening response profiles compared with
healthy control participants. In this study, adults with CFS who had not experienced
emotional maltreatment during childhood exhibited normal cortisol profiles. The
authors suggest that childhood trauma might cause long-term impairment in terms
of the individual’s ability to adapt successfully to stress, for example, via disturbances
to the hypothalamic–pituitary–adrenal axis, thereby conveying a risk of developing
CFS.
There have been three longitudinal studies investigating the relationships between
activity levels in childhood and the onset of CFS in adults. In the first, lower levels of
exercise in childhood were associated with a greater risk of CFS in later life (Viner &
Hotopf, 2004). Conversely, a second study, which defined high levels of exercise as
“engaging in sporting activities weekly,” in childhood through to adulthood (13 years
to 43 years) found that high levels of exercise were associated with an increased future
risk of CFS in adulthood (Harvey, Wadsworth, Wessely, & Hotopf, 2008b). A third
study did not replicate either of these studies, finding no prospective association with
either little exercise or lots of exercise in childhood and CFS in adulthood (Goodwin,
White, Hotopf, Stansfield, & Clark, 2011).
Many patients link the onset of their symptoms to infection and, while it is
unlikely that serious viral illness perpetuates fatigue in CFS, serious infections such as
mononucleosis, hepatitis, meningitis, and Q fever are known to trigger onset in some
individuals (Cleare & Wessely, 1996). Other risk factors for developing CFS include
previous psychological illness (Harvey, Wadsworth, Wessely, & Hotopf, 2008a) and
negative life events or difficulties in the months before onset (Hatcher & House,
2003).
A wide range of factors may act to perpetuate chronic fatigue. Coping responses
to acute fatigue are important determinants of prolonged fatigue: Extreme physical
activity after an acute illness may allow insufficient time for recovery whereas prolonged
bed rest may cause physical deconditioning and further exacerbate symptoms. Illness
beliefs and the attribution of symptoms to a physical cause, with minimization of
psychological or personal contributions, are also important and have been related
to increased symptoms and worse outcomes in CFS (see Chalder & Hill, 2012, for
a review). Similarly, catastrophic beliefs that exercise will be damaging or worsen
symptoms lead to the avoidance of physical and mental activities and greater disability
(Petrie, Moss-Morris, & Weinman, 1995). Disrupted sleep patterns resulting from
excessive daytime rest may contribute to fatigue, muscle pain, and poor concentration.
The response and attitudes of others are also important in determining the course
of fatigue. Overly concerned carers may reinforce patients’ maladaptive beliefs and
coping strategies by inadvertently encouraging disability. Skeptical or stigmatizing
reactions from relatives, health professionals, or work colleagues can cause frustration
and leave the patient feeling isolated and unsupported (Deale & Wessely, 2001; Van
Houdenhove et al., 2002).
The Cognitive Behavioral Model and the Treatment

of Chronic Fatigue Syndrome
Early cognitive behavioral models focused on the perpetuation of symptoms and

disability associated with CFS (Chalder, Butler, & Wessely, 1996). The essence
of cognitive behavioral therapy (CBT) is to help patients to change behavioral
and cognitive factors, focusing specifically on changing avoidance behavior, unhealthy
sleep patterns, and unhelpful beliefs in order to improve levels of fatigue and disability.
The focus is largely on the here and now and the model applies whether the outcome
is fatigue or psychiatric disorder or both. While treatment trials, recently reviewed
in a meta-analysis (Castell, Kazantzis, & Moss-Morris, 2011), have provided some
validity for the model, a developmental perspective is probably needed to understand
more fully the development of CFS.
Surawy, Hackmann, Hawton, and Sharpe (1995) described a cognitive model
of understanding CFS. They suggested that a patient’s interpretation of somatic
symptoms such as fatigue as being physical as opposed to psychological was vital
for the development and continuation of the disorder. The model advocated that
these physical illness attributions may have evolved as a consequence of childhood
experiences in which the expression of negative emotion would have been met with
unsympathetic or hostile responses. The model proposed that a somatic attribution
(attributing symptoms to a physical cause) makes the patient’s symptoms and illness
easier to understand. The diagnosis of CFS, in a sense, can be seen as a protective
mechanism that the individual has employed in order to preserve identity and self-
esteem. Over time the individual’s focus on the symptom of fatigue leads him or her
to try and control it. The downside to this is that the individual then purportedly
gets into a vicious circle in which the desire to control symptoms leads to avoidance
in general. Although avoidant coping strategies may help in the short term, the long-
term consequences are potentially extremely unhelpful. The side effects of behavioral
avoidance or inactivity are well understood, whether related to disease processes
or not.
The evidence suggests that the most effective treatments for CFS are CBT and graded
exercise therapy (GET). The CBT model attempts to incorporate the heterogeneous
nature of the condition and stresses the role of perpetuating factors. The treatment
for CFS therefore involves planned activity and rest, graded increases in activity, a
sleep routine, and cognitive restructuring of unhelpful beliefs and assumptions.
Assessment
The assessment should include not only a detailed description of symptoms but also,
more importantly, a detailed behavioral analysis of what the individual is able to do
in relation to work, home, private, and social aspects of their lives. The quality and
quantity of sleep should be enquired about. A detailed account of activity, rest, and
sleep patterns should be obtained by asking the patient to keep a diary for 2 weeks.
This will be used as a guide for setting the initial behavioral goals and can be used
throughout treatment to monitor progress. Specific fears about the consequences
of activity and exercise should be elicited, as should more general ideas about the
nature of the illness. Circumstances surrounding the onset should be discussed, as
this information may be useful when giving the patient a rationale for treatment,
and lifestyle factors may need to be addressed during treatment. It is also extremely
helpful to elicit compassionately the patient’s family and personal history. Previous
trauma in childhood is associated with CFS in adulthood, and making links between
trauma and fatigue may be helpful during the process of therapy. The presence of
depression and/or anxiety should be assessed; if severe, such disorders may require
treatment in their own right, either before CBT or concurrently.
Engagement
Engaging the patient and his or her significant other in treatment and forming a
therapeutic alliance is a continual process. During the assessment, the individual, who
may be sensitive to being disbelieved, may be on the lookout for evidence that the
therapist thinks the problem is “all in the mind.” During the early stage of treatment
it is helpful for the therapist to be explicit in conveying belief in the real and physical
nature of the symptoms. Careful attention should be paid to the language that is used.
The term “psychological” is probably best avoided; first, because it is a broad term
which means different things to different people, but also because it may set the scene
for unnecessary disagreement between the patient and the therapist. The patient’s
symptoms are real and it helps to state and restate this. Rather than debating whether
the problem is physical or psychological—a mind/body split which is unhelpful in
any illness—it is far more useful to direct the discussion toward how the problem can
best be managed, taking into account physiological, behavioral, and cognitive factors.
Rationale for Treatment

Once a thorough assessment has been carried out, the therapist should share with
the patient an initial formulation of the problem. While openly acknowledging that
this is to some extent hypothetical, it should help the process of engagement and will
form part of the rationale for treatment, a prerequisite for any intervention. It stands
to reason that having an understanding of how and why treatment works will aid
compliance.
The rationale will obviously vary depending on the individual’s circumstances, but
essentially the patient should be told that the emphasis in treatment in the early
phases will be on perpetuating factors. Initially, keeping a diary of activity and sleep
patterns will highlight areas of inconsistency. These are used to set goals with a
view to establishing a consistent level of activity every day regardless of symptoms.
The amount of activity is then gradually increased and rest decreased as the patient
becomes more confident. It can be helpful to point out that rest is useful in an acute
illness but is rarely restorative in the longer term. A sleep routine should also be
established as quickly as possible.
The rationale may be discussed several times throughout treatment. It can be useful
to ask the patient to describe how he or she thinks the approach works in order to
check whether the potential benefits of treatment have been clearly understood, and
to discuss any concerns. Before commencing treatment it is important that the patient
and his or her family are clear about what it entails. The aims of treatment should
be explicitly negotiated and agreed with the patient. These aims are best defined in
terms of specific and realistic achievements or behavioral goals that are worked toward
gradually, and depend on individual needs.
Structure
Patients are usually seen fortnightly for up to 15 sessions of face-to-face treatment.
Follow-ups are carried out at 3 and 6 months and then 1 year to monitor progress
and tackle any residual problems. Written material and self-help books are offered
(Burgess & Chalder, 2005; Chalder, 1995) to supplement verbal interactions.
Questionnaires are given to assess fatigue and disability before and after treatment
and at follow-up. The Chalder Fatigue Scale is an 11-item scale used to assess both
physical and mental fatigue. There are two ways of scoring it. The bimodal scoring
system can be used (0, 0, 1, 1) and those who score 4 or more are considered a
fatigue case. Alternatively the Likert scoring system can be used (0, 1, 2, 3) (Cella
& Chalder, 2010; Chalder et al., 1993). The work and social adjustment scale is a
5-item scale which assesses the impact of fatigue on an individual’s ability to go to
work, manage the home, engage in social or private leisure activities, and maintain
relationships (Cella, Sharpe, & Chalder, 2011). It is brief, simple, and sensitive to
change after CBT.
At the beginning of treatment long-term targets are negotiated with the patient to
ensure the therapist, patient, and significant other are working toward similar goals.
At every subsequent session short-term goals are agreed upon. Patients keep records
of their activity and rest throughout treatment so that progress can be monitored and
problems discussed.
Problems are anticipated and problem-solving strategies are used to elicit effective
coping. Discussion during sessions often revolves around exploring issues that may
be preventing the patient from making changes. A variety of techniques are used to
facilitate change. Socratic questions are used to explore specific concerns or difficulties.
The therapist may need to slow down the expectation of success. Less pressure to
succeed often results in quicker success, on the part of the therapist and the patient.
Activity Scheduling
Goals usually include a mixture of social and leisure-related activities as well as activities
related to responsibilities. Short walks or tasks carried out in even chunks throughout
the day are ideal and are interspersed with rests. The emphasis is on consistency and
breaking the association between experiencing symptoms and stopping activity. The
goals (e.g., for someone less disabled, walking for 10 minutes three times daily) are
gradually built up as tolerance to symptoms increases, until the longer-term targets
are reached. Fatigue levels do not decrease very much initially, but during the process
of treatment marked reductions in fatigue might be expected. Tasks that require
concentration, such as reading, can be included, but mental functioning does seem
to improve in synchrony with physical functioning.
Establishing a Sleep Routine

Early on in treatment patients are asked to keep a diary of bedtime, sleep time,
wake up time, and get up time. The total number of hours spent asleep is calculated
and a variety of strategies can then be used to improve both the quality and
quantity of sleep. A routine of going to bed and getting up at a preplanned time,
while simultaneously cutting out daytime naps, helps to improve both hypersomnia
and insomnia. Change in sleep routine can be brought about slowly, depending
on the severity of the problem. For those who sleep too much, the amount of
time they spend asleep can be reduced gradually. A detailed description of how
to manage sleep problems is provided by Morin and Espie (2003). It can be
difficult for people with CFS to establish a sleep routine, particularly when they are
not at work or in education. Some flexibility should be built into the negotiated
program.
Modifying Negative and Unhelpful Thinking

The initial aim of this component is to prevent unhelpful thoughts from blocking
progressive increases in activity. Information about the nature of CFS and the process
of rehabilitation should be shared with the individual throughout treatment, as
many patients will have been given incorrect or misleading information about their
illness. Explanations regarding the physiological effects of inactivity can help patients
understand the rationale for activity scheduling, while demonstrating the effect of
attention on symptoms can also help patients use enjoyable activities as a form of
distraction.
Information to assist self-help, given at various stages of treatment, can be helpful.
In reality, unhelpful beliefs about the harmful effects of exercise will diminish as the
patient becomes more active and confident. However, some will need more structured
cognitive therapy using traditional methods. Specific negative thoughts such as, “My
muscles will be damaged by exercising too much” should be recorded in a diary.
Patients should be encouraged to elicit alternative, less catastrophic interpretations of
events. These too should be recorded in a diary and discussed during consultations.
Core beliefs and dysfunctional assumptions relating to perfectionism or self-worth
may be discussed with some patients.
Treating Comorbidity
Some patients with severe depression may benefit from antidepressants. Others will
find their mood improves with activity scheduling and cognitive restructuring. For
those with an anxiety disorder, discussion about the physiological aspects of anxiety
can be helpful. Many patients are unaware of the physiological aspects of anxiety and
the associated physical symptoms. Giving information about the nature of autonomic
arousal often helps explain the patient’s experience of intrusive, frightening somatic
sensations.
Tackling Psychosocial Problems and Trauma

Related social or psychological difficulties will often emerge during treatment. It is
important that these are tackled in a problem-solving fashion, otherwise they may
prevent further progress. However, the focus needs to be on rehabilitation. Being
distracted from the main task in hand may lead to treatment failure. Improvements in
one particular area of a patient’s life will usually generalize to other areas. However,
should the patient reveal early life trauma, the therapist should try to facilitate
emotional processing in an evidence-based way. Compassion may not be what the
patient is used to, and he or she may experience some difficulty in revealing past
trauma.
Employment
There is no black-and-white rule about how to negotiate employment. From a
therapeutic perspective, several factors need to be considered: the patient’s level of
fear, degree of disability, age, and plans for the future; the employer’s view, when
relevant, and the degree of support from the employer. The long-term goal may
involve a return to work, but some patients may be negotiating medical retirement.
Others may be on state benefits, which makes recovery more difficult. Clearly, the
longer a person is away from work the less confident the person will become, making
a return even more daunting.
Facilitating Change
Resistance to change is maintained by dissonance reduction. It can be recognized

by the way in which patients respond to situations or information that challenge or
contradict their beliefs. A reluctance to accept an interpretation or advice is often a
consequence of efforts to maintain a consistent interpersonal stance. Change has to
occur slowly in order to maintain an adaptive and socially acceptable level of historical
continuity. In the first instance, the therapist should support the patient’s point of
view, thus accepting and working with his or her attributions of cause and control.
Therapeutic change can then occur slowly without arousing too much dissonance
(Kirmayer, 1990).
Contrary to popular belief, it is not necessary to challenge individuals’ beliefs about
the etiology of the illness directly. Rather, specific cognitions about the danger of
activity and exercise can be examined and, if necessary, addressed. Joining and accom-
modating to the individual’s beliefs is far more advantageous to the process of change.
Telephone Treatment
Many patients are unable to travel to specialist units for treatment. In addition, there is
a shortage of specialists who are suitably qualified to deliver CBT. To overcome these
problems, a telephone treatment package of CBT, consisting of 13 telephone and two
face-to-face sessions, was developed. In an initial pilot study, nine patients with a diag-
nosis of CFS who were unable to attend regular outpatient appointments were offered
telephone treatment after an initial face-to-face assessment. Patients were given a self-
help manual and were phoned fortnightly for up to half an hour to discuss progress,
problem solve any difficulties, review diaries sent by post to the therapist, and discuss
plans for the coming fortnight. Patients also attended a face-to-face discharge appoint-
ment. Eight patients completed treatment, and improvement was seen on all measures
at discharge; fatigue had improved by 75%. At 6-month follow-up, levels of function-
ing had continued to improve. This pilot study demonstrated that telephone CBT
resulted in a reduction in fatigue and improvement in disability (Burgess & Chalder,
2001). The advantage of a telephone-based approach is that it is less time-consuming
for the therapist, therefore allowing more patients to be treated. The advantages for
patients are that it is less time-consuming and less disruptive to their lives.
Given the promising results of the pilot study, the next obvious step was to compare
telephone CBT with face-to-face CBT. Significant improvements in the primary
outcomes of physical functioning and fatigue occurred and were maintained to 1-year
follow-up after discharge from treatment. Improvements in social adjustment and

global outcome were also noted and patient satisfaction was similar in both groups.
Despite these encouraging results, the dropout rate was relatively high and therapists
should be aware of this potential problem (Burgess, Andiappan, & Chalder, 2011).
Treatment Evidence
A systematic review showed that CBT administered in specialist centers by skilled

therapists led to improved physical functioning and quality of life compared with
relaxation therapy or standard medical care (Price, Mitchell, Tidy, & Hunot, 2008).
Randomized controlled trials (RCTs) evaluating GET have found that it improves
measures of fatigue and physical functioning compared with flexibility training and
relaxation training or general advice (Reid, Chalder, Cleare, Hotopf, & Wessely,
2004). More recently, a meta-regression examining CBT and GET for adults with
CFS showed a dose effect, with those who received more sessions showing better
outcomes (Castell, Kazantzis, & Moss-Morris, 2011).
The recently published PACE trial found that CBT and GET were more effective in
reducing both fatigue and physical disability than adaptive pacing therapy, when each
was added to specialist medical care, and more effective than specialist medical care
alone (White et al., 2011). Recovery was defined operationally using multiple criteria,
and compared the proportions of participants meeting each individual criterion as well
as two composite criteria, defined as (a) recovery in the context of the trial, and (b)
clinical recovery from the current episode of the illness, however defined, both at 52
weeks after randomization. The percentages (number/total) meeting trial criteria for
recovery were 22% after CBT and after GET, 8% after adaptive pacing therapy, and 7%
after specialist medical care. Similar proportions met criteria for clinical recovery. The
odds ratio (OR, 95% CI) for trial recovery after CBT was 3.36 (1.64, 6.88) and for
GET 3.38 (1.65, 6.93), when compared to adaptive pacing therapy. This confirmed
that recovery from CFS is possible, and that CBT and GET are the therapies most
likely to lead to recovery (White, Goldsmith, Johnson, Chalder, & Sharpe, 2013).
There is insufficient evidence to suggest that antidepressants, corticosteroids,
or other pharmacological agents are beneficial in the treatment of CFS, and no
reliable evidence that dietary supplements, evening primrose oil, or intra-muscular
magnesium are helpful (Reid et al., 2004). Prolonged rest cannot be recommended
as a treatment for CFS and may actually perpetuate or increase fatigue in people
recovering from a viral illness. A literature review of treatments for CFS reported
both limited benefits and substantial adverse effects with immunoglobulin therapy
(Rimes & Chalder, 2005). There is insufficient evidence for the use of interferon as
an effective treatment for CFS.
Mediators of Change
Several studies have attempted to examine mediators of change in relation to treatment

outcome in CFS. Identifying mechanisms of change may elucidate ways in which
treatment can be developed, tailored, or optimized to suit the needs of different

individuals (Laurenceau, Hayes, & Feldman, 2007). It may also provide information
about the clinical utility of the model on which treatment is based.
Patients receiving GET who reported overall improvement were no more physically
fit than those not improving, but did perceive less effort with exercise, and those who
improved their physical function had a smaller heart rate response to submaximal
exercise (i.e., they were fitter) (Fulcher & White, 2000). Another trial of GET found
a reduction in symptom focusing and an increased ability to exert oneself as assessed
by maximal heart rate mediated change in mental and physical fatigue (Moss-Morris,
Sharon, Tobin, & Baldi, 2005).
In the context of CBT a reduction in fearful cognitions was associated with better
outcomes in an early trial comparing CBT with relaxation (Deale, Chalder, & Wessely,
1998). Several years later a Dutch group found that a decrease in focusing on fatigue
mediated the effect of CBT on fatigue and impairment in a trial of CBT compared to
two control conditions (Wiborg, Knoop, Prins, & Bleijenberg, 2011). In summary,
then, change in symptom focusing mediated treatment outcome in both CBT and
GET.
Interestingly, in the context of a trial of CBT compared with counseling for
chronic fatigue (not CFS) in primary care, a good fatigue outcome was associated
with the patient acknowledging, expressing, and accepting distress (Godfrey, Chalder,
Ridsdale, Seed, & Ogden, 2007).
Acceptance
Research on patients with chronic pain has suggested that attempting to control
pain which is uncontrollable (i.e., lack of acceptance) is associated with distress and
frustration (Aldrich, Eccleston, & Crombez, 2000) and reduced physical functioning
(McCracken, Carson, Eccleston, & Keefe, 2004). Lack of acceptance has also been
shown to be inversely related to the ability to undergo positive, personal change
for better health and well-being (Afrell, Biguet, & Rudebeck, 2007). Conversely,
increased acceptance—giving up attempts to control pain—has been associated
with less psychological distress and better well-being and adjustment (McCracken,
1998).
Despite the wealth of research into acceptance and chronic pain, the concept of
acceptance in relation to chronic fatigue is discussed much less. One study that does
consider the relationship between acceptance and CFS symptoms found that higher
levels of acceptance were associated with greater psychological well-being and less
distress in patients with CFS (Van Damme, Crombez, Van Houdenhove, Mariman, &
Michielsen, 2006). In another study, lack of acceptance was the key factor associated
with impaired physical functioning and work and social adjustment cross-sectionally.
After a course of CBT, patients showed significantly increased acceptance, as well as
reduced concern over mistakes (negative perfectionism), less fatigue and impairment
of physical functioning, and improved work and social adjustment (Brooks, Rimes, &
Chalder, 2011).
This study showed that acceptance increased after CBT despite not being directly
incorporated into the cognitive behavioral model of CFS. It may be useful therefore to
address acceptance directly during a course of CBT, as this may lead to improved phys-
ical and social functioning and less fatigue. While “willingness” is incorporated into
CBT, acceptance is often not directly addressed, with CBT focusing more on graded
increases in activity, sleep management, and addressing unhelpful cognitions concern-
ing symptoms, coping strategies, and perfectionism. CBT could focus on acceptance
of the symptom of fatigue using attentional strategies to facilitate this. It must be
stressed, however, that acceptance of disability is not being advocated here. Indeed
the research demonstrates that disability can improve with rehabilitative therapies.
Perfectionism
Unhelpful aspects of perfectionism have been linked to CFS. Several studies (Deary
& Chalder, 2010; Kempke et al., 2011; White & Schweitzer, 2000) have found a
link between CFS and negative aspects of perfectionism (e.g., doubts about actions,
concern over mistakes). More specifically, “self-critical” perfectionism has been shown
to be related to increased stress sensitivity and depression in CFS patients (Luyten
et al., 2011). Patients report change for the positive in certain aspects of perfectionism
after CBT (Brooks et al., 2011). However, it is possible that enduring perfectionist
traits may hinder improvement and/or put people at risk for future episodes of CFS
or depression.
Prognosis
CFS is not associated with an increased mortality rate and rarely constitutes a missed
medical diagnosis when an attempt has been made to exclude organic illness prior
to making the diagnosis. A systematic review of studies describing the prognosis of
CFS identified 14 studies that used operational criteria to define cohorts of patients
with CFS (Cairns & Hotopf, 2005). Full recovery from untreated CFS is rare and an
improvement in symptoms is a more commonly reported outcome than full recovery.
The median full recovery rate was 5% (range 0–31%) and the median proportion of
patients who improved during follow-up was 39.5% (range 38–64%). Less fatigue
severity at baseline, a sense of control over symptoms, and not attributing illness to
a physical cause were all associated with a good outcome. Psychiatric disorder was
associated with poorer outcomes. The review looked at the course of CFS without
systematic intervention but, as we have seen, there is now increasing evidence for the
effectiveness of CBT and GET. More recent evidence suggests that recovery from CFS
is possible and that CBT and GET are the therapies most likely to lead to recovery
(White et al., 2013).
References
Afari, N., & Buchwald, D. (2003). Chronic fatigue syndrome: A review. American Journal of
Afrell, M., Biguet, G., & Rudebeck, C. E. (2007). Living with a body in pain: Between
acceptance and denial. Scandinavian Journal of Caring Sciences, 21, 291–296.
Aldrich, S., Eccleston, C., & Crombez, G. (2000). Worrying about chronic pain: Vigilance to
threat and misdirected problem solving. Behavioural Research Therapy, 38, 457–470.
Brooks, S. K., Rimes, K. A., & Chalder, T. (2011). The role of acceptance in chronic fatigue
syndrome. Journal of Psychosomatic Research, 71, 411–415.
Burgess, M., Andiappan, M., & Chalder, T. (2011). Cognitive behaviour therapy for chronic
fatigue syndrome in adults: Face to face versus telephone treatment—A randomised
controlled trial. Behavioural and Cognitive Psychotherapy, 40, 175–191.
Burgess, M., & Chalder, T. (2001). Telephone/postal cognitive behaviour therapy for chronic
fatigue syndrome in secondary care: A pilot study. Behavioural and Cognitive Psychother-
apy, 29, 447–455.
Burgess, M., & Chalder, T. (2005). Overcoming chronic fatigue: A self-help guide using cognitive
techniques, London, England: Constable & Robinson.
Cairns, R., & Hotopf, M. (2005). Review article: The prognosis of chronic fatigue syndrome.
Occupational Medicine (London), 55, 20–31.
Castell, B. D., Kazantzis, N., & Moss-Morris, R. E. (2011). Cognitive behavioral therapy and
graded exercise for chronic fatigue syndrome: A meta-analysis. Clinical Psychology, 18,
311–324. doi:10.1111/j.1468-2850.2011.01262.x
Cella, M., & Chalder, T. (2010). Measuring fatigue in clinical and community settings. Journal
of Psychosomatic Research, 69, 17–22.
Cella, M., Sharpe, M., & Chalder, T. (2011). Measuring disability in patients with chronic
fatigue syndrome: Reliability and validity of the work and social adjustment scale. Journal
of Psychosomatic Research, 71, 124–128.
Chalder, T. (1995). Coping with chronic fatigue: Overcoming common problems. London,
England: Sheldon Press.
Chalder, T., Berelowitz, G., Pawlikowska, T., Watts, L., Wessely, S., Wright, D., & Wallace,
P. (1993). The development of a Fatigue Scale. Journal of Psychosomatic Research, 37 ,
147–153.
Chalder, T., Butler, S., & Wessely, S. (1996). In-patient treatment of chronic fatigue syndrome.
Behavioural and Cognitive Psychotherapy, 24, 351–365.
Chalder, T., & Hill, K. (2012). Emotional processing and chronic fatigue syndrome. Psycho-
analytic Psychotherapy, 26, 141–156.
Cleare, A. J., & Wessely, S. C. (1996). Chronic fatigue syndrome: A stress disorder? British
Journal of Hospital Medicine, 55, 571–574.
Deale, A., Chalder, T., & Wessely, S. (1998). Illness beliefs and treatment outcome in chronic
fatigue syndrome. Journal of Psychosomatic Research, 45, 77–83.
Deale, A., & Wessely, S. (2001). Patients’ perceptions of medical care in chronic fatigue
syndrome. Social Science & Medicine, 52, 1859–1864.
Deary, V., & Chalder, T. (2010). Personality and perfectionism in chronic fatigue syndrome:
A closer look. Psychology and Health, 25, 465–475.
Fisher, L., & Chalder, T. (2003). Childhood experiences of illness and parenting in adults with
chronic fatigue syndrome. Journal of Psychosomatic Research, 54, 439–443.
Fukuda, K., Straus, S., Hickie, I., Sharpe, M., Dobbins, J., & Komaroff, A. (1994). The
chronic fatigue syndrome: A comprehensive approach to its definition and study. Annals
of Internal Medicine, 121, 953–959.
Fulcher, K., & White, P. D. (2000). Strength and physiological response to exercise in patients
with chronic fatigue syndrome. Journal of Neurology, Neurosurgery & Psychiatry, 69,
302–307.
Godfrey, E., Chalder, T., Ridsdale, L., Seed, P., & Ogden, J. (2007). Investigating the “active
ingredients” of cognitive behaviour therapy and counselling for patients with chronic
fatigue in primary care: Developing a new process measure to assess treatment fidelity and
predict outcome. British Journal of Clinical Psychology, 46, 253–272.
Goodwin, L., White, P. D., Hotopf, M., Stansfield, S. A., & Clark, C. (2011). Psychopathology
and physical activity as predictors of chronic fatigue syndrome in the 1958 British birth
cohort: A replication study of the 1946 and 1970 birth cohorts. Annals of Epidemiology,
21, 343–350.
Harvey, S. B., Wadsworth, M., Wessely, S., & Hotopf, M. (2008a). The relationship between
prior psychiatric disorder and chronic fatigue: Evidence from a national birth cohort study.
Harvey, S. B., Wadsworth, M., Wessely, S., & Hotopf, M. (2008b). Etiology of chronic fatigue
syndrome: Testing popular hypotheses using a national birth cohort study. Psychosomatic
Medicine, 70, 488–495.
Hatcher, S., & House, A. (2003). Life events, difficulties and dilemmas in the onset of chronic
fatigue syndrome: A case–control study. Psychological Medicine, 33, 1185–1192.
Heim, C., Nater, U. M., Maloney, E., Boneva, R., Jones, J. F., & Reeves, W. C. (2009).
Childhood trauma and risk for chronic fatigue syndrome. Archives of General Psychiatry,
66, 72–78.
Heim, C., Wagner, D., Maloney, E., Papanicolaou, D. A., Solomon, L., Jones, J. F., … Reeves,
W. C. (2006). Early adverse experience and risk for chronic fatigue syndrome. Archives of
Kato, K., Sullivan, P. F., Evengard, B., & Pedersen, N. L. (2006). Premorbid predictors of
chronic fatigue. Archives of General Psychiatry, 63, 1267–1272.
Kempke, S., Van Houdenhove, B., Luyten, P., Goossens, L., Bekaert, P., & Van Wambeke,
P. (2011). Unraveling the role of perfectionism in chronic fatigue syndrome: Is there
a distinction between adaptive and maladaptive perfectionism? Psychiatry Research, 186,
373–377.
Kirmayer, L. J. (1990). Resistance, reactance and reluctance to change: A cognitive attributional
approach to strategic interventions. Journal of Cognitive Psychotherapy, 4, 83–104.
Laurenceau, J-P., Hayes, A. M., & Feldman, G. C. (2007). Some methodological and statistical
issues in the study of change processes in psychotherapy. Clinical Psychology Review, 27 ,
682–695.
Luyten, P., Kempke, S., Van Wambeke, P., Claes, S., Blatt, S. J., & Van Houdenhove, B.
(2011). Self-critical perfectionism, stress generation, and stress sensitivity in patients with
chronic fatigue syndrome: Relationship with severity of depression. Psychiatry, 74, 21–30.
McCracken, L. M. (1998). Learning to live with the pain: Acceptance of pain predicts
adjustments in persons with chronic pain. Pain, 74, 21–27.
McCracken, L. M., Carson, J. W., Eccleston, C., & Keefe, F. J. (2004). Acceptance and change
in the context of chronic pain. Pain, 109, 4–7.
Morin, C. M., & Espie, C. (2003). Insomnia: A clinician’s guide to assessment and treatment.
New York, NY: Springer.
Moss-Morris, R., Sharon, C., Tobin, R., & Baldi, J. C. (2005). A randomised controlled
graded exercise trial for chronic fatigue syndrome: Outcomes and mechanisms of change.
Journal of Health Psychology, 10, 245–259.
Petrie, K., Moss-Morris, R., & Weinman, J. (1995). Catastrophic beliefs and their implications
in chronic fatigue syndrome. Journal of Psychosomatic Research, 39, 31–37.
Price, J. R., Mitchell, E., Tidy, E., & Hunot, V. (2008). Cognitive behaviour therapy for
chronic fatigue syndrome in adults. Cochrane Database of Systematic Reviews, CD001027.
Reid, S., Chalder, T., Cleare, A., Hotopf, M., & Wessely, S. (2004). Chronic fatigue syndrome.
Clinical Evidence, 11, 1–3.
Rimes, K. A., & Chalder, T. (2005). Treatments for chronic fatigue syndrome. Occupational
Sharpe, M., Arcard, L. C., Banatvala, J. E., Borysiewicz, L. K., Clare, A. W., David, A., … Lane,
R. J. (1991). A report—Chronic fatigue syndrome: Guidelines for research. Journal of
the Royal Society of Medicine, 84, 118–121.
Surawy, C., Hackmann, A., Hawton, K., & Sharpe, M. (1995). Chronic fatigue syndrome: A
cognitive approach. Behaviour Research and Therapy, 33, 535–544.
Van Damme, S., Crombez, G., Van Houdenhove, B., Mariman, A., & Michielsen, W. (2006).
Well-being in patients with chronic fatigue syndrome: The role of acceptance. Journal of
Van Houdenhove, B., Neerinckx, E., Onghena, P., Vingerhoets, A., Lysens, A., Lysens, R.,
& Vertommen, H. (2002). Daily hassles reported by chronic fatigue syndrome and
fibromyalgia patients in tertiary care: A controlled quantitative and qualitative study.
Psychotherapy and Psychosomatics, 71, 207–213.
Viner, R. H., & Hotopf, M. (2004). Childhood predictors of self-reported chronic fatigue syn-
drome/myalgic encephalomyelitis in adults: National birth cohort study. British Medical
Journal, 329, 941–945.
Wessely, S. (1995). The epidemiology of chronic fatigue syndrome. Epidemiological Reviews,
17 , 139–151.
Wessely, S., Chalder, T., Hirsch, S., Wallace, P., & Wright, D. (1997). The prevalence and
morbidity of chronic fatigue and chronic fatigue syndrome: A prospective primary care
study. American Journal of Public Health, 87 , 1449–1454.
Wessely, S., Hotopf, M., & Sharpe, M. (1998). Chronic fatigue and its syndromes. New York,
White, P. D., Goldsmith, K., Johnson, A. L., Chalder, T., & Sharpe, M. (2013). Recovery from
chronic fatigue syndrome after treatments given in the PACE trial. Psychological Medicine.
doi:10.1017/S0033291713000020
White, P. D., Goldsmith, K. A., Johnson, A. L., Potts, L., Walwyn, R., DeCesare, J. C., …
on behalf of the PACE Trial Management Group (2011). Comparison of adaptive pacing
therapy, cognitive behaviour therapy, graded exercise therapy, and specialist medical care
for chronic fatigue syndrome (PACE): A randomised trial. Lancet, 377 , 823–836.
White, C., & Schweitzer, R. (2000). The role of personality in the development and perpetua-
tion of chronic fatigue syndrome. Journal of Psychosomatic Research, 48, 515–524.
Wiborg, J. F., Knoop, H., Prins, J. B., & Bleijenberg, G. (2011). Does a decrease in avoidance
behavior and focusing on fatigue mediate the effect of cognitive behavior therapy for
chronic fatigue syndrome? Journal of Psychosomatic Research, 70, 306–10.
24
Insomnia
Allison G. Harvey and Lauren D. Asarnow
University of California, Berkeley, United States
Humans spend approximately one-third of their lives sleeping. Although the study of
human sleep is a relatively young science and many fascinating mysteries remain to
be solved, there have been rapid advances in knowledge on the function of sleep, the
consequences of inadequate sleep (for cognition, mood, and health), sleep disorders,
and treatments for sleep disorders. Sleep disorders are a major public health problem
and there are insufficient numbers of professionals equipped to deliver the powerful
evidence-based treatments available. Hence, there is growing need for the budding
science of dissemination to be applied in this area. The present chapter provides a
brief overview of the basics of sleep and relevant theory before moving on to discuss
the most prevalent sleep disorder—insomnia—in terms of diagnosis, assessment, case
formation, and treatment.
Sleep Basics
Human sleep can be divided into (a) non-rapid eye movement (NREM) sleep that
can be subdivided into four stages (Stages 1, 2, 3, and 4) through which sleep
progressively deepens and (b) rapid eye movement (REM) sleep. Stage 1 and 2
sleep improves the ability to learn. Stage 3 and 4 sleep is important for growth,
repair, metabolic regulation and immunity, and solidifying memories. REM sleep is
important for learning and unlearning information, memory consolidation, emotional
processing, and mood/emotion regulation.
It is well established that sleep deprivation has detrimental effects on multiple
domains. There is robust evidence that sleep deprivation undermines emotion regula-
tion the following day (Yoo, Gujar, Hu, Jolesz, & Walker, 2007). Adverse and severe
effects of sleep deprivation on cognitive functioning have been clearly demonstrated

DOI: 10.1002/9781118528563.wbcbt24
(e.g., Van Dongen, Maislin, Mullington, & Dinges, 2003). Sleep deprivation increases
appetite, weight gain, and insulin tolerance (Spiegel, Tasali, Penev, & Van Cauter,
2004). Indeed, in a recent meta-analysis involving 30 studies (12 in children) and
634,511 participants, an association between short sleep and obesity was observed
across the lifespan (Cappuccio et al., 2008). There is accruing evidence that sleep
disturbance and sleep loss signal increased risk for suicidality (see Bernert & Joiner,
2007, for a review). Given these important functions, disorders of sleep have major
public health implications.
Sleep need varies across ages. The National Sleep Foundation recommends 12–18
hours for newborns (0–2 months), 14–15 hours for infants (3–11 months), 12–14
hours for toddlers (1–3 years), 11–13 hours for preschoolers (3–5 years), 10–11
hours for school-aged children (5–10 years), 8.5–9.25 hours for teens (10–17 years),
and 7–9 hours for adults.
Two processes govern the sleep–wake cycle (Borbely & Wirz-Justice, 1982). The
first is the circadian process, which arises from the endogenous pacemaker in the
suprachiasmatic nuclei (SCN). At the molecular level, intrinsically rhythmic cells
within the SCN generate rhythmicity via an autoregulatory transcription–translation
feedback loop regulating expression of circadian genes. The process by which the
pacemaker is set to a 24-hour period and kept in appropriate phase with seasonally
shifting day length is called entrainment, which occurs via zeitgebers. The primary
zeitgeber is the daily alteration of light and dark. Hence, behavioral interventions
for sleep disorders can incorporate timed light exposure (Wirz-Justice, Benedetti,
& Terman, 2009), as discussed later. The SCN is also responsive to non-photic
cues such as arousal/locomotor activity, social cues, feeding, sleep deprivation, and
temperature (Mistlberger, Antle, Glass, & Miller, 2000). Hence, interventions for
sleep problems can take advantage of powerful non-photic cues such as meal times
and exercise, as described in interpersonal and social rhythm therapy (Frank, 2005),
also discussed later.
The second process governing the sleep–wake cycle is the homeostatic process.
This process regulates the duration and structure of sleep based on prior sleep and
wakefulness. Specifically, sleep pressure increases during wake and dissipates during
sleep. Sleep homeostasis influences sleep propensity; that is, sleep homeostasis results
in an increased tendency to sleep when a person has been sleep-deprived, and a
decreased tendency to sleep after having had a substantial amount of sleep. Cognitive
behavioral therapy for insomnia (CBT-I) includes methods to increase homeostatic
drive to sleep via short-term sleep deprivation. This chapter describes CBT-I in
detail.
Insomnia
In this chapter we focus on insomnia, as it is the most common sleep disorder. Insom-
nia is a chronic difficulty getting to sleep, maintaining sleep, or waking in the morning
not feeling restored. It is a prevalent problem, reported by approximately 10% of
the population (Ohayon, 2002). The consequences are severe and include func-
tional impairment, work absenteeism, impaired concentration and memory, increased
Insomnia 543
use of medical services and increased risk of accident, health problems, and the
development of psychiatric disorders (Kyle, Morgan, & Colin, 2010; Riemann &
Voderholzer, 2003). Not surprisingly given the prevalence and associated impair-
ments, the cost to society is enormous (Daley, Morin, LeBlanc, Gregoire, & Savard,
2009).
Diagnostic Criteria
There are three classification systems for sleep disorders; the International Classifica-
tion of Sleep Disorders (2nd ed.; ICSD-2; American Academy of Sleep Medicine, 2005),
the Research Diagnostic Criteria (RDC; Edinger et al., 2004), and the Diagnostic
and Statistical Manual of Mental Disorders (5th ed., DSM-5; American Psychiatric
Association, 2013). Here we focus on the RDC criteria because these were derived
via a thorough published literature review conducted by a workgroup commissioned
by the American Academy of Sleep Medicine.
According to the RDC, a diagnosis of insomnia disorder may be given when there is
a subjective complaint of trouble falling asleep, staying asleep, or obtaining restorative
sleep. Additionally, these difficulties must be associated with daytime impairment,
and must occur despite the allowance of adequate time periods and circumstances for
sleep. The RDC defines a diagnosis of primary insomnia as persisting for one month
and is independent from and not better accounted for by any psychiatric diagnosis,
another primary sleep disorder (e.g., parasomnia or narcolepsy), substance use or
withdrawal from psychiatric medications, or a general medical condition. A number
of subtypes are also defined.
Epidemiology
Children. Up to 30% of primary school-aged children experience symptoms of
insomnia (Gregory & O’Connor, 2002) such as difficulties initiating and, to a lesser
extent, maintaining sleep, as well as behavioral difficulties including bedtime resistance
and reluctance/refusal to sleep alone (Gregory, Cox, Crawford, Holland, & Harvey,
2009). The only pediatric insomnia disorder covered in the ICSD-2 is behavioral
insomnia of childhood. Behavioral insomnia is a sleep disorder in which school-aged
children typically require parental presence in order to fall asleep. In addition to
decrements in physical health (Cappuccio et al., 2008), inadequate or disturbed sleep
in childhood forecasts the later development of anxiety and depression (Gregory et al.,
2005).
Teens. The rapid body and brain development associated with the onset of, and
progression through, puberty is associated with greater sleep need (Carskadon,
Acebo, & Jenni, 2004). Moreover, a key feature of sleep, preceding and during the
adolescent years, can be the delay in circadian phase and corresponding delay in sleep
onset, often shifting past midnight to the early morning hours (Carskadon, 2002).
This effect may be attributable to a number of influences, which include a tendency
toward increasing autonomy in deciding what time to go to bed, which coincides
with both a natural biological delay in the circadian cycle and irregularity in the
sleep schedule associated with psychosocial stress and social activities (Carskadon,
2002). This tendency toward a delayed circadian phase, combined with early school
start times (Carskadon, Wolfson, Acebo, Tzischinsky, & Seifer, 1998) and paid work
responsibilities, means that adolescents often do not obtain sufficient sleep. Indeed,
many studies indicate an epidemic of sleep deprivation in youth (Gibson et al.,
2006). Sleep deprivation of varying severity is reported by 10–40% of high school
youth (Carskadon, 1999); 12.4% of youth report insomnia symptoms nearly every
day of the past month, with higher rates for girls and youth of lower socioeconomic
status (Roberts, Lee, Hemandez, & Solari, 2004). Lifetime prevalence of DSM-IV
defined insomnia through age 18 has been reported as 10.7%, with an increased risk
among postpubertal girls (Johnson, Roth, Schultz, & Breslau, 2006). Youth DSM-IV
insomnia has 30-day prevalence of 4.7% (Roberts, Roberts, & Chan, 2006) and point
prevalence of 4.0% (Ohayon, Roberts, Zulley, Smirme, & Priest, 2000). Insomnia is
even higher (>70%) among depressed youth (Liu et al., 2007).
Adults. About 6% of the general adult population meets diagnostic criteria for a
formal diagnosis of insomnia. Approximately one-third of the general population
reports some significant symptoms of insomnia (Morin, LeBlanc, Daley, Gregoire,
& Merette, 2006; Ohayon, 2002). The rate of insomnia is higher among older
adults. Insomnia in older adults is often accompanied by medical illnesses, which
may complicate issues of assessment and treatment, further compounding burden and
cost.
Comorbidity. In a large epidemiological study, Ford and Kamerow (1989) found that
there is approximately a 50% comorbidity rate between insomnia and other psychiatric
or medical illnesses. More recent studies have yielded a rate as high as 75% (Lichstein,
2000). In cases of comorbid insomnia, additional empirical and clinical attention may
be especially important as there appears to be a bidirectional relationship whereby
worsening sleep problems lead to a decline in general health as well as the maintenance
of daytime distress and mood symptoms. Then daytime distress and mood symptoms
worsen the sleep problems the next night (Harvey, 2008). Hence, a very important
recent shift in the field was documented as part of the National Institutes of Health
(NIH) State of the Science Conference (NIH, 2005). It was concluded that the term
“secondary” insomnia should be replaced with the term “comorbid insomnia” on the
basis of accumulating evidence that insomnia that is comorbid with another disorder
likely contributes to the maintenance of that disorder (Harvey, 2001; Smith, Huang,
& Manber, 2005).
Theory to Guide Treatment
We begin this section by discussing an influential overarching framework, the Spiel-

man model. We then move on to describe a sample of the behavioral, cognitive,
hyperarousal, neurocognitive, and hybrid models of insomnia, selecting those models
that help guide the delivery of psychosocial interventions for insomnia.
Insomnia 545
Three-Factor Model
This is a diathesis–stress model that is often referred to as the three-factor model
or the three-P model. According to Spielman, Caruso, and Glovinsky (1987), acute
or short-term insomnia occurs as a result of predisposing factors (e.g., traits) and
precipitating factors (e.g., life stressors). This acute form can then develop into
a chronic or longer-term disorder as a result of perpetuating factors (e.g., poor
coping strategies). Predisposing factors (such as a tendency to worry) constitute a
vulnerability for insomnia, and this vulnerability remains across the life of the disorder.
Precipitating factors trigger acute insomnia, but their influence tends to wane over
time. In contrast, perpetuating factors take hold and serve to maintain insomnia.
Behavioral Model: Stimulus Control Model

The most important behavioral model is the stimulus control model (Bootzin, 1972).
It is based on the conditioning principle that insomnia occurs when the bed or
bedroom ceases to be paired specifically with sleep, but has become paired with many
possible responses (e.g., being awake and anxious about not sleeping). As will become
evident later in this chapter, this theory has led to the development of an intervention
with strong efficacy.
Cognitive Model
One cognitive model of insomnia aims to specify the cognitive processes that serve to
perpetuate insomnia (Harvey, 2002). According to this conceptualization, insomnia
is maintained by a cascade of cognitive processes that operate at night and during
the day. The equal emphasis on the nighttime and daytime processes is an important
feature of this model. The key cognitive processes that comprise the cascade are (a)
worry and rumination, (b) selective attention and monitoring, (c) misperception of
sleep and daytime deficits, (d) dysfunctional beliefs about sleep (based on Morin,
1993), and (e) counterproductive safety behaviors that serve to maintain beliefs.
Many of the specific predictions generated by this model have been empirically tested,
leading to refinement of the model (Harvey, 2005) and a new cognitive therapy
treatment approach that has preliminary support in an open trial (Harvey, Sharpley,
Ree, Stinson, & Clark, 2007).
Hyperarousal Models
The hypothesis that physiological hyperarousal serves to perpetuate insomnia has
attracted interest for several decades, since the classic work of Monroe (1967) in
which significantly increased physiological activation (increased rectal temperature,
heart rate, basal skin resistance, and aphasic vasoconstrictions) was found 30 minutes
before and during sleep in persons with insomnia, as compared to good sleepers.
More recently, in a series of elegant studies, Bonnet and Arand (1992) experimentally
induced a chronic physiological activation via caffeine intake in good sleepers. The caf-
feine resulted in decreased sleep efficiency and increased daytime fatigue. In addition,
Bonnet and Arand (1995) measured whole body VO2 , which was conceptualized
as an index of hyperarousal, at intervals across the day and during sleep. VO2 was
consistently elevated at all measurement points in individuals with insomnia, relative
to the good sleepers. The authors concluded that the 24-hour increase in metabolic
rate observed may be an important maintainer of insomnia.
Neurocognitive Model
The neurocognitive model (Perlis, Giles, Mendelson, Bootzin, & Wyatt, 1997; Perlis,
Merica, Smith, & Giles, 2001) extends the behavioral model by explicitly allowing for
the possibility that conditioned arousal may act as a perpetuating factor. The concept
of arousal is expressed in terms of somatic, cognitive, and cortical arousal.
Somatic arousal corresponds to measures of metabolic rate, cognitive arousal
typically refers to mental constructs like worry and rumination, and cortical arousal
refers to the level of cortical activation (but may also include all of central nervous
system arousal). Cortical arousal, it is hypothesized, occurs as a result of classical
conditioning and allows for abnormal levels of sensory and information processing,
and long-term memory formation. These phenomena, in turn, are directly linked to
sleep continuity disturbance and/or sleep state misperception. Specifically, enhanced
sensory processing (detection of stimuli and potentially the emission of a startle and/or
orienting responses) around sleep onset and during NREM sleep is thought to make
the individual particularly vulnerable to perturbation by environmental stimuli (e.g.,
a noise outside on the street), which in turn interferes with sleep initiation and/or
maintenance. Enhanced information processing (detection of, and discrimination
between, stimuli and the formation of a short-term memory of the stimulating event)
during NREM sleep may blur the phenomenologic distinction between sleep and
wakefulness. That is, one cue for “knowing” that one is asleep is the lack of awareness
of events occurring during sleep. Enhanced information processing may therefore
account for the tendency in insomnia to judge polysomnography-defined sleep as
wakefulness.
Finally, enhanced long-term memory (detection of, and discrimination between,
stimuli and recollection of a stimulating event hours after its occurrence) around sleep
onset and during NREM sleep may interfere with the subjective experience of sleep
initiation and duration. Normally, individuals cannot recall information from periods
immediately prior to sleep, during sleep, or during brief arousals from sleep. An
enhanced ability to encode and retrieve information in insomnia would be expected
to influence judgments about sleep latency, wakefulness after sleep onset, and sleep
duration.
Hybrid Models
At least three models have been proposed that incorporate a range of levels of
explanation (e.g., behavioral, physiological) and across various points of the disorder
(e.g., precipitating factors, perpetuating factors). These will now be described.
Morin’s (1993) cognitive behavioral model of insomnia incorporates cognitive,
temporal, and environmental variables as both precipitating and perpetuating factors.
Insomnia 547
Morin places hyperarousal as the key precipitating factor of insomnia. The hyperarousal
can be cognitive-affective, behavioral, or physiological. Stimulus conditioning can then
exacerbate this arousal. For example, a person may associate temporal (e.g., bedtime
routines) and environmental (e.g., bedroom) stimuli with fear of being unable to
sleep. Worry and rumination may then result. Additional perpetuating factors may
ensue, including, as in the cognitive model, daytime fatigue, worry and emotional
distress about sleep loss, and maladaptive habits (e.g., excessive time in bed). Thus,
hyperarousal may serve as a trigger, but a multitude of factors perpetuate the negative
cycle. However, the consequences of sleeplessness can also serve as a trigger for the
cycle.
Lundh’s (1998) cognitive behavioral model of insomnia also considers cognitive
and physiological arousal, as well as stressful life events, as factors. However, Lundh’s
model proposes sleep interpreting processes as additional factors. Sleep interpreting
processes are thoughts about sleep, including perceptions about sleep onset latency,
total sleep time, and sleep quality; thoughts about sleep quantity requirements and the
consequences of not meeting these requirements; how variations in sleep quality are
explained; and the degree to which negative aspects of daily functioning are attributed
to poor sleep. Thus, a central tenet of this model is that individuals’ cognitions and
perceptions about their poor sleep and their consequent daytime functioning play key
roles in maintaining insomnia.
Espie’s (2002) psychobiological inhibition model posits that insomnia is a disorder
of the automaticity of homeostatic and circadian processes. That is, in good sleepers,
these two processes naturally default to good sleep and can adjust to some variability,
but in persons with insomnia, the central problem is with inhibition of dearousal
processes critical to good sleep. The attention–intention–effort pathway (Espie,
Broomfield, MacMahon, Macphee, & Taylor, 2006) extends this model by providing
an explanation for how insomnia develops and what critical factors maintain it.
More specifically, this pathway suggests that sleep–wake automaticity is inhibited by
selectively attending to sleep, by explicitly intending to sleep, and by introducing
effort into the sleep engagement process.
The impact of the environment on insomnia is an understudied area. The interpersonal
context of sleep is an important contributor to insomnia; bed partners can interfere
with each other’s sleep, whether by snoring sounds, movement, or out of sync
bedtimes; noisy or otherwise uncomfortable environments could also create sleep
disturbance; and unsafe bedroom environments likely result in hypervigilance (Troxel
et al., 2010; Troxel, Robles, Hall, & Buysse, 2007).
Also, increased technology use and busier schedules may have an effect on insomnia.
Technology options (television, movies, video games, Internet, music, cell phones,
and text-messaging) and busier schedules (increased homework, part-time employ-
ment, and increased time spent on sports and other extracurricular activities) surely
contribute to the bright light and arousing conditions that are not conducive to
sleep.
Assessment and Formulation of Insomnia
The assessment of insomnia varies depending on whether it is being done in a

clinical or research context. As the latter has already been well articulated (Buysse,
Ancoli-Israel, Edinger, Lichstein, & Morin, 2006), this next section will focus on the
assessment of insomnia for clinical purposes.
Subjective Estimates
As evident from the RDC criteria, insomnia is defined subjectively. As such, three
levels of self-reported sleep data are collected from patients during an assessment for
insomnia. First, a clinical sleep history is taken to assess for the diagnostic criteria and
the presence of comorbid psychiatric and medical problems. It can be valuable to take
a “wide lens” as well as a “focused lens” approach to the assessment of the current
sleep schedule. The wide lens approach is a broad overview and involves asking the
patient retrospectively to recall his or her sleep before it became a problem. Typically
the focus is on the past week or the past month. The focused lens approach focuses
more specifically on a particular typical night of insomnia.
The broad overview starts by determining which of the following is the patient’s
predominant complaint: not enough sleep, trouble falling asleep, difficulty staying
asleep, early morning awakening, light or nonrefreshing sleep, inability to sleep
without sleeping pills, or sleep that is unpredictable. Then there is a move to more
specificity by obtaining information about the frequency of nights of insomnia and
the night-to-night variability (Spielman & Anderson, 1999). Other topics to work
through systematically are: the time the patient retires to bed (many patients go to bed
very early in an attempt to maximize the amount of sleep they obtain), the activities
engaged in once in bed, time of lights out (including how the decision to turn the
lights out is made), sleep onset latency (the difference between the time of lights out
and the time of falling asleep), awakenings (the number, timing, and duration; the
experience of awakenings, particularly any distress experienced and how the patient
copes), wake-up time (which can be determined by environmental disturbances, and
can be variable or unvarying which is suggestive of a circadian component to the
insomnia), out of bed time (does the patient linger in bed and occasionally fall back
to sleep? If so, this is suggestive of poor sleep hygiene), and total sleep time (does it
vary on the weekdays versus the weekends? If so, this gives a clue that work stress may
be contributing or that circadian factors such as a delayed sleep phase may need to be
considered) (Spielman & Anderson, 1999). In addition, an appreciation of what sleep
and daytime functioning were like before the onset of the sleep problem provides a
comparison for assessing response to treatment.
The more focused lens approach involves a detailed functional analysis of a typical
recent night. The goal is to build up a picture of how various emotional, behavioral,
and cognitive processes are linked to, and feed into, each other (Harvey, 2006). It
essentially involves a detailed discussion of a recent, specific, typical night of poor
sleep. A very specific episode is a situation that happened on one particular day (e.g.,
last Monday) and at a particular time (e.g., while trying to get to sleep). Focusing
Insomnia 549
on this night, a few minutes should be spent asking questions to start to get an
idea of the contexts (e.g., “How was your day?,” “What had you been doing in the
evening?”). These questions help to determine antecedents or events that might have
had a bearing on the insomnia experienced that night (e.g., conflict with a spouse, a
late exercise session). Then a very detailed description should be obtained of exactly
what happened and the consequences of it. By working through the events, and
corresponding thoughts, feelings, and behaviors across one night, a vicious cycle is
drawn out, demonstrating their contribution to the insomnia (Harvey, 2006).
Second, one or more validated questionnaire measures can be used to index the
presence and severity of sleep disturbance (e.g., Pittsburgh Sleep Quality Index;
Buysse, Reynolds, Monk, Berman, & Kupfer, 1989), insomnia (e.g., Insomnia
Severity Index; Bastien, Vallieres, & Morin, 2001), and daytime sleepiness (e.g.,
Stanford Sleepiness Scale; Hoddes, Zarcone, Smythe, Phillips, & Dement, 1973).
Third, the patient can be asked to complete a sleep diary each morning as soon
as possible after waking for 2 weeks to provide prospective estimates of sleep. A
standardized and recommended sleep diary has been published (Carney et al., 2012).
A sleep diary provides a wealth of information including night-to-night variability in
sleeping difficulty and sleep–wake patterns and can be used to determine the presence
of circadian rhythm problems, such as a delayed sleep phase or an advance sleep phase.
Also, sleep diaries reduce several problems associated with the methods just discussed
that rely on retrospective report, such as answering on the basis of saliency (i.e., the
worst night) or recency (i.e., the previous night) (Smith, Nowakowski, Soeffing, Orff,
& Perlis, 2003). Interestingly, the “enhanced awareness” of sleep patterns facilitated
by diary keeping can reduce anxiety over sleep loss and thus contribute to better sleep
(Morin, 1993, p. 71).
Objective Estimates
The gold standard measure of sleep is polysomnography (PSG). PSG is used to classify
sleep into the aforementioned stages. It involves placing surface electrodes on the
scalp and face to measure electrical brain activity (electroencephalogram, EEG), eye
movement (electro-oculogram, EOG), and muscle tone (electromyogram, EMG).
The data obtained are used to classify each epoch of data by sleep stage and in terms
of sleep cycles (NREM and REM). Disadvantages associated with PSG include its
expense, discomfort for participants, and labor-intensive nature. Although PSG is
not needed for the routine assessment of insomnia, it is important if the patient is
suspected of having a comorbid sleep disorder such as sleep apnea or periodic limb
movement disorder (Chesson et al., 2004) or if treatment is not effective.
Actigraphy is an alternative means of providing an objective estimate of sleep.
Actigraphs are small, wrist-worn devices, within which are located a sensor, a processor,
and memory storage. The sensor samples physical motion; the processor translates
it into numerical digital data, summarizing the frequency of motions into epochs
of specified time duration and storing the summary in memory. These data are
then downloaded to a computer and analyzed to generate various sleep parameters
(but cannot differentiate stages of sleep). Because the body becomes more quiescent
during sleep, actigraphy can be used to differentiate between periods of wakefulness
and periods of sleep. In fact, the correlation between actigraphy- and PSG-defined
estimates of total sleep time is quite strong, ranging from 0.88 to 0.97 in adult
nonpatients (Jean-Louis et al., 1997). Although actigraphy is not required for the
assessment of insomnia, it provides an overview of the sleep–wake cycle in a way that
is minimally intrusive.
Interventions
A number of treatments are available to address insomnia. As most of the research

to date has focused on cognitive behavioral therapy for insomnia (CBT-I), this will
also be our focus. We note that there are several very helpful “how to do CBT-I”
manuals (e.g., Morin & Espie, 2003; Perlis, Aloia, & Kuhn, 2011; Perlis & Lichstein,
2003). Adaptations for other populations, including children (Gradisar et al., 2011)
and adolescents (Clarke & Harvey, 2012; Dahl & Harvey, 2007), are also available.
Cognitive Behavioral Therapy for Insomnia

The primary goal of CBT-I is to address the cognitive and behavioral maintaining
mechanisms involved in perpetuating sleep disturbance. A second important goal
is to teach coping techniques that patients can use in instances of residual sleep
difficulty. CBT-I is currently considered the treatment of choice for insomnia. It is a
multicomponent treatment that is typically comprised of one or more of the following
components: stimulus control, sleep restriction, sleep hygiene, paradoxical intention,
relaxation therapy, imagery training, and cognitive restructuring for unhelpful beliefs
about sleep. Each of these components will now be described.
Stimulus control. The rationale for stimulus control therapy lies in the notion that
insomnia is a result of conditioning that occurs when the bed becomes associated
with inability to sleep. As described by Bootzin, Epstein, and Wood (1991), stimulus
control requires patients to (a) use the bed only for sleep (i.e., no watching television
or talking on cell phones), (b) go to bed only when sleepy, (c) get out of bed and go
to another room when unable to fall asleep or return to sleep within approximately
15–20 minutes, and return to bed only when sleepy again, and (d) arise in the
morning at the same time each day (no more than 2 hours later on weekends)
(Bootzin & Stevens, 2005). The goal is gradually to move toward a regular schedule
7 days a week. It is very clear that as a stand-alone intervention, stimulus control is
an effective treatment (Morin et al., 2006), although it is easy to combine with sleep
restriction and deliver the two together.
Sleep restriction. Sleep restriction therapy, as developed by Spielman, Saskin, and

Thorpy (1987), rests on the general premise that time in bed should be limited to
maximize the sleep drive and so that the association between the bed and sleeping is
strengthened. This behavioral treatment begins with a reduction of time spent in bed
so that time in bed is equivalent to the time the patient estimates he or she spends
sleeping. Thus, for instance, if an individual thinks he or she gets approximately
Insomnia 551
6 hours of sleep per night, but usually spends about 2 additional hours trying to
get to sleep, the sleep restriction therapy would begin by limiting his or her time
spent in bed to 6 hours. This initial reduction in time spent in bed is intended to
heighten a person’s homeostatic sleep drive (Perlis & Lichstein, 2003). Following this
restriction, sleep gradually becomes more efficient, at which point time spent in bed
is gradually increased to reach an optimal sleep efficiency. Sleep efficiency is defined as
total sleep time divided by time in bed multiplied by 100. The goal is to increase sleep
efficiency to more than 85–90%. It is very clear that as a stand-alone intervention,
sleep restriction is an effective treatment (Morin, Bootzin, et al., 2006).
Sleep hygiene. Information about sleep, sleep-incompatible behaviors, and the daytime
consequences of sleep disturbance is often given to inform patients of the basic steps
that they can take to improve their sleep. Although sleep hygiene education is
typically included as one component of CBT-I, its use as the sole intervention in
treating insomnia has not been empirically supported (Morin, Bootzin, et al., 2006).
Paradoxical intention. In paradoxical intention, patients are instructed to stay awake

for as long as possible. The aim is to reduce performance anxiety related to sleep.
Paradoxical intention aims to replace the tendency to try actively to get to sleep
that is often employed by individuals struggling with insomnia. Because employing
an active focus and strategy to induce sleep is actually generally sleep-incompatible
(Espie, 2002), paradoxical intention places patients in the role of passive observer,
thereby decreasing anxiety and increasing the likelihood of sleep onset.
Relaxation therapy. Patients are taught to implement a variety of exercises while in

the therapy session. They are then encouraged to practice these exercises as much as
they can between sessions, but the emphasis is on practice during the day (as opposed
to using them only at night as an effort to get to sleep). Practice is essential and is
often aided by making a tape of the relaxation instructions that the patient can use at
home.
Cognitive restructuring/therapy. The formal cognitive therapy component of CBT-I,

often administered in one session, involves altering faulty beliefs about sleep by
education and discussion about sleep requirements, the biological clock, and the
effects of sleep loss on sleep–wake functions (e.g., Edinger, Wohlgemuth, Radtke,
Marsh, & Quillian, 2001). This approach is distinct to the intervention we referred
to earlier in which the entire treatment is focused on reversing cognitive maintaining
processes (e.g., Harvey, 2005). An empirical question that remains to be answered
is whether combining CBT-I and the cognitive therapy intervention will improve
overall outcome.
Evidence for components of cognitive behavioral therapy for insomnia. A number of

randomized controlled trials (RCTs) have compared one or more components of
CBT-I to each other and/or to placebo. In a recent review of CBT-I, the Standards
of Practice Committee of the American Academy of Sleep Medicine found CBT-I
to be highly effective and to have sustainable gains over long-term follow-up up
to 24 months in adult and older adult samples (Morin, Bootzin, et al., 2006).
This review used the American Psychological Association criteria for well-supported
empirically-based treatments (Chambless & Hollon, 1998) and concluded that these
criteria are met by stimulus control, paradoxical intention, relaxation, sleep restriction
approaches, and the administration of multiple components in the form of CBT-I.
The sleep hygiene intervention alone has not been found to be effective as a treatment
for insomnia. Cognitive therapy for insomnia is a promising new approach, but RCTs
are still needed in order for it to meet American Psychological Association criteria for
an empirically supported treatment.
Implementation. Four to 10 weekly sessions of CBT-I are typically needed to admin-

ister the components chosen from those described above. These sessions have been
conducted in individual therapy, in group therapy, and with the addition of self-help
interventions.
Treatment of comorbid insomnia. Until relatively recently, it had often been assumed
that insomnia that is comorbid with another psychiatric or medical disorder could
not be successfully treated if the primary condition with which it was associated was
not treated first. While it is certainly true that cases of comorbid insomnia present
additional challenges, evidence is accumulating to suggest that insomnia does respond
to treatment when it is treated with CBT-I, even if the psychiatric or medical disorder
is not under control. Moreover, consistent with the growing evidence that insomnia
and the comorbid disorders mutually maintain each other, treating insomnia can
reduce symptoms and processes associated with the comorbid disorder. For example,
Manber et al. (2008) gave all patients an antidepressant treatment (escitalopram). Half
also received CBT-I while the other half received placebo psychotherapy for sleep. The
addition of CBT-I to the antidepressant treatment resulted in greater remission from
insomnia (50%) and a substantially higher rate of remission of depression (61.5%),
relative to a placebo psychotherapy (remission from insomnia 7.7%; remission from
depression 33.3%). These startling outcomes have encouraged researchers to treat
insomnia comorbid with a range of other medical and psychiatric conditions, including
cancer, HIV, posttraumatic stress disorder, and bipolar disorder.
Psychological versus Pharmacological Interventions

It is important to conduct a thorough efficacy and cost–benefit analysis for the
different available treatment options in order to determine the best course of action
in addressing insomnia. Primarily, a choice between CBT-I, pharmacology, or a
combination of the two must be made. There are a range of reasons that focusing on
nonpharmacologic interventions may be preferable in certain circumstances:
1. The ideal intervention for sleep disturbance in patients who are taking medica-
tions for other psychiatric or medical conditions is one that alleviates the sleep
disturbance without causing adverse interactions with the prescribed medication
and without causing adverse side effects. Nonpharmacologic interventions meet
those criteria.
Insomnia 553
2. There is evidence that nonpharmacologic interventions for insomnia are more

acceptable to patients than medication treatments (Morin, Gaulier, Barry, &
Kowatch, 1992; Vincent & Lionberg, 2001).
3. The leading nonpharmacologic treatment for insomnia, CBT-I, produces more
durable effects, relative to hypnotic medications (Jacobs, Pace-Schott, Stickgold,
& Otto, 2004; Morin, Colecchi, Stone, Sood, & Brink, 1999b; Sivertsen et al.,
2006).
4. If a patient is at risk of substance use problems (Grant et al., 2004; Levin &
Hennessy, 2004), the prescription of certain classes of medications to treat sleep
disturbance may increase risk.
5. Pharmacologically induced sleep may not provide the health benefits that humans
have specifically evolved to obtain from sleep (Seibt et al., 2008).
In terms of the specific sources of evidence, a meta-analysis of 21 RCTs of

CBT-I (primarily stimulus control and sleep restriction therapies) and pharmacological
(benzodiazepine receptor agonist; BzRA) treatments for primary insomnia concluded
that treatment effects for the two treatment modalities were comparable in the short
term, but CBT-I is more effective in decreasing sleep onset latency (Smith et al.,
2002). As longer-term posttreatment follow-ups are often not included in studies of
pharmacological interventions, it is not yet possible to answer questions of comparable
efficacy several months after treatment has ceased. However, a study by Sivertsen et al.
(2006) compared CBT-I, zopiclone, and placebo. The results clearly favored CBT-I,
which resulted in improved short- and long-term functioning relative to zopiclone
on three out of the four outcome measures. Moreover, for most outcomes zopiclone
was no better than placebo.
Addressing the issue of whether a combined pharmacological plus CBT-I approach
is indicated, Morin, Colecchi, et al. (1999a) compared pharmacological treatment
alone (temazepam, with an initial dosage of 7.5 mg and a maximum dosage of
30 mg per night), CBT-I alone (delivered in eight weekly sessions), temazepam
plus CBT-I (combination treatment), and placebo medication as treatments for
insomnia in older adults. All three active treatments were associated with short-
term clinical gains, while placebo was not. However, only individuals who received
CBT-I were found to sustain treatment gains over time (up to 24-month follow-
up). The combination treatment was associated with some sustained gains but more
attrition in efficacy over follow-up than in the CBT-I-alone group. Additionally,
study participants, their significant others, and their treating clinicians rated the
CBT-I to be more effective than and preferable to pharmacotherapy alone (Morin,
Colecchi, et al., 1999a). Morin, Vallieres, et al. (2009) subsequently studied the
added value of medication over CBT alone for acute treatment of insomnia and the
effects of maintenance therapies on long-term outcome in adults (mean age = 50).
CBT alone was followed by either 6 months of extended therapy or no additional
treatment, while an initial 6-month combined treatment of CBT plus 10 mg per
day of zolpidem was followed by 6 months of extended CBT plus intermittent use
of zolpidem or CBT only. Across both treatment groups, 60% of patients achieved
some treatment response and no added value was found in combining medication
with CBT, at least during the initial 6-week treatment phase. After the 6-week
treatment phase 42% were in remission and these rates increased to between 65
and 51% after 6 months of extended treatment. Patients treated with a combined
approach of CBT plus zolpidem during the initial 6-week treatment phase achieved
better long-term outcomes when zolpidem was discontinued after the initial 6-week
trial compared to those who continued taking the medication on an intermittent
schedule.
In a report of a sample of 334 adolescents aged 12 to 18 years with major
depressive disorder who had not responded to a 2-month initial treatment with a
selective serotonin reuptake inhibitor, adolescents with treatment resistant depression
who used adjunctive sleep medication were less likely to respond to treatment (Brent
et al., 2008), again pointing to the possible advantage of psychosocial treatments for
sleep problems.
Brief Overview of Other Sleep Disorders
Although a full description of other sleep disorders and their treatment is beyond
the scope of this chapter, we provide a very brief description of other major sleep
disorders here. It is important to be aware of, and assess for, the presence of these
other sleep disorders. Each of these disorders is relatively common and can have
serious consequences for the health and daytime functioning of the sufferer. For
further information on these disorders we refer the reader to Kryger, Roth, and
Dement (2005) and Perlis et al. (2011).
Circadian Rhythm Disorders

There are two main circadian rhythm disorders; advance phase or “larks” (common
among older adults) which involves falling asleep early and waking up early, and
delayed sleep phase or “owls” (common among adolescents and clients with mood
disorders) which involves not being able to fall asleep until the early hours in the
morning and sleeping well into the next day. Powerful behavioral adjustments can be
helpful for patients seeking help for these problems.
Practice parameters (Sack et al., 2007) indicate evidence for timed light exposure
(with a light box) and planned and regular sleep schedules (chronotherapy). For
clients who are not interested in using a light box we recommend using a behavioral
approach to encourage exposure to natural morning bright sun light (even when
it is cloudy) and evening dim light (including an electronic curfew). Traditional
chronotherapy for clients with very late bedtimes (“owls”), involving progressively
delaying bedtimes and waketimes until reaching the desired alignment, tends to
be highly disruptive to family and work schedules (Czeisler et al., 1981; Thorpy,
Korman, Spielman, & Glovinsky, 1988; Weitzman et al., 1981), so another approach
is to adopt a planned sleep modification protocol derived from circadian principles
involving moving bedtimes earlier by 20 to 30 minutes per week.
There is accruing evidence for the importance of light and dark therapy in the
treatment of the mood disorders. A recently published “how to” manual is highly
recommended (Wirz-Justice et al., 2009). Within this manual the accumulating
Insomnia 555
evidence base is presented. To give a couple of examples, a preliminary trial of dark

therapy was published by Barbini et al. (2005). The 16 patients with bipolar disorder
who were experiencing a manic episode lived and slept in 14 hours of darkness for
3 consecutive days (6 p.m. to 8 a.m.). Those who received dark therapy exhibited
a decrease in manic symptoms relative to the 16 patients in the treatment as usual
group. The conclusion drawn was that dark therapy can diminish manic symptoms as
rapidly as conventional antipsychotics. Bright light exposure is a well-established first
line treatment for depressions with a seasonal pattern, and has also proven effective
(although to a lesser extent) in purely nonseasonal depression (Even, Schröder,
Friedman, & Rouillon, 2008; Golden et al., 2005; Tuunainen, Kripke, & Endo,
2004).
Treating Hypersomnia
The pharmacologic treatment of hypersomnia is underresearched (Harvey & Li,
2009) and psychological treatments are in development (Kaplan & Harvey, 2009).
One tricky aspect of the treatment of hypersomnia at this point in knowledge is
to ascertain whether hypersomnia is a disorder of excessive sleep or a disorder of
excessive time in bed. If, as the literature is suggesting, many cases of hypersomnia
are a function of excessive time in bed, the treatment is likely to be focused on
setting daytime goals, adjusting the sleep–wake schedule, and planning for waking
up (see Kaplan & Harvey, 2009, for more details). In cases where hypersomnia
truly involves excessive sleep, after rule outs for disorders such as narcolepsy, CBT-I
approaches involving sleep compression, sleep education, detailed planning of wind-
down and brisk wake-up period, and regularizing the sleep–wake schedule may be
indicated.
Sleep Apnea
Transient closure of the upper airway during sleep is associated with disruption to
sleep. The nighttime symptoms can include snoring, pauses in breathing during
sleep, shortness of breath during sleep, choking during sleep, headaches on waking,
and difficulty getting breath or breathlessness on waking. The adverse outcomes
include daytime sleepiness and cardiovascular problems. Continuous positive airway
pressure (CPAP) is an effective therapy for most patients with obstructive sleep
apnea (OSA). Cognitive behavioral therapy has been used to increase adherence to
CPAP (Perlis et al., 2011). The psychoeducation approach focuses on educating
patients that the most effective treatment for OSA is CPAP and highlights the
psychiatric and health risks of untreated OSA. The modeling approach is presented
in a group setting, with other patients as well as partners and family members to
engage social support. Following an education component, a “modeling video” is
shown that presents real cases of successful CPAP usage, emphasizing the long-
term health benefits of using CPAP. Other useful interventions for CPAP adherence
include exposure therapy for claustrophobic reactions to CPAP and motivational
enhancement therapy.
Narcolepsy
This is a disorder characterized by excessive sleepiness. Episodes of short uncontrol-
lable naps during the day are typical. Often the nap is associated with cataplexy (loss
of muscle tone triggered by strong emotion), sleep paralysis, or hypnogogic hallu-
cinations. Behavioral interventions for patients with narcolepsy include regularizing
the sleep–wake schedule and scheduled naps. For example, a single 120-minute nap
may be more effective than several short naps for reduction in daytime sleepiness
symptoms (Perlis et al., 2011).
Restless Legs Syndrome and Periodic Limb Movement Disorder

Restless legs syndrome (RLS) and periodic limb movement disorder (PLMD) are
two relatively common conditions that should be assessed and, if present, referred
to a sleep specialist. The symptoms of RLS are a sensation of an urge to move the
limbs (usually the legs) and a feeling of restlessness because of sensations in the limbs
(usually the legs). The sensations start or get worse when resting, relaxing, or first
going to bed and are temporarily relieved by movement or pressure. Symptoms are
typically most severe at night and can have a profound effect on sleep quality. A
clear circadian pattern must be present. The hallmark feature of PLMD is repetitive
episodes of limb movements during sleep, usually the legs. Periodic limb movements
in sleep are repetitive movements, most typically in the lower limbs, that occur about
every 20–40 seconds. The movements are associated with a partial or full awakening.
Other Treatment Approaches
Sleep Deprivation
A startling improvement in mood has been observed in 40–60% of depressed
bipolar patients following total or partial sleep deprivation (Barbini et al., 1998). As
symptoms of depression quickly return when the patient sleeps, several approaches
are being tested in the hope of extending the therapeutic effects of sleep deprivation
by combining sleep deprivation with antidepressant medications, lithium, and light
therapy (Giedke & Schwarzler, 2002; Riemann et al., 1999; Wirz-Justice & Van
den Hoofdakker, 1999). The initial results are promising (Benedetti et al., 2001;
Benedetti et al., 2007). Intriguingly, it is increasingly widely agreed that sleep
deprivation operates via mechanisms similar to antidepressant medication, namely, by
inducing activation of serotonergic transmission (Adrien, 2002).
Social Rhythms
As already noted, exogenous factors have a powerful impact on the circadian/sleep
systems. Indeed, stronger social rhythms are associated with better subjective sleep
quality (Monk, Petrie, Hayes, & Kupfer, 1994). As these exogenous factors are
relatively easy to modify, they have become the target of a powerful psychosocial
Insomnia 557
intervention; namely, interpersonal and social rhythm therapy (Frank, 2005). This
approach is effective for bipolar disorder (Frank et al., 2005). The regularization of
daily rhythms such as meals, exercise, and social contact is likely to be a helpful part
of many interventions to improve sleep.
Meditation
Studies incorporating mindfulness skills, such as letting go, acceptance, and non-
striving, in combination with behavioral treatment for insomnia, reported significant
improvements in presleep arousal, sleep effort, and dysfunctional sleep-related cogni-
tions (Ong, Shapiro, & Manber, 2008). Interestingly, mindfulness may target specific
psychological aspects of sleep-related arousal, such as high levels of rumination and
more negative sleep-related cognitions. Mindfulness meditation represents something
of a departure from traditional cognitive therapy techniques as, rather than chal-
lenging and changing the content of one’s thoughts, one would observe and accept
one’s thoughts. Future research examining the effects of mindfulness meditation
techniques on specific contributors to presleep arousal is an exciting domain for the
future.
Summary
In this chapter we have focused on the most common sleep disorder; namely, chronic
insomnia. We have provided a description of the disorder, an overview of the various
theories of the factors that predispose an individual to developing insomnia, that
precipitate insomnia, and that perpetuate insomnia. In addition, we have included
an overview of the assessment and treatment of insomnia and a brief introduction
to other sleep disorders. Although we spend approximately one-third of our lives
sleeping, sleep is a relatively new topic of scientific study. As such, there is a myriad of
mysteries and questions about the function of sleep and sleep disorders that are yet to
be answered. The results that have emerged to date clearly place sleep as critical for
the health and well-being of humans throughout the lifespan. As such, it is a domain
that holds a large number of exciting opportunities for future research. Before closing
we wish to draw attention to three of the many interesting questions that remain to
be answered relating to chronic insomnia and the role of sleep in other psychiatric
and medical disorders.
Sleep across Development

There is clear evidence for the efficacy and effectiveness of CBT-I for both adults
and older adults. However, what about adolescents, children, toddlers, and infants?
We know that sleep varies substantially across the lifespan. In newborns, average total
sleep time is approximately 16–18 hours, organized into 3- to 4-hour sleep periods
across the 24-hour cycle. The average amount of sleep obtained by a 5-year-old
is 11.1 hours and by a 9-year-old is 10.2 hours (Hoban, 2004). In adolescence,
nighttime sleep reduces from an average of 9 hours at age 13 to 7.9 hours at age
16 (Hoban, 2004). Average nighttime sleep varies between 7 and 9 hours in young
adults and between 6 and 8 hours in the middle adult years. There are also alterations
in sleep architecture over the course of development. Newborn infants are thought
to start sleep with REM and then move into NREM, with each REM–NREM
cycle lasting about 50 minutes (Carskadon & Dement, 2005). In newborns REM
and NREM phases are called “active” and “quiet” sleep, respectively, because of
the difficulty in differentiating sleep stages at this age. Whereas newborns spend
approximately 50% of sleep in “active” sleep, once a child is 2 years of age this
percentage reduces to 20–30% of total sleep time. Between the ages of 6 and 11, the
amount of Stage 3 and 4 sleep reduces and Stage 2 sleep increases (Hoban, 2004).
Across the adolescent years, the “adult” sleep cycle length becomes established, with
Stages 3 and 4 further decreasing in length, accompanied by increases in Stage 2 sleep
(Carskadon & Dement, 2005). During the adolescent years there is a delay in circadian
phase and a corresponding delay in sleep onset, often shifting past midnight to the
early morning hours (Carskadon, 2002; Tate, Richardson, & Carskadon, 2002).
This has been attributable to a number of influences, which include a tendency
toward increasing autonomy in deciding what time to go to bed, which coincides
with both a natural biological delay in the circadian cycle with the onset of puberty
and irregularity in the sleep schedule associated with psychosocial stress and social
activities (Carskadon, 2002; Hoban, 2004). There is a small evidence base reporting
on the effectiveness of some interventions (including those described previously in
the “Circadian Rhythm Disorders” section) with children and adolescents who suffer
from sleep disturbance (Bootzin & Stevens, 2005; Owens, France, & Wiggs, 1999;
Sadeh, 2005). However, this domain has not been adequately investigated given the
scope of the problem.
Improving Treatments
There is no doubt that CBT-I is an effective treatment, as evidenced by two meta-
analyses (Morin, Culbert, & Schwartz, 1994; Murtagh & Greenwood, 1995) and a
review conducted by the Standards of Practice Committee of the American Academy
of Sleep Medicine (Chesson et al., 1999; Morin, Hauri, et al., 1999) which has
been updated (Morin, Bootzin, et al., 2006). However, the field is not as yet at a
point where patients can be offered a maximally effective psychological treatment,
as indicated by (a) the significant subset of patients who do not improve following
CBT-I (19–26%), (b) the average overall improvement being in the range of 50–60%
(Morin, Culbert, et al., 1994; Murtagh & Greenwood, 1995), and (c) the fact that
only a minority of patients reach a high end state (i.e., become good sleepers; Harvey
& Tang, 2003). Furthermore, the widely held assumption that a treatment that
addresses sleep will also effectively address the daytime consequences of insomnia,
has not yet been supported (Means, Lichstein, Epperson, & Johnson, 2000). In fact,
there is some evidence that aspects of the daytime impairment suffered by patients
with insomnia are independent of nighttime sleep (Neitzert Semler & Harvey, 2005).
Hence, treatment development efforts that improve outcome and target daytime
symptoms are an important direction for the future.
Insomnia 559
Comorbidity
Several investigators have concluded that the outcome data suggest that improvement
in sleep following CBT-I treatment has great potential to facilitate improvement in
medical and psychological symptoms of the so-called “primary” psychiatric or medical
disorder (Harvey, 2008; Smith et al., 2005). This is an exciting direction for future
exploration. Theoretically this links back to the idea, discussed earlier in this chapter,
that sleep likely has a regulatory role in mood and emotion as well as in bodily repair
and immune system functioning. Hence, sleep disturbance is likely to contribute to
the exacerbation of symptoms in psychiatric and medical disorders and treatment of
sleep disturbance may be critical for full recovery. Initial results are consistent with
these ideas in the context of depression (Manber et al., 2008), nightmares (Germain,
Shear, Hall, & Buysse, 2007), chronic pain (Currie, Wilson, & Curran, 2002), and
substance use problems (Arnedt et al., 2007).
References
Adrien, J. (2002). Neurobiological bases for the relation between sleep and depression. Sleep
Medicine Reviews, 6, 341–351.
American Academy of Sleep Medicine. (2005). International classification of sleep disorders
(ICSD): Diagnostic and coding manual (2nd ed.). Westchester, IL: Author.
Arnedt, J. T., Conrov, D., Rutt, J., Aloia, M. S., Brower, K. J., & Armitage, R. (2007). An open
trial of cognitive-behavioral treatment for insomnia comorbid with alcohol dependence.
Sleep Medicine, 8, 176–180.
Barbini, B., Benedetti, F., Colombo, C., Dotoli, D., Bernasconi, A., Cigala-Fulgosi, M., …
Smeraldi, E. (2005). Dark therapy for mania: A pilot study. Bipolar Disorders, 7 , 98–101.
Barbini, B., Colombo, C., Benedetti, F., Campori, E., Bellodi, L., & Smeraldi, E. (1998). The
unipolar-bipolar dichotomy and the response to sleep deprivation. Psychiatry Research,
79, 43–50.
Bastien, C. H., Vallieres, A., & Morin, C. M. (2001). Validation of the Insomnia Severity
Index as an outcome measure for insomnia research. Sleep Medicine, 2, 297–307.
Benedetti, F., Barbini, B., Campori, E., Fulgosi, M. C., Pontiggia, A., & Colombo, C.
(2001). Sleep phase advance and lithium to sustain the antidepressant effect of total
sleep deprivation in bipolar depression: New findings supporting the internal coincidence
model? Journal of Psychiatric Research, 35, 323–329.
Benedetti, F., Dallaspezia, S., Fulgosi, M. C., Barbini, B., Colombo, C., & Smeraldi, E. (2007).
Phase advance is an actimetric correlate of antidepressant response to sleep deprivation
and light therapy in bipolar depression. Chronobiology International, 24, 921–937.
Bernert, R. A., & Joiner, T. E. (2007). Sleep disturbances and suicide risk: A review of the
literature. Neuropsychiatric Disease and Treatment, 3, 735–743.
Bonnet, M. H., & Arand, D. L. (1992). Caffeine use as a model of acute and chronic insomnia.
Sleep, 15, 526–536.
Bonnet, M. H., & Arand, D. L. (1995). 24-hour metabolic rate in insomniacs and matched
normal sleepers. Sleep, 18, 581–588.
Bootzin, R. R. (1972). Stimulus control treatment for insomnia. Proceedings of the American
Psychological Association, 7 , 395–396.
Bootzin, R. R., Epstein, D., & Wood, J. M. (1991). Stimulus control instructions. In P. J.
Hauri (Ed.), Case studies in insomnia (pp. 19–28). New York, NY: Springer.
Bootzin, R. R., & Stevens, S. J. (2005). Adolescents, substance abuse, and the treatment of
insomnia and daytime sleepiness. Clinical Psychology Review, 25, 629–644.
Borbely, A., & Wirz-Justice, A. (1982). Sleep, sleep deprivation and depression. Human
Neurobiology, 1, 205–210.
Brent, D., Emslie, G., Clarke, G., Wagner, K. D., Asarnow, J. R., Keller, M., … Zelazny, J.
(2008). Switching to another SSRI or to venlafaxine with or without cognitive behav-
ioral therapy for adolescents with SSRI-resistant depression: The TORDIA randomized
controlled trial. Journal of the American Medical Association, 299, 901–913.
Buysse, D. J., Ancoli-Israel, S., Edinger, J., D., Lichstein, K. L., & Morin, C. M. (2006).
Recommendations for a standard research assessment of insomnia. Sleep, 29, 1155–1173.
Buysse, D. J., Reynolds, C. F., Monk, T. H., Berman, S. R., & Kupfer, D. J. (1989). The
Pittsburgh Sleep Quality Index: A new instrument for psychiatric practice and research.
Psychiatry Research, 28, 193–213.
Cappuccio, F. P., Taggart, F. M., Kandala, N. B., Currie, A., Peile, E., Stranges, S., & Miller,
M. A. (2008). Meta-analysis of short sleep duration and obesity in children and adults.
Sleep, 31, 619–626.
Carney, C. E., Buysse, D. J., Ancoli-Israel, S., Edinger, J. D., Krystal, A. D., Lichstein, K. L.,
& Morin, C. M. (2012). The Consensus Sleep Diary: Standardizing prospective sleep
self-monitoring. Sleep, 35, 287–302.
Carskadon, M. A. (1999). Adolescent sleep patterns: Biological, social, and psychological influences.
New York, NY: Cambridge University Press.
Carskadon, M. A. (2002). Factors influencing sleep patterns of adolescents. In M. A. Carskadon
(Ed.), Adolescent sleep patterns: Biological, social, and psychological influences (pp. 4–26).
New York, NY: Cambridge University Press.
Carskadon, M. A., Acebo, C., & Jenni, O. G. (2004). Regulation of adolescent sleep:
Implications for behavior. Annals of the New York Academy of Sciences, 1021, 276–291.
Carskadon, M. A., & Dement, W. C. (2005). Normal human sleep: An overview. In M. H.
Kryger, T. Roth, & W. C. Dement (Eds.), Principles and practice of sleep medicine (4th
ed., pp. 16–26). Philadelphia, PA: Elsevier.
Carskadon, M. A., Wolfson, A. R., Acebo, C., Tzischinsky, O., & Seifer, R. (1998). Adolescent
sleep patterns, circadian timing, and sleepiness at a transition to early school days. Sleep,
21, 871–881.
Chambless, D. L., & Hollon, S. D. (1998). Defining empirically supported theories. Journal
Chesson, A. L., Jr., Anderson, W. M., Littner, M., Davila, D., Hartse, K., Johnson, S., …
Rafecas, J. (1999). Practice parameters for the nonpharmacologic treatment of chronic
insomnia. An American Academy of Sleep Medicine report. Standards of Practice Com-
mittee of the American Academy of Sleep Medicine. Sleep, 22, 1128–1133.
Chesson, A., Jr., Hartse, K., Anderson, W. M., Davila, D., Johnson, S., Littner, M., … Rafecas,
J. (2000). Practice parameters for the evaluation of chronic insomnia. An American
Academy of Sleep Medicine report. Standards of Practice Committee of the American
Academy of Sleep Medicine. Sleep, 23, 237–241.
Clarke, G., & Harvey, A. G. (2012). The complex role of sleep in adolescent depression. Child
and Adolescent Psychiatric Clinics of North America, 21, 385–400.
Currie, S. R., Wilson, K. G., & Curran, D. (2002). Clinical significance and predictors of
treatment response to cognitive-behavior therapy for insomnia secondary to chronic pain.
Journal of Behavioral Medicine, 25, 135–153.
Insomnia 561
Czeisler, C. A., Richardson, G. S., Coleman, R. M., Zimmerman, J. C., Moore-Ede, M. C.,
Dement, W. C., & Weitzman, E. D. (1981). Chronotherapy: Resetting the circadian
clocks of patients with delayed sleep phase insomnia. Sleep, 4, 1–21.
Dahl, R. E., & Harvey, A. G. (2007). Sleep in children and adolescents with psychiatric or
emotional disorders. Sleep Medicine Clinics, 2, 501–511.
Daley, M., Morin, C. M., LeBlanc, M., Gregoire, J. P., & Savard, J. (2009). The economic
burden of insomnia: Direct and indirect costs for individuals with insomnia syndrome,
insomnia symptoms, and good sleepers. Sleep, 32, 55–64.
Edinger, J. D., Bonnet, M. H., Bootzin, R. R., Doghramji, K., Dorsey, C. M., Espie,
C. A., … American Academy of Sleep Medicine Work Group (2004). Derivation of
research diagnostic criteria for insomnia: Report of an American Academy of Sleep
Medicine Work Group. Sleep, 27 , 1567–1596.
Edinger, J. D., Wohlgemuth, W. K., Radtke, R. A., Marsh, G. R., & Quillian, R. E. (2001).
Cognitive behavioral therapy for treatment of chronic primary insomnia: A randomized
Espie, C. A. (2002). Insomnia: Conceptual issues in the development, persistence, and
treatment of sleep disorder in adults. Annual Review of Psychology, 53, 215–243.
Espie, C. A., Broomfield, N. M., MacMahon, K. M., Macphee, L. M., & Taylor, L. M.
(2006). The attention-intention-effort pathway in the development of psychophysiologic
insomnia: A theoretical review. Sleep Medicine Reviews, 10, 215–245.
Even, C., Schröder, C. M., Friedman, S., & Rouillon, F. (2008). Efficacy of light therapy in
nonseasonal depression: A systematic review. Journal of Affective Disorders, 108, 11–23.
Ford, D. E., & Kamerow, D. B. (1989). Epidemiologic study of sleep disturbances and
psychiatric disorders: An opportunity for prevention? Journal of the American Medical
Association, 262, 1479–1484.
Frank, E. (2005). Treating bipolar disorder: A clinician’s guide to interpersonal and social
rhythm therapy. New York, NY: Guilford Press.
Frank, E., Kupfer, D. J., Thase, M. E., Mallinger, A. G., Swartz, H. A., Eagiolini, A. M., …
Monk, T. (2005). Two-year outcomes for interpersonal and social rhythm therapy in
individuals with bipolar I disorder. Archives of General Psychiatry, 62, 996–1004.
Germain, A., Shear, M. K., Hall, M., & Buysse, D. J. (2007). Effects of a brief behavioral
treatment for PTSD-related sleep disturbances: A pilot study. Behaviour Research and
Therapy, 45, 627–632.
Gibson, E., Powles, A. C. P., Thabane, L., O’Brien, S., Molnar, D., Trajanovic, N., …
Chilcott-Tanser, L. (2006). “Sleepiness” is serious in adolescence: Two surveys of 3235
Canadian students. BMC Public Health, 6, 116.
Giedke, H., & Schwarzler, F. (2002). Therapeutic use of sleep deprivation in depression. Sleep
Medicine Reviews, 6, 361–377.
Golden, R. N., Gaynes, B. N., Ekstrom, R. D., Hamer, R. M., Jacobsen, F. M., Suppes,
T., … Nemeroff, C. B. (2005). The efficacy of light therapy in the treatment of mood
disorders: A review and meta-analysis of the evidence. American Journal of Psychiatry,
162, 656–662.
Gradisar, M., Dohnt, H., Gardner, G., Paine, S., Starkey, K., Menne, A., … Trenowden, S.
(2011). A randomized controlled trial of cognitive-behavior therapy plus bright light
therapy for adolescent delayed sleep phase disorder. Sleep, 34, 1671–1680.
Grant, B. F., Stinson, F. S., Dawson, D. A., Chou, S. P., Dufour, M. C., Compton, W., …
Kaplan, K. (2004). Prevalence and co-occurrence of substance use disorders and inde-
pendent mood and anxiety disorders: Results from the National Epidemiologic Survey on
Alcohol and Related Conditions. Archives of General Psychiatry, 61, 807–816.
Gregory, A. M., Caspi, A., Eley, T. C., Moffitt, T. E., O’Connor, T. G., & Poulton, R. (2005).
Prospective longitudinal associations between persistent sleep problems in childhood and
anxiety and depression disorders in adulthood. Journal of Abnormal Child Psychology, 33,
157–163.
Gregory, A. M., Cox, J., Crawford, M. R., Holland, J., & Harvey, A. G. (2009). Dysfunctional
beliefs and attitudes about sleep in children. Journal of Sleep Research, 18, 422–426.
Gregory, A. M., & O’Connor, T. G. (2002). Sleep problems in childhood: A longitudinal
study of developmental change and association with behavioral problems. Journal of the
American Academy of Child and Adolescent Psychiatry, 41, 964–971.
Harvey, A. G. (2001). Insomnia: Symptom or diagnosis? Clinical Psychology Review, 21,
1037–1059.
Harvey, A. G. (2002). A cognitive model of insomnia. Behaviour Research and Therapy, 40,
869–894.
Harvey, A. G. (2005). A cognitive theory of and therapy for chronic insomnia. Journal of
Cognitive Psychotherapy: An International Quarterly, 19, 41–60.
Harvey, A. G. (2006). What about patients who can’t sleep? Case formulation for insomnia.
In N. Tarrier (Ed.), Case formulation in cognitive behaviour therapy: The treatment of
challenging and complex clinical cases (pp. 293–311). New York, NY: Brunner-Routledge.
Harvey, A. G. (2008). Insomnia, psychiatric disorders, and the transdiagnostic perspective.
Current Directions in Psychological Science, 17 , 299–303.
Harvey, A. G., & Li, D. (2009). Managing sleep disturbance in bipolar disorder. Current
Psychiatry Reviews, 5, 182–193.
Harvey, A. G., Sharpley, A., Ree, M. J., Stinson, K., & Clark, D. M. (2007). An open trial of
cognitive therapy for chronic insomnia. Behavior Research and Therapy, 45, 2491–2501.
Harvey, A. G., & Tang, N. K. J. (2003). Cognitive behavior therapy for insomnia: Can we rest
yet? Sleep Medicine Reviews, 7 , 237–262.
Hoban, T. F. (2004). Sleep and its disorders in children. Seminars in Neurology, 24, 327–340.
Hoddes, E., Zarcone, V., Smythe, H., Phillips, R., & Dement, W. C. (1973). Quantification
of sleepiness: A new approach. Psychophysiology, 10, 431–436.
Jacobs, G. D., Pace-Schott, E. F., Stickgold, R., & Otto, M. W. (2004). Cognitive behavior
therapy and pharmacotherapy for insomnia: A randomized controlled trial and direct
comparison. Archives of Internal Medicine, 164, 1888–1896.
Jean-Louis, G., von Gizycki, H., Zizi, F., Spielman, A., Hauri, P., & Taub, H. (1997).
The actigraph data analysis software: II. A novel approach to scoring and interpreting
sleep-wake activity. Perceptual and Motor Skills, 85, 219–226.
Johnson, E. O., Roth, T., Schultz, L., & Breslau, N. (2006). Epidemiology of DSM-
IV insomnia in adolescence: Lifetime prevalence, chronicity, and an emergent gender
difference. Pediatrics, 117 , e247–256.
Kaplan, K. A., & Harvey, A. G. (2009). Hypersomnia across mood disorders: A review and
synthesis. Sleep Medicine Reviews, 13, 275–285.
Kryger, M. H., Roth, T., & Dement, W. C. (2005). Principles and practice of sleep medicine
(4th ed.). Philadelphia, PA: W. B. Saunders.
Kyle, S. D., Morgan, K., & Colin, A. E. (2010). Insomnia and health-related quality of life.
Sleep Medicine Reviews, 14, 69–82.
Levin, F. R., & Hennessy, G. (2004). Bipolar disorder and substance abuse. Biological
Lichstein, K. (2000). Secondary insomnia. In K. Lichstein & C. Morin (Eds.), Treatment of
late-life insomnia (pp. 297–319). Thousand Oaks, CA: Sage.
Insomnia 563
Liu, X., Buysse, D. J., Gentzler, A. L., Kiss, E., Mayer, L., Kapornai, K., … Kovacs, M. (2007).
Insomnia and hypersomnia associated with depressive phenomenology and comorbidity
in childhood depression. Sleep, 30, 83–90.
Lundh, L.-G. (1998). Cognitive-behavioural analysis and treatment of insomnia. Scandinavian
Journal of Behaviour Therapy, 27 , 10–29.
Manber, R., Edinger, J. D., Gress, J. L., San Pedro-Salcedo, M. G., Kuo, T. F., & Kalista,
T. (2008). Cognitive behavioral therapy for insomnia enhances depression outcome in
patients with comorbid major depressive disorder and insomnia. Sleep, 31, 489–495.
Means, M. K., Lichstein, K. L., Epperson, M. T., & Johnson, C. T. (2000). Relaxation
therapy for insomnia: Nighttime and daytime effects. Behaviour Research and Therapy,
38, 665–678.
Mistlberger, R. E., Antle, M. C., Glass, J. D., & Miller, J. D. (2000). Behavioral and
serotonergic regulation of circadian rhythms. Biological Rhythm Research, 31, 240–283.
Monk, T. H., Petrie, S. R., Hayes, A. J., & Kupfer, D. J. (1994). Regularity of daily life in
relation to personality, age, gender, sleep quality and circadian rhythms. Journal of Sleep
Research, 3, 196–205.
Monroe, L. J. (1967). Psychological and physiological differences between good and poor
sleepers. Journal of Abnormal Psychology, 72, 255–264.
Morin, C. M. (1993). Insomnia: Psychological assessment and management. New York, NY:
Guilford Press.
Morin, C. M., Bootzin, R. R., Buysse, D. J., Edinger, J. D., Espie, C. A., & Lichstein, K. L.
(2006). Psychological and behavioral treatment of insomnia: An update of recent evidence
(1998–2004). Sleep, 29, 1396–1406.
Morin, C. M., Colecchi, C., Stone, J., Sood, R., & Brink, D. (1999a). Behavioral and phar-
macological therapies for late-life insomnia. Journal of the American Medical Association,
281, 991–999.
Morin, C. M., Colecchi, C., Stone, J., Sood, R., & Brink, D. (1999b). Behavioral and
pharmacological therapies for late-life insomnia: A randomized controlled trial. Journal of
the American Medical Association, 281, 991–999.
Morin, C. M., Culbert, J. P., & Schwartz, S. M. (1994). Nonpharmacological interventions
for insomnia: A meta-analysis of treatment efficacy. American Journal of Psychiatry, 151,
1172–1180.
Morin, C. M., & Espie, C. A. (2003). Insomnia: A clinical guide to assessment and treatment.
New York, NY: Kluwer Academic/Plenum.
Morin, C. M., Gaulier, B., Barry, T., & Kowatch, R. A. (1992). Patients’ acceptance of
psychological and pharmacological therapies for insomnia. Sleep, 15, 302–305.
Morin, C. M., Hauri, P. J., Espie, C. A., Spielman, A. J., Buysse, D. J., & Bootzin, R. R.
(1999). Nonpharmacologic treatment of chronic insomnia. An American Academy of
Sleep Medicine review. Sleep, 22, 1134–1156.
Morin, C. M., LeBlanc, M., Daley, M., Gregoire, J. P., & Merette, C. (2006). Epidemiology
of insomnia: Prevalence, self-help treatments, consultations, and determinants of help-
seeking behaviors. Sleep Medicine, 7 , 123–130.
Morin, C. M., Vallieres, A., Guay, B., Ivers, H., Savard, J., Merette, C., … Baillargeon, L.
(2009). Cognitive behavioral therapy, singly and combined with medication, for persistent
insomnia: A randomized controlled trial. JAMA, 301, 2005–2015.
Murtagh, D. R., & Greenwood, K. M. (1995). Identifying effective psychological treatments
for insomnia: A meta-analysis. Journal of Consulting and Clinical Psychology, 63, 79–89.
National Institutes of Health. (2005). National Institutes of Health State of the Science
Conference Statement: Manifestations and management of chronic insomnia in adults.
June 13–15, 2005. Sleep, 28, 1049–1057.
Neitzert Semler, C., & Harvey, A. G. (2005). Misperception of sleep can adversely affect
daytime functioning in insomnia. Behaviour Research and Therapy, 43, 843–856.
Ohayon, M. M. (2002). Epidemiology of insomnia: What we know and what we still need to
learn. Sleep Medicine Reviews, 6, 97–111.
Ohayon, M. M., Roberts, R. E., Zulley, J., Smirme, S., & Priest, R. G. (2000). Prevalence and
patterns of problematic sleep among older adolescents. Journal of the American Academy
of Child & Adolescent Psychiatry, 39, 1549–1556.
Ong, J. C., Shapiro, S. L., & Manber, R. (2008). Combining mindfulness meditation
with cognitive-behavior therapy for insomnia: A treatment-development study. Behavior
Therapy, 39, 171–182.
Owens, J. L., France, K. G., & Wiggs, L. (1999). Behavioural and cognitive-behavioural
interventions for sleep disorders in infants and children: A review. Sleep Medicine Reviews,
3, 281–302.
Perlis, M. L., Aloia, M., & Kuhn, B. (2011). Behavioral treatment for sleep disorders: A
comprehensive primer of behavioral sleep medicine. Amsterdam, The Netherlands: Elsevier.
Perlis, M. L., Giles, D. E., Mendelson, W. B., Bootzin, R. R., & Wyatt, J. K. (1997).
Psychophysiological insomnia: The behavioural model and a neurocognitive perspective.
Journal of Sleep Research, 6, 179–188.
Perlis, M., & Lichstein, K. (Eds.). (2003). Treating sleep disorders: Principles and practice of
behavioral sleep medicine. New York, NY: John Wiley & Sons, Inc.
Perlis, M. L., Merica, H., Smith, M. T., & Giles, D. E. (2001). Beta EEG activity and insomnia.
Sleep Medicine Reviews, 5, 363–374.
Riemann, D., Konig, A., Hohagen, F., Kiemen, A., Voderholzer, U., Backhaus, J., … Berger,
M. (1999). How to preserve the antidepressive effect of sleep deprivation: A comparison
of sleep phase advance and sleep phase delay. European Archives of Psychiatry and Clinical
Riemann, D., & Voderholzer, U. (2003). Primary insomnia: A risk factor to develop depression?
Journal of Affective Disorders, 76, 255–259.
Roberts, R. E., Lee, E. S., Hemandez, M., & Solari, A. C. (2004). Symptoms of insomnia
among adolescents in the lower Rio Grande Valley of Texas. Sleep, 27 , 751–760.
Roberts, R. E., Roberts, C. R., & Chan, W. (2006). Ethnic differences in symptoms of insomnia
among adolescents. Sleep, 29, 359–365.
Sack, R. L., Auckley, D., Carskadon, M. A., Wright, K. P. J., Vitiello, M. V., & Zhdanova,
I. V. (2007). Circadian rhythm sleep disorders, Part II: Advanced sleep phase disorder,
delayed sleep phase disorder, free-running disorder, and irregular sleep-wake rhythm: An
American Academy of Sleep Medicine review. Sleep, 30, 1484–1501.
Sadeh, A. (2005). Cognitive-behavioral treatment for childhood sleep disorders. Clinical
Seibt, J., Aton, S. J., Jha, S. K., Coleman, T., Dumoulin, M. C., & Frank, M. G. (2008). The
non-benzodiazepine hypnotic zolpidem impairs sleep-dependent cortical plasticity. Sleep,
31, 1381–1391.
Sivertsen, B., Omvik, S., Pallesen, S., Bjorvatn, B., Havik, O. E., Kvale, G., … Nordhus, A.
H. (2006). Cognitive behavioral therapy vs zopiclone for treatment of chronic primary
insomnia in older adults: A randomized controlled trial. Journal of the American Medical
Association, 295, 2851–2858.
Smith, L. J., Nowakowski, S., Soeffing, J. P., Orff, H. J., & Perlis, M. L. (2003). The
measurement of sleep. In M. L. Perlis & K. L. Lichstein (Eds.), Treating sleep disorders:
Principles and practice of behavioral sleep medicine (pp. 29–73). New York, NY: John
Wiley & Sons, Inc.
Insomnia 565
Smith, M. T., Huang, M. I., & Manber, R. (2005). Cognitive behavior therapy for chronic
insomnia occurring within the context of medical and psychiatric disorders. Clinical
Smith, M. T., Perlis, M. L., Park, A., Smith, M. S., Pennington, J., Giles, D. E., & Buysse,
D. J. (2002). Comparative meta-analysis of pharmacotherapy and behavior therapy for
persistent insomnia. American Journal of Psychiatry, 159, 5–11.
Spiegel, K., Tasali, E., Penev, P., & Van Cauter, E. (2004). Brief communication: Sleep
curtailment in healthy young men is associated with decreased leptin levels, elevated
ghrelin levels, and increased hunger and appetite. Annals of Internal Medicine, 141,
846–850.
Spielman, A. J., & Anderson, M. W. (1999). The clinical interview and treatment planning
as a guide to understanding the nature of insomnia: The CCNY insomnia interview. In
S. Chokroverty (Ed.), Sleep disorders medicine: Basic science, technical considerations, and
clinical aspects (2nd ed., pp. 385–426). Boston, MA: Butterworth-Heinemann.
Spielman, A. J., Caruso, L. S., & Glovinsky, P. B. (1987). A behavioral perspective on insomnia
treatment. Psychiatric Clinics of North America, 10, 541–553.
Spielman, A. J., Saskin, P., & Thorpy, M. J. (1987). Treatment of chronic insomnia by
restriction of time in bed. Sleep, 10, 45–56.
Tate, B. A., Richardson, G. S., & Carskadon, M. A. (2002). Maturational changes in sleep-wake
timing: Longitudinal studies of the circadian activity rhythm of a diurnal rodent. In M.
A. Carskadon (Ed.), Adolescent sleep patterns: Biological, social, and psychological influences
(pp. 40–49). New York, NY: Cambridge University Press.
Thorpy, M. J., Korman, E., Spielman, A. J., & Glovinsky, P. B. (1988). Delayed sleep phase
syndrome in adolescents. Journal of Adolescent Health Care, 9, 22–27.
Troxel, W. M., Buysse, D. J., Matthews, K. A., Kip, K. E., Strollo, P. J., Hall, M., … Reis, S.
E. (2010). Sleep symptoms predict the development of the metabolic syndrome. Sleep,
33, 1633–1640.
Troxel, W. M., Robles, T. F., Hall, M., & Buysse, D. J. (2007). Marital quality and the marital
bed: Examining the covariation between relationship quality and sleep. Sleep Medicine
Reviews, 11, 389–404.
Tuunainen, A., Kripke, D. F., & Endo, T. (2004). Light therapy for non-seasonal depression.
Cochrane Database of Systematic Reviews, 2, CD004050.
Van Dongen, H. P., Maislin, G., Mullington, J. M., & Dinges, D. F. (2003). The cumulative
cost of additional wakefulness: Dose–response effects on neurobehavioral functions and
sleep physiology from chronic sleep restriction and total sleep deprivation. Sleep, 26,
117–126.
Vincent, N., & Lionberg, C. (2001). Treatment preference and patient satisfaction in chronic
insomnia. Sleep, 24, 411–417.
Weitzman, E. D., Czeisler, C. A., Coleman, R. M., Spielman, A. J., Zimmerman, J. C.,
Dement, W., … Pollak, C. P. (1981). Delayed sleep phase syndrome: A chronobiological
disorder with sleep-onset insomnia. Archives of General Psychiatry, 38, 737–746.
Wirz-Justice, A., Benedetti, F., & Terman, M. (2009). Chronotherapeutics for affective disorders:
A clinician’s manual for light & wake therapy. Basel, Switzerland: Karger.
Wirz-Justice, A., & Van den Hoofdakker, R. H. (1999). Sleep deprivation in depression: What
do we know, where do we go? Biological Psychiatry, 46, 445–453.
Yoo, S. S., Gujar, N., Hu, P., Jolesz, F. A., & Walker, M. P. (2007). The human emotional
brain without sleep—a prefrontal amygdala disconnect. Current Biology, 17 , R877–878.
25
Anorexia Nervosa and Bulimia
Nervosa
Jennifer Svaldi and Brunna Tuschen-Caffier
University of Freiburg, Germany
Symptoms and Classification of Anorexia Nervosa and

Bulimia Nervosa
Eating disorders such as anorexia nervosa (AN) and bulimia nervosa (BN) are
characterized by disturbed eating behavior as well as body weight and shape concerns.
Subjects with AN strive to be extremely thin and show pathological fear of gaining
weight. While the Diagnostic and Statistical Manual of Mental Disorders (4th ed., text
rev.; DSM-IV-TR; American Psychiatric Association [APA], 2000) stresses that this
fear persists even though individuals with AN are underweight, the Eating Disorder
Work Group of the DSM-5 (www.dsm5.org) recommends substituting the term
“underweight” with the phrase “markedly low weight”. In the DSM-IV-TR (APA,
2000), normal weight and underweight are established by means of the body mass
index (BMI = body weight in kg/body height in m2 ). A BMI less than or equal to
17.5 is considered underweight, suggesting that an individual’s weight is less than 85%
of the weight considered to be normal for his or her age and height. For the revision
of the DSM (DSM-5), the Eating Disorders Work Group proposes to renounce the
quantification of underweight. Rather, whether weight is inappropriately low should
be defined taking into consideration the person’s age, gender, and physical health
status (see also www.dsm5.org).
In the case of BN it is typical for affected subjects to suffer from repetitive episodes
of binge eating. During these episodes, mainly high caloric and easily accessible
food (e.g., cake, ice cream, bread, pasta, fast food) is consumed, which is generally
avoided during regular meals. Due to fears of weight gain many individuals with
BN engage in self-induced vomiting after a binge-eating episode. Alternatively or
additionally, they misuse laxatives, diuretics, or enemas, or other medications. This
form of BN is subtyped as BN purging type (APA, 2000). Binge-eating episodes
are a necessary criterion for the classification of BN according to the DSM-IV (APA,

DOI: 10.1002/9781118528563.wbcbt25
2000). However, it is still unclear how large the amount of food eaten needs to
be in order to qualify as an “objective”—rather than a “subjective”—binge attack.
This aside, binge attacks are episodes which occur in a discrete period of time
and are accompanied by a sense of loss of control. While in the current DSM-
IV binge-eating episodes and compensatory behaviors have to occur on average at
least twice a week over a period of 3 months, the Eating Disorder Work Group
recommends that the required minimum frequency in the DSM-5 be reduced to once
a week over the last 3 months (www.dsm5.org), as individuals who report a lower
frequency than twice per week are comparable to those meeting the current DSM-IV
criterion.
Even though individuals with BN are in general of normal weight, they often are
concerned about their body shape and weight. Additionally, their self-evaluation is
strongly dependent on how satisfied or unsatisfied they are with their body weight
or shape (APA, 2000). A diagnosis of BN, however, should not be given if the
disturbance occurs only in the course of AN.
While the DSM-IV requires the specification of the BN purging subtype and the
nonpurging subtype, the expert group recommends a deletion of the two subtypes
as it is unclear how to define nonpurging inappropriate behavior. Additionally,
the nonpurging subtype has received little attention both empirically and clinically.
Finally, it is unclear insofar as individuals with this subtype of BN more closely
resemble individuals with binge eating disorder (www.dsm5.org).
Overvaluation of Body Weight and Shape as a Core Feature of

Anorexia Nervosa and Bulimia Nervosa
Overvaluation of body weight and shape and associated body dissatisfaction are core
features of AN as well as BN (APA, 2000). It has been shown that overvaluation
of body weight and shape plays a central role in the development and maintenance
of eating disordered symptoms (Jacobi, Hayward, de Zwaan, Kraemer, & Agras,
2004). According to schema-theoretical conceptions (Vitousek & Hollon, 1990;
Williamson, White, York-Crowe, & Stewart, 2004), body dissatisfaction represents
the negative cognitive and affective connotation of one’s own body represented in
the body schema. From a developmental perspective, a negative body schema is the
result of past negative experiences activated by exposure to body-related cues (e.g.,
a mirror). Such activated negative body-related self-schema is further presumed to
direct eating disordered patients’ attention to body-related stimuli. At the behavioral
level such distortions in information processing are presumed to be observable as
body checking and avoidance of body-related information, but also restrictive eating
and compensatory behavior (Williamson et al., 2004).
According to the presented model, shape- and weight-related worries in AN present
themselves not only at the emotional (e.g., shame, disgust) and cognitive level (e.g.,
undue influence of body weight and shape on self-evaluation), but also at different
levels of information processing; for example, the allocation of attention toward
specific body parts. Empirical evidence for the model comes, for instance, from a
study by Rieger et al. (1998): Subjects with AN and BN responded faster to a probe
Anorexia Nervosa and Bulimia Nervosa 569
when it was at the location of a word cue denoting a large body. Likewise, in a pictorial
dot-probe paradigm, Shafran, Lee, Cooper, Palmer, and Fairburn (2007) found that
relative to body-unrelated cues, attention was allocated more toward both neutral and
negative body-related cues in eating disordered patients. While these studies did not
assess whether the processed stimuli were dependent on their level of self-reference,
other studies investigated whether eating disordered individuals process their own
and other bodies in fundamentally different ways. For example, Jansen, Nederkoorn,
and Mulkens (2005) consecutively presented eating symptomatic and normal control
participants with a photo of themselves (self-body) and a picture of a weight-matched
control body (other-body) while continuously measuring eye movements. Eating
symptomatic participants allocated their gaze more toward their own self-termed ugly
body parts than to their own beautiful body parts. When looking at the other-body,
the eating symptomatic group paid most attention to the beautiful body parts of
the other-body. By contrast, normal controls showed the opposite gaze pattern.
Comparably, when looking at body pictures, women with high body dissatisfaction
were found to allocate their attention significantly more often and longer toward
hips, waist, legs, and arms than women with low body dissatisfaction did (Hewig,
Cooper, Trippe, Hecht, Straube, & Miltner, 2008). Moreover, Blechert, Ansorge,
and Tuschen-Caffier (2010) analyzed attentional processes of patients with AN and
BN using a modified dot-probe paradigm. The aim of the study was to test whether
individuals with AN and BN show an attentional bias toward a photo of their own body
(self-photo) relative to a photo of a matched control participant’s body (other-photo).
Saccade latency was used as an index of covert attention to the cue photos. In the AN
group saccades were faster when the self-photo was the target whereas in the BN group
there was a numerically opposite but nonsignificant pattern. The bias for self-photos
correlated with body dissatisfaction in the AN group (the more dissatisfied AN patients
were, the stronger was the attentional bias toward the self-photos). Taken together,
there is evidence that patients with eating disturbances seem to show an attentional
bias (vigilance) toward ugly body parts (Jansen et al., 2005) and toward their own
body, rather than avoidance behavior (Blechert et al., 2010; Shafran et al., 2007).
This is an important aspect for body image treatment (discussed later in this chapter).
Associated Psychopathology
Comorbid mental disorders (Axis I disorders) and/or personality disorders (Axis II

disorders) often co-occur in AN and BN. The most frequent comorbid disorders
are affective disorders, anxiety disorders, and disorders with substance dependence
(Striegel-Moore, Garvin, Dohm, & Rosenheck, 1999). As such, approximately 70% of
females with BN are affected by an anxiety disorder at least once in their life. Thereby,
the most frequent diagnoses include social phobia, generalized anxiety disorder,
and posttraumatic stress disorder. With regard to personality disorders, borderline
personality disorder is particularly prominent.
There is further a range of physical sequelae associated with AN and BN. For
instance, malnutrition increases the risk for other symptoms: Iron deficiency may lead
to tiredness and headaches, while chronic potassium deficiency can lead to kidney
failure and to muscular weakness and cramps, obstipation, hypotonia, and cardiac
arrhythmias. Moreover, severe underweight may result in estrogen deficiency lead-
ing to bone loss, which is associated with an increased fracture risk. In addition,
metabolism problems and electrolyte imbalance may lead to cardiovascular complica-
tions, or cardiac insufficiency, which can also lead to death by cardiac arrest. As such,
the mortality risk in AN and BN is significantly increased compared to the normal
population (Arcelus, Mitchell, Wales, & Nielsen, 2011; Crow et al., 2009; Herzog
et al., 2000; Keel, Mitchell, Miller, Davis, & Crow, 1999).
Physiological dysfunction includes amenorrhea, which is usually a consequence of
the weight loss. While the DSM-IV (APA, 2000) requires amenorrhea for diagnostic
fulfillment, the Eating Disorder Work Group of the DSM-5 suggests a deletion of
this criterion, as a subgroup of AN patients continues to have at least some menstrual
activity though fulfilling all other symptoms of AN. Moreover, amenorrhea cannot
be applied to men, nor to premenarchal and postmenopausal females, nor to females
taking oral contraceptives (www.dsm5.org).
Development and Maintenance of Anorexia

Nervosa and Bulimia Nervosa
Eating disorders such as AN and BN are seen as multidetermined serious mental

disorders. Using a biopsychosocial model as a framework for the categorization of risk
factors, biological (e.g., genetic), social (e.g., family), and psychological (e.g., self-
esteem) factors, among others, are important for the development and maintenance
of eating disorders (see Figure 25.1 for an etiological and maintenance working
model). The following sections highlight some of the main risk factors that have been
identified by empirical studies.
Genetic Predisposition
There is evidence that a genetic predisposition may increase vulnerability for AN and
BN (Fichter & Noegel, 1990; Strober, Freeman, Lampert, Diamond, & Kaye, 2000).
For instance, the concordance rate concerning eating disorders for monozygotic twins
amounted to 56–65%; in dizygotic twins concordance rates were substantially lower
at 7–8% (Crisp, Hall, & Holland, 1985; Holland, Sicotte, & Treasure, 1988). Genes
seem to be important for the development of AN in particular (e.g., Bulik et al.,
2006; Klump, Wonderlich, Lehoux, Lilenfeld, & Bulik, 2002).
In patients with BN concordance rates have been reported at between 22.9 and
35% for monozygotic twins, and for dizygotic females between 8.7 and 29% (Holland
et al., 1988; Kendler et al., 1991). This could indicate a lower involvement of
genetic factors in BN compared to AN. On the basis of a review on cultural and
genetic influences in eating disorders, Keel and Klump (2003) have drawn a similar
conclusion. However, another review (Fairburn, Cowen, & Harrison, 1999) gives
evidence of a wide range in the determined concordance rates both in AN and BN
twin studies. This wide range may also be determined by the varying methodologies
and sample sizes used in the studies.
Etiological working model
Predispositions and triggers

Genetics
Personality (e.g., low self-esteem, perfectionism)
Learning history
(concerning food
and body)
Weight concern,
Stressful life events Dieting, weight
body image
(e.g., interpersonal loss behavior
disturbance
problems)
Positive short-term
Biological
effects (e.g., emotion
changes
regulation)
Disturbed eating
(e.g., binge eating)
Figure 25.1 Etiological and maintenance model of anorexia and bulimia

nervosa.
Sociocultural Influences
In Western industrialized societies there is an abundance of palatable foods, appe-
tizing beyond the extent of physical hunger. Moreover, opulent and versatile food
is of high significance on social occasions. At the same time, though, Western
societies have an extremely thin body ideal, favoring slim and flat bodies. Women
in particular are exposed to a strong normative pressure to conform to this body
ideal. From an early age, girls more than boys learn that positive evaluations and
care are strongly dependent on their physical appearance (Striegel-Moore, Silber-
stein, & Rodin, 1986), and their self-esteem correlates significantly with body
build (Guyot, Fairchild, & Hill, 1981). Many of them have concerns about their
weight and appearance even in childhood and try to restrict their food intake
(Hawkins, Turell, & Jackson, 1983). This problem aggravates in puberty during
the genetically determined increase of body fat in females; accordingly, the per-
centage of those who resort to dieting increases (Thelen, Powell, Lawrence, &
Kuhnert, 1992). Body dissatisfaction is very prominent in adult women as well.
Thirty percent of those in the normal weight range try to lose weight by dieting
or exercise in order to improve general health and increase attractiveness (Green
et al., 1997). The mentioned characteristics—concerns about body shape, size, and
weight, and efforts at dietary restriction—are also typical features of AN and BN.
Therefore, it is assumed that there is a continuum from an accepting attitude toward
one’s body with a dietary intake oriented at internal signals, to strong concerns
about one’s body with a deliberate restriction of caloric intake, up to clinical eat-
ing disorders (Heatherton & Polivy, 1992; Rodin, Silberstein, & Striegel-Moore,
1984).
Familial Factors
There is evidence that mothers of daughters with disordered eating report more
dissatisfaction with the general functioning of the family system than mothers of
daughters without disturbed eating (Pike & Rodin, 1991). However, the inference
that these abnormalities are responsible for the development of eating disorders is
problematic, as their characteristics may well be a consequence of eating disorders.
Nevertheless, unfavorable familial ties can become a source of pressure, independent
of whether they are of a primary or secondary nature, thus contributing to the
maintenance of the disorder.
However, it is likely that the eating-related behavior of mothers and their attitudes
toward body and weight are of special importance. Mothers of daughters with
disordered eating differ in their dieting history from mothers of girls without disturbed
eating. They themselves more often show disturbed eating patterns and have a
problematic attitude toward the body shape and weight of their eating disturbed
daughters (Pike & Rodin, 1991). Possible effects of modeling (observational learning)
are given by a study of girls with mothers with restrained eating: These girls have
stronger fears of getting fat, and in the laboratory they eat more after a preload
than girls with mothers without restrained eating (Franzen & Florin, 1995). As
such, children of mothers with restrained eating could have a higher risk for the
development of an eating disorder. However, it is still unclear whether modeling
explains the transmission of the maternal eating behavior to the daughters. For
instance, evidence for a familial transmission of eating behavior from mothers to
daughters through direct modeling has not been found yet (Byely, Archibald, Graber,
& Brooks-Gunn, 2000; Griffiths & McCabe, 2000). Moreover, it has been shown
that girls show higher restrained eating if their mothers report a low belief in their own
autonomy (Ogden & Steward, 2000). Furthermore, the development of disturbed
eating may be the consequence of an interaction between parental eating style and
other aspects of parental behavior such as overprotection (Tata, Fox, & Cooper,
2001) or shame-proneness (Murray, Waller, & Legg, 2000).
Behavioral and Cognitive Aspects

Several individuals affected by BN report that a longer period of fasting or a phase
of dietary restriction preceded the onset of the eating disorder (Mitchell, Hatsukami,
Eckert, & Pyle, 1985). In addition, longitudinal studies show that the risk for an
eating disorder is up to eight times higher for dieting adolescent girls compared to
nondieters (e.g., Patton, Johnson-Sabine, Wood, Mann, & Wakeling, 1990).
Empirical evidence suggests that dieting is not only correlationally but also causally
linked to binge-eating episodes (Jacobi et al., 2004). Usually, in the course of a
diet aimed at weight reduction, important nutrients, especially carbohydrates and
fats, are omitted. As a consequence, the body may crave the omitted nutrients
and accordingly the thoughts center around food. Moreover, using a cue reactivity
paradigm it has been shown that patients with AN and BN respond to high and
low calorie pictures with enhanced attentional processing indicated by early event
related potentials (ERPs; Blechert, Feige, Joos, Zeeck, & Tuschen-Caffier, 2011).
This indicates that patients with AN and BN show a generalized attentional bias for
food images, regardless of caloric value, and may explain the persistent preoccupation
with food in these individuals. Further, it has been found that restrained eaters
(Herman & Mack, 1975), as a risk group for the development of eating disorders,
show typical attentional processing toward food items: Restrained eaters respond less
strongly in their electrocortical responses (as displayed by early ERPs) to high caloric
food cues which they expect to eat subsequently compared to food cues which they do
not expect to eat, a difference that was not evident in nonrestrained eaters (Blechert,
Feige, Hajcak, & Tuschen-Caffier, 2010). This result may indicate that restrained
eaters downregulate their reactivity to available food cues in order to maintain their
dietary rules.
Further, experimental studies with women high on restrained eating yield evidence
that cognitive control of restrained eating behavior can be lost under various circum-
stances. In particular, under preload conditions (e.g., letting participants taste a food
item prior to a taste test), but also at the smell or the sight of food, under stress for
any number of reasons, as well as under negative and positive mood, individuals with
high restrained eating react with disinhibited eating (Cools, Schotte, & McNally,
1992; Jansen, 1996; Mills & Palandra, 2008; Schotte, Cools, & McNally, 1990).
Specifically, whereas unrestrained eaters eat less under the described circumstances,
restrained eaters tend to eat more. This phenomenon of counter-regulation is con-
sidered an analogue of binge episodes, which are a central feature of BN and AN
binge-eating/purging subtype. It is interesting that in individuals with AN and BN
the control over the eating behavior is lost under comparable circumstances as in
individuals with restrained eating.
Physiological Reactions
When exposed to food, individuals display anticipatory reactions (Powley & Berthoud,
1985) including increased salivation and insulin response. Subsequently, blood glu-
cose level goes down and intestinal motility increases to prepare the organism for
food intake (see Power & Schulkin, 2008, for other such anticipatory reactions,
also called cephalic phase responses). It seems plausible that such cephalic phase
responses are particularly distinct in food-deprived individuals. Contrary to expec-
tation, patients with AN (restricting type), who consequently maintain a strict diet
and accordingly are strongly food-deprived, react with a significantly lower sali-
vary response at the sight of food stimuli than women with BN, whose dietary
restriction is subject to strong fluctuations (LeGoff, Leichner, & Spigelman, 1988).
Jansen’s (1994) classical conditioning model yields a good explanation for this
counterintuitive result. Accordingly, food intake as an unconditioned stimulus acti-
vates unconditioned metabolic processes. If an abundant food intake often succeeds
the sight or smell of food, the latter themselves can become conditioned stimuli,
thereby triggering cephalic phase responses without prior food intake. Similarly,
arbitrary other external and internal conditions (being alone in front of the tele-
vision, agitation, depressed mood, pressure to perform) can become conditioned
stimuli for anticipatory physiological reactions directed at food intake, if they are
always succeeded by food intake. In patients with AN of the restricting subtype,
however, the chances of such conditioning processes occurring are fairly low. They
frequently expose themselves to eating-related stimuli, for example, by studying
cooking recipes, preparing palatable meals for others, and occasionally confronting
themselves with the smell and the sight of food—in general, though, without
noteworthy food intake occurring. Thereby, AN patients have, to a certain extent,
established an extinction program for anticipatory, physiological reactions and there-
fore have created a favorable premise to further maintain their dietary restriction.
Patients with BN, on the other hand, switch between dieting or fasting periods
and phases, during which they eat abundantly. Overeating often occurs in the
evening, when they are alone, when they have expressed restrained eating over the
whole day, and often when they feel under pressure. In this way these external
and internal conditions can easily reach the stage of conditioned stimuli for the
anticipatory, physiological reactions. In restricted food intake and fasting periods
as well behavioral strategies, patients with BN differ from those with AN. In these
periods individuals with BN are constantly concerned with food. However, these
thoughts center around the question of how the confrontation with food can be
avoided, or they are oriented toward the availability of food for a later binge-eating
episode.
Sexual Trauma
Eating disordered patients share some features with victims of sexual trauma, such as a
negative attitude towards one’s body and a sense of self loaded with shame and guilt, as
well as a negative attitude toward sexuality. However, these common features do not
allow the conclusion that traumatic experiences, especially in childhood and adoles-
cence, increase vulnerability, particularly for the development of an eating disorder. In
methodologically well-conducted studies, the assumption of an increased vulnerability
for eating disorders after traumatic experiences compared to other mental disorders
was not confirmed (Pope & Hudson, 1992; Welch & Fairburn, 1996). Some studies
suggest that women with eating disorders do not differ from women without eating
disorders with regard to the frequency of sexual trauma prior to the onset of the disor-
der (Pope & Hudson, 1992; Pope, Mangweth, Negrao, Hudson, & Cordas, 1994).
In other studies clear differences between patients with mental disorders (DSM-III-R,
Axis I) and healthy controls were found; however, differences were not found between
women with eating disorders and those with other Axis I disorders (Palmer, Chaloner,
& Oppenheimer, 1992; Welch & Fairburn, 1994). The latter results point more
toward an increased risk for the development of mental disorders in general (DSM-III-
R, Axis I), and therefore also for the possible development of an eating disorder, fol-
lowing trauma. However, trauma does not represent a specific risk factor for the devel-
opment of eating disorders. In accordance with this, the probability of past traumatic
experiences in eating disordered individuals is higher with the presence of comorbid
Axis I disorders (Roty, Yager, & Rossotto, 1994) or comorbid personality disorders
(McClelland, Mynors-Wallis, Fahy, & Treasure, 1991) than when such comorbidity
is absent. Nevertheless, even though not specific for the development of AN and BN,
traumatic experiences, if present, should be a target in the treatment of AN and BN.
Stressful Life Events

There is some evidence that patients with BN report more stressful life events before
the onset of the eating disorder (e.g., Fairburn, Welch, Doll, Davies, & O’Connor,
1997). Similarly, other studies found adverse experiences to be a risk factor for the
development of eating disorders (Jacobi et al., 2004). Interpersonal problems may
be stressful life events that trigger food intake. For instance, experimental studies
have shown that individuals suffering from BN react with an increase in the desire
to eat when confronted with interpersonal conflict situations (e.g., Tuschen-Caffier
& Vögele, 1999). It is assumed that in BN, low self-esteem, and deficits in social
competencies (Williams et al., 1993) add to an increase in experienced burden in
interpersonal relationships and conflict situations (Fairburn, 1993).
Personality and Psychological Mechanisms

Personality variables such as perfectionism, impulsivity, and low self-esteem, and
psychological mechanisms such as deficits in affect regulation, have been assumed
to play a role in the development and maintenance of AN and BN (e.g., Cassin &
von Ranson, 2005; Mauler, Hamm, Weike, & Tuschen-Caffier, 2006). Performance
situations may be an important factor contributing to the maintenance of eating
disorder symptoms. As such, both in the clinical and research context individuals
with eating disorders are described as persons who are strongly performance-oriented,
aiming to achieve their goals perfectly (Blouin, Zuro, & Blouin, 1990; Heatherton
& Baumeister, 1991). Newer studies have been able to show that elevated concerns
over mistakes were associated with AN and BN but not with other mental disorders
(Bulik et al., 2003). Notwithstanding, a range of prospective studies were not able to
demonstrate that perfectionism is indeed a predisposing risk factor for eating disorders
(Stice, 2001).
Dysregulation of Affect
A subgroup of eating disordered individuals may have difficulties coping with intensive
emotions, especially anger and sadness, or may experience them in an especially
intensive manner. In this context, Fairburn, Cooper, and Shafran (2003) speak
of mood intolerance. It is assumed that eating disordered individuals affected by
mood intolerance do have difficulties in the acceptance of mood fluctuations and in
reacting adequately to them. Instead, they engage in dysfunctional strategies, such
as overeating, in order to distract themselves from aversive emotional states and
associated thoughts. There is some evidence that binge eating in patients with BN
is triggered by negative affect (e.g., Alpers & Tuschen-Caffier, 2001; Haedt-Matt &
Keel, 2011; Hilbert & Tuschen-Caffier, 2007).
Moreover, Svaldi, Griepenstroh, Tuschen-Caffier, and Ehring (2012) systemati-
cally investigated emotion regulation difficulties across patients with AN, BN, and
binge-eating disorder (BED) using a large range of emotion regulation variables.
Additionally, as emotion regulation difficulties have been found across a wide range
of emotional disorders (e.g., Campbell-Sills & Barlow, 2006) patients with borderline
personality disorder (BPD) and individuals with major depressive disorder (MDD)
were included. Compared to healthy subjects, all clinical groups reported significantly
higher levels of emotion intensity, lower acceptance of emotions, less emotional aware-
ness and clarity, more self-reported emotion regulation problems, and decreased use
of functional and increased use of dysfunctional emotion regulation strategies. Thus,
results point toward emotion regulation difficulties being a transdiagnostic risk or
maintenance factor, rather than being typical for specific mental disorders.
Low Self-Esteem
Empirical evidence further suggests that eating disordered individuals often display
low self-esteem (Button, Loan, Davies, & Sonuga-Barke, 1997; Cooper & Fairburn,
1993). In addition, several studies found associations between self-esteem and eating
pathology in eating disturbed individuals (for an overview, see Shisslak, Crago,
Renger, & Clark-Wagner, 1998). It is still unclear, however, whether low self-esteem
is the consequence of an eating disorder and as such contributes to its maintenance,
or whether low self-esteem is also relevant for the incidence of an eating disorder.
Toward an Integrative View
Overall, empirical evidence suggests that the development and maintenance of eating
disorders is most probably multifactorial. A key component of AN and BN is that
the importance of body shape and weight is strongly overvalued. In this context
(both preceding and following the incidence of the disorder) eating-behavior-related
abnormalities emerge (restricted food intake, increased food intake). With the aim
of weight reduction different means of weight control (e.g., intermittent fasting) are
adopted, thus leading to biological changes (e.g., reduction of the basal metabolism),
which in turn increase the probability of disturbed eating behavior. Most likely, the
immediate consequences of pathological eating behavior (e.g., restricted food intake
in AN) play a central role in the maintenance of eating disorders (e.g., positive
reinforcement in the sense of an increased control over one’s body in AN; negative
reinforcement in the sense of a distraction from aversive emotions by focusing on
binge episodes in BN).
For the primary incidence of the psychopathological phenomena associated with
eating disorders, it is very likely that interdependent factors play a crucial role. As such,
biological processes such as the reduction of the basal metabolism through frequent
dieting, or the conditioning of metabolic processes (cephalic phase responses) as a
consequence of the frequent linkage of arbitrary internal or external stimuli (e.g.,
agitation, negative mood, performance orientation) with food intake (e.g., in BN),
probably play an important role. These processes have to be considered in the context
of social factors (e.g., excessive orientation toward a thin body ideal) and individual
factors of a person’s learning history (e.g., food as a comforter, the importance of
the thin body ideal in the family). Personality variables (e.g., self-esteem problems,
a pronounced need for control) can contribute to a narrowing of one’s sense of
self and self-definition to one’s body shape and weight (see also Fairburn, Shafran,
& Cooper, 1999), thereby leading to the necessity to become or remain thin.
Alternatively, in BN increased food consumption may be a means of affect regulation
in the sense of a negative reinforcement (Alpers & Tuschen-Caffier, 2001; Fairburn,
Cooper, et al., 2003; Heatherton & Baumeister, 1991). Critical life events or periods
(e.g., interpersonal problems in the form of a closeness–distance regulation problem
in close relationships) not infrequently precede the onset of the first incidence of
eating disorder symptoms; at the same time, though, these factors also contribute
to the maintenance of the disorder (see also Cattanach, Malley, & Rodin, 1988;
Tuschen-Caffier & Vögele, 1999).
Taking into consideration contemporary studies and developments in the concep-
tualization of eating disorders, it can be assumed that the various eating disorders
share more commonalities than differences with regard to mechanisms of develop-
ment and maintenance (Fairburn, Cooper, et al., 2003). This justifies the adoption
of an integrative view on risk factors in their possible effect on the development and
maintenance of the various forms of eating disorders.
Cognitive Behavioral Treatment of Anorexia

Nervosa and Bulimia Nervosa
For the treatment of AN and BN, cognitive behavioral approaches adopt a therapeutic
structure that directly focuses on the distinctive features of the disorder: nutritional
management and normalization of food intake, alteration of body image disturbances
and negative feelings towards one’s body, and alteration of the functional relation of
stress and eating behavior (Fairburn, Cooper, et al., 2003; Tuschen-Caffier, Pook,
& Frank, 2001; Wilson, Fairburn, Agras, Walsh, & Kraemer, 2002). Within these
treatment blocks, most cognitive behavioral treatment programs adopt behaviorally-
oriented interventions, but also cognitive interventions that are thought to motivate
patients to question their views and beliefs, and, where necessary, achieve a shift
toward more realistic thoughts and attitudes, as well as emotional patterns that
enhance well-being.
Psychological Preparation for Psychotherapy

The therapist and patient have to develop a plausible model for the explanation,
etiology, and maintenance of the eating disorder. The principles of the therapy are
then derived from the model in a way that the patient is capable of understanding.
According to the model of explanation for AN and BN, for instance, the therapist
pays attention to the excessive concern about weight and shape. The therapist points
out that, from the 1960s onward, an extremely slim ideal has been promoted in
Western industrialized countries. Many women try to correspond to this ideal by
repeated dieting or by eating extremely low-caloric food. These statements must be
put forward in a way that does not make the patient feel pathological about her diets
or even her vomiting. For this reason it is helpful for the therapist to emphasize that
the concern about weight and figure as well as the dieting are understandable: Against
the background of the ideal that society promotes, becoming slim or staying slim has
developed into a central goal in life. Society conveys the impression that the value
of a woman depends, to a great extent, upon her figure or weight. Considering this
background, it is understandable if a woman develops a massive concern or fear about
her figure not corresponding with this ideal. It is further understandable that this
could lead someone to start dieting, eating low-caloric food, or even vomiting. These
general statements should be complemented, if possible, by individual experiences of
the patient. They should also be able to describe why the patient was overly concerned
with figure and weight at the time the eating disorder began to occur.
Depending on the results of the individual analysis of the problem, the therapist will
also point out the connection between eating behavior and psychological impairment
due to stressful situations. These can be interpersonal conflicts, pressure to achieve, or
intense feelings (e.g., feeling angry, sad, bored, excited, or lonely). One mechanism
that can be used to explain the connection between stressful situations and eating is
distraction. A preoccupation with eating and vomiting (in the case of BN) or with the
aim of not eating (in the case of AN) provides a distraction from disturbing thoughts
and feelings.
Alternatively, it can be explained to patients with BN that psychological stressors,
and specifically the accompanying feelings and thoughts, can become conditioned
stimuli for anticipatory bodily reactions focusing on food intake (e.g., raised insulin),
as long as they are repeatedly followed by eating (Jansen, 1994). The principle of
counter-regulation can also be explained to the patients: In situations that are not
stressful, they are capable of controlling or suppressing the craving for food that is
produced by their body. However, in stressful situations this energy is needed to cope
with the problems.
Knowledge of the disorder and the ability to use specific therapeutic measures in
treating AN and BN are of great importance for the success of therapy. It further
requires a positive attitude toward the therapy on the part of the therapist, as well as a
high motivation to cooperate actively with therapy on the part of the person seeking
treatment.
The next section of this chapter focuses on cognitive behavioral interventions in
the context of symptom-oriented therapy.
Nutritional Management
Long time-spans between meals, frequent fasting, and a diet low in carbohydrates
and fats are typical for both AN and BN. In both disorders the aim is to implement
regular eating patterns, including a balanced intake of macronutrients (carbohydrates,
protein, fats). To counteract malnutrition and the co-occurring psychobiological
aftereffects (e.g., binge-eating episodes, depressed mood, constant preoccupation
with food), patients are guided to eat three meals a day, and, additionally, two small
daily snacks between the meals. As both AN and BN patients are characterized by
distinct fears about weight gain when being on a regular meal schedule, exclusively
educative interventions in the sense of a nutrition consultation are in general not
enough to motivate patients to change their eating patterns in the long run (e.g.,
Pike, Walsh, Vitousek, Wilson, & Bauer, 2003). Motivational interviewing techniques
are used to support patients in adherence to a regular eating pattern and to motivate
patients toward self-responsible decisions and behaviors (DiMarco et al., 2009).
In AN, weight restoration is a major aim of the implementation of a regular meal
intake. Experts advise aiming for a weight gain of about 500 g to a maximum of
1,000 g per week in the inpatient setting; in the outpatient setting the weight gain is
usually smaller (200–500 g per week). The magnitude of the weekly weight gain has
to be planned according to the physical condition of the patient. A medical checkup
of the patient’s health status is essential. To promote personal responsibility and self-
control for the progression of a healthy eating style, and because of possible severe
medical complications, there is a tendency to refrain from total parenteral nutrition.
However, in cases where underweight may prove fatal, there may be an indication for
parenteral nutrition, which occurs under medical assistance in the inpatient setting.
In addition to the regular meal intakes, patients’ general levels of activity have a
crucial influence on whether the intended weight gain is achieved. Therefore, patients
are motivated to avoid excessive exercise and to reduce their general level of activity
for their daily errands (e.g., by taking the elevator instead of using the stairs). In
severe cases, patients need to have bed rest.
In contrast to patients with BN, most of whom can be treated in an outpatient
setting, for many patients with AN inpatient treatment may be necessary before
starting treatment in an outpatient setting. In the context of nutritional management,
all patients are guided to learn an eating behavior that they can maintain in the
long term, without feeling psychologically or biologically deprived and without
experiencing fear toward specific foods, which can themselves function as risk factors
for relapse. Therefore, from the beginning “forbidden foods” are integrated into the
regular meal plan and patients learn to eat them in moderate amounts. Usually, these
forbidden foods are of high caloric content (e.g., chocolate, cake), which patients
actually like to eat, but in general deny themselves out of a fear of becoming fat or
losing control. The fact that these foods in particular are eaten in large amounts during
the course of a binge episode repeatedly leads to rigorous attempts to eliminate them
from the daily meal plan. Therefore patients are prompted gradually to overcome their
phobic fears concerning specific foods and to develop realistic beliefs with regard to the
probability of weight gain. Furthermore, in the context of these exposures patients
with binge-eating episodes are guided to eat the preferred binge food attentively
(i.e., eating slowly, identifying and naming the taste and the smell of the relevant
food).
Treatment of Body Image Disturbances

Patients with eating disorders display various forms of body image disturbance. For
example, they overestimate the size of their body width, are dissatisfied with their body
shape, and display an excessive pursuit of thinness and/or strong emotional reactions
(e.g., fear, disgust, sadness) at the sight of their body (APA, 2000; Cash & Deagle,
1997; Cash & Pruzinsky, 2004; Rosen, 1997). Clinical observations furthermore
suggest that eating disordered patients often evaluate themselves exclusively on
the dimensions of fat and thin. To modify negative reactions toward one’s body,
and to widen patients’ evaluative dimensions, exposure sessions, video, and mirror
confrontation are useful techniques. The aim of these techniques is to confront the
patients with their body and their body experience systematically (e.g., Delinsky &
G. T. Wilson, 2006; Hilbert & Tuschen-Caffier, 2004; Tuschen-Caffier, Pook, et al.,
2001; Tuschen-Caffier, Vögele, Bracht, & Hilbert, 2003). During mirror exposure,
patients are guided to describe their appearance in detail, rather than evaluating
themselves on the dimensions of fat and thin. Initially, patients wear their habitual
clothes, in which they feel comfortable. Often, these are articles of clothing that veil
the patient’s body shape. The therapist prompts the patient to observe him- or herself
in a full-length mirror. With the help of gull-wing doors, patients are also able to
observe the back side of their body. In general, patients start with a description of
their face. Without the guidance of the therapist self-descriptions remain at a rather
global, superficial level (e.g., “Apart from my fat cheeks my face looks quite normal”).
By means of directed specifications (e.g., “Skin can be fine-pored or large-pored,
pigmented light-colored or dark. What does your skin on the face look like?”),
patients are gradually guided toward a more differentiated perception and evaluation
of their physical appearance.
Having described their body in detail, patients are prompted to reflect the overall
impression of their person. In doing so they should attribute emotions (e.g., “I look
rather sad and reserved”), the state of their personal needs (e.g., “If I met myself at a
party, I would think: She wants to be alone. She doesn’t want to be approached by
anyone”), and behavior tendencies (e.g., “My posture looks as if I would like to steal
off”) to their overall appearance.
Mirror exposures are carried out at different times of the day (e.g., prior to and
after meal intake) and when patients are in different emotional states. Furthermore,
patients are asked to wear different clothing (elegant, figure-accentuating dresses;
sports clothes) in order to experiment with their appearance (e.g., changing hair-style,
putting on make-up, wearing jewelry). By means of such a playful/experimental
handling of their look, many patients become more flexible in the way they dress and
the image they want to represent.
It is especially difficult for patients to do the mirror exposures in skin-tight clothing.
It is important that the therapist pays attention that the patient does not use avoidance
strategies (e.g., diverting his or her gaze). On the one hand, patients verbalize their
thoughts and feelings at the sight of their body; on the other hand, they are prompted
to give a detailed self-description. The respective mirror exposure sessions are not
terminated until the patient has calmed down considerably. Over the course of
exposure sessions patients gradually get used to the sight of their body, and they learn
to widen the evaluative dimensions regarding their physical attractiveness and to accept
negative features of their physical appearance, without overly emphasizing them.
Skills-Based Interventions
These interventions are useful for patients who have skill deficits (e.g., deficits in
problem solving, deficits in strategies for overcoming stressful situations), or for
patients who display overly strong emotional reactions to stressful events. Moreover,
they are helpful for patients who show a reduced tolerance for aversive situations and
emotions (e.g., Fairburn, Marcus, & Wilson, 1993). Patients are asked to describe
and define what they experience their problem to be; then the therapist prompts
them to generate, preferably in an uncensored manner, all potential solutions that
come to mind. Subsequently, they evaluate the various generated alternatives in terms
of their effectiveness for the solution of the problem. In the following phase of the
training patients are prompted to choose an alternative solution (or combination of
alternatives) and to try it. After the “testing stage” patients evaluate the alternative(s),
with regard to how successfully they were able to implement the strategy and to what
extent they were able to solve their problem effectively. If the result is unsatisfactory,
patient and therapist together try to find a plausible explanation for the unfavorable
problem-solving result (e.g., Was the problem-solving strategy implemented
adequately? Was the strategy unsuitable for the solution of the problem?). This is
then followed by a further test phase, either using the problem-solving strategy that
was originally implemented, or choosing and testing a new strategy.
Exposure Therapy
If patients show overly strong reactions to stressful events, or their tolerance for
aversive situations and emotions is rather low, exposure therapy may be a promising
option. During exposure therapy, patients are exposed to aversive situations and
emotions without being able to resort to pathological eating behavior. As such, by
means of several techniques (e.g., videofeedback, audiofeedback, special therapeutic
conversation strategies), patients are mentally exposed to the specific situations and
emotions (e.g., negative recall of a former relationship; unreached goals) that usually
lead to binge eating. At the same time they are confronted with the foods they usually
eat during a binge-eating episode. They are repeatedly prompted to describe the food
in detail, to smell it, to describe what they smell, and to have a small bite of the food
in order to identify it. During the course of the prolonged exposure the high level
of stress gradually decreases, and the anticipated physiological craving (cephalic phase
responses) is probably extinguished, thereby gradually reducing the desire to eat (see
also Jansen, 1994). In this way patients learn that they have the ability to bear stressful
situations and their co-occurring feelings and thoughts without having to give in to
the craving for food.
Cognitive Intervention
In most cognitive behavioral treatments, the three main therapeutic blocks (nutritional
management, alteration of body image disturbances, and improvement of stress
management) are supplemented by specific cognitive strategies, which help patients
overcome their rigid, often dichotomous thinking. As such, for the development of
more realistic thoughts in eating disordered patients, Fairburn et al. (1993) suggest
an orientation toward the developed strategy of cognitive restructuring (e.g., Beck,
2011). In the first step of this process, participants are asked to identify and specify
a problematic thought. Following that, they are asked to evaluate the evidence for
and against the expressed thought. In the final step, patients have to weigh the pros
and cons against each other and finally come to a reasoned conclusion. This shift in
thinking is then thought to guide patients’ future behavior. Thereby, at the beginning
of this restructuring process it is not pivotal that patients have actually internalized
their shift in attention; rather, they should acquire the knowledge regarding which
perspective (e.g., with regard to weight cycling) is appropriate and reasonable,
and orient their behavior toward this perspective. In sum, the aim of cognitive
interventions is to help patients to become aware of the respective advantages and
disadvantages of their behavior and objectives and to decide for themselves, giving
consideration to all aspects (e.g., health risks vs. risks regarding central aspects of their
perception of attractiveness) in favor of or against each alternative in a self-determined
and self-responsible manner.
Stabilization and Prevention of Relapses

Toward the end of psychotherapy the therapist guides patients to develop realistic
expectations concerning the further course of their improvement. The therapist
points out that lots of patients experience periods of relapse during certain situations
in life; for instance, when feeling under pressure. The therapist emphasizes that the
reoccurrence of symptoms of the eating disorder is nothing to get too upset about
and does not mean that the therapy was of no use or that the patient is back to where
he or she was at the beginning. The therapist encourages patients to understand the
reoccurrence of binge eating as a chance to make use of what they learned in the
therapy for themselves (e.g., exposure to food, establishing a normal and healthy
eating style). The therapist also makes clear that the maintenance of a regular and
balanced way of eating is crucial to the long-term success of therapy. He or she
also encourages patients to contact their therapist again if necessary during a difficult
period in life in order to refresh what they learned in psychotherapy.
Efficacy of Cognitive Behavioral Therapy
In general, cognitive behavioral therapy (CBT) programs for the treatment of eat-
ing disorders include the treatment blocks described earlier in the chapter. For the
treatment of BN, CBT is considered the treatment of choice; as such, in numerous
controlled treatment studies CBT emerged as the more effective treatment com-
pared to other forms of treatment (e.g., pharmacological treatment, interpersonal
psychotherapy) (Walsh et al., 1997; Wilson & Fairburn, 2002; Wilson et al., 1999).
A meta-analysis considered 26 studies with a total of 460 patients with BN
for the treatment of BN by CBT; the studies compared patients treated with
CBT with patients treated with alternative psychological therapies or no treatment
(Whittal, Agras, & Gould, 1999). Effect sizes for CBT were very good throughout
(effect size [ES] for reduction of binges = 1.28; ES for reduction of compensatory
behavior = 1.22; ES for reduction of symptoms of depression = 1.31; ES for
reduction of dysfunctional thoughts with regard to eating = 1.35). Furthermore, this
meta-analysis showed that CBT was superior to pharmacological approaches on all
four outcome variables. Moreover, clinical studies have provided evidence that CBT
leads to a long-term reduction of bulimic symptoms in 70–75% of patients (Fichter
& Quadflieg, 2004; Tuschen-Caffier et al., 2001).
With regard to AN, only a few controlled treatment studies have been conducted
to date. At this point, there is no empirical support for whether CBT should be
the treatment of choice for AN as well. However, clinical studies yield evidence
that CBT treatment leads to a substantial reduction of symptoms in the majority
of patients. As such, Fichter, Quadflieg, and Hedlund (2006) described the 12-year
course of patients with AN (N = 103) after inpatient cognitive behavioral treatment.
Accordingly, over 50% were free of any eating disorder.
Effectiveness studies for the evaluation of CBT usually refer to an investigation of
the treatment blocks described earlier. In the following sections, the three treatment
blocks (nutritional management, body image therapy, and stress management) will
be considered separately with regard to their (supposed) effectiveness.
Efficacy of Nutritional Management

A treatment study compared the effectiveness of nutritional management and stress
management in patients with BN (Laessle et al., 1991). Both treatment conditions
were administered in a group setting with 15 sessions per condition over a period of
3 months. Both treatment conditions resulted in a reduction of bulimic symptoms.
However, nutritional management resulted in a faster decrease of binge frequency
and a higher abstinence rate from binge eating (3 weeks after treatment beginning:
36.4% in the nutritional management condition vs. 15.4% in the stress management
condition; and posttreatment: 50% vs. 26.9%, respectively). At 1-year follow-up, the
binge abstinence rate was 56% in the nutritional management condition compared to
25% in the stress management condition. Hence, in BN a symptom-oriented approach
seems to have a better outcome than a more comprehensive approach. On the other
hand, a simplified behavior therapy focusing on nutritional counseling does not seem
to be sufficient for the treatment of BN (Fairburn et al., 1991). For AN, nutritional
management as a stand-alone intervention is not effective enough for such a serious
mental disorder. For instance, Pike et al. (2003) compared nutritional management
with CBT as an add-on to an inpatient treatment approach. CBT was much more
effective than nutritional management.
Efficacy of Mirror Exposure

The mirror exposure therapy described earlier has been evaluated as a treatment
component for BN in both the inpatient and outpatient setting, and can be consid-
ered a promising treatment strategy (Tuschen-Caffier et al., 2001). In women with
extreme shape and weight concerns, mirror exposure compared to a nondirective body
image treatment resulted in a significant improvement in body checking and avoid-
ance, weight and shape concerns, body dissatisfaction, and overall psychopathology
(Delinsky & G. T. Wilson, 2006). In line with the concept of habituation, one study
with a mixed sample of eating disordered patients showed a significant reduction
of negative emotions and cognitions over the course of a single mirror exposure
session (Vocks, Legenbauer, Wachter, Wucherer, & Kosfelder, 2007). Finally, Vocks,
Wachter, Wucherer, and Kosfelder (2008) assessed body-related emotions and cog-
nitions in eating disordered patients and a control group during an unguided mirror
exposure session both prior to and after a body image therapy session including
at least three sessions of guided mirror exposure. Results revealed that the extent
of negative body-related emotions and cognitions was significantly reduced in the
unguided post- compared to the unguided pre-mirror exposure session in the eating
disordered group, while emotions and cognitions remained stable in the control
group.
Further, Delinsky and D. M. Wilson (2010) found considerable decreases in distress
within and between exposure sessions in a BN case example with three repeated mirror
exposures. Moreover, Trentowska, Bender, and Tuschen-Caffier (2013) have shown
that subjective distress as well as negative cognitions and emotions improved during
four sessions of body image training with repeated mirror exposure in women
diagnosed with eating disorder not otherwise specified (EDNOS) and BN.
In sum, there is evidence that mirror exposure is a promising intervention for
the treatment of body dissatisfaction for individuals with subclinical eating symp-
tomatology (Delinsky & G. T. Wilson, 2006; Moreno-Dom ı́nguez et al., 2012),
binge-eating disorder (Hilbert & Tuschen-Caffier, 2004; Hilbert, Tuschen-Caffier,
& Vögele, 2002), BN, and EDNOS (Trentowska et al., 2013; Vocks et al., 2007;
Vocks et al., 2008). By contrast, studies testing the effects of mirror exposure in AN
are scarce. In fact, disregarding studies which included extremely small samples of
AN patients and thus could not make evaluations in this subsample only (n < 6;
Vocks, et al., 2007; Vocks et al., 2008), to our knowledge only three studies so far
have tested the effects of body image therapy in AN. One study showed that body
image therapy with mirror exposure was significantly better with regard to reduction
of body dissatisfaction, body anxiety, and avoidance behaviors than standard body
image treatment with only one mirror exposure (Key et al., 2002). However, the
sample size in this study was very small (n = 6 for the standard treatment, n = 9
for the mirror exposure group). In addition, patients with AN were admitted to the
study only after weight restoration. Using exposure by videofeedback, another study
(Rushford & Ostermeyer, 1997) found that sensations of fatness and comparative
size responses decreased significantly over the course of body exposure. By contrast,
a recent fMRI study (Vocks et al., 2010) found an increase in the activity of the
extrastriate body area by body image therapy, but no pre-post differences were found
at the self-report level of the AN patients with regard to the cognitive affective
dimension towards one’s body. The authors interpreted the neural findings in terms
of a reduction of an avoidant information processing of body-related stimuli instigated
by the body image therapy. However, only a more direct measure of visual attention
during exposure to one’s body can give more insight into the role of attentional
processes in the maintenance and modification of body dissatisfaction in body image
therapy.
In summary, even though it seems promising, at present there is a lack of evidence
on the long-term effects of body image therapy using mirror exposure and/or other
confrontation methods (e.g., videofeedback). Furthermore, future research has yet
to reveal the underlying mechanisms of the effectiveness of mirror exposure. Mirror
exposure has been shown to trigger negative emotions toward one’s body that
gradually decrease during the course of repeated exposure (Tuschen-Caffier et al.,
2003), but it is still unclear whether this effect is a consequence of habituation or can
be explained by other mechanisms. Furthermore, because it is an integrative part of

a cognitive behavioral treatment approach, the specific rate of its effectiveness is yet
unclear, as effectiveness studies on its single contribution are still pending.
Efficacy of Stress Management Training

With regard to BN, empirical evidence suggests that interventions aiming exclusively
at an improvement of social competencies in the management of stress are less
effective than symptom-oriented approaches in the reduction of bulimic symptoms
(see Laessle et al., 1991). With regard to BN, the evidence suggests the superiority
of symptom-oriented treatment approaches over interpersonal therapy (Agras, Walsh,
Fairburn, Wilson, & Kraemer, 2000).
Concluding Remarks
Fundamental research and treatment studies have contributed to an empirical vali-

dation of assumptions with regard to the etiology and treatment concepts of eating
disorders. As such, plausible conceptualizations concerning the etiology and mainte-
nance of eating disorders have been developed and have been subjected to empirical
evaluation. Furthermore, therapeutic approaches have been developed that lead to a
remission or improvement of the disorder, thereby also reducing co-occurring and
long-term problems. Against the background of the empirical evidence, the National
Institute for Health and Care Excellence (2004) has developed guidelines for the
treatment of eating disorders, which should be considered as a guideline for health
professionals and individuals affected by eating disorders. Accordingly, psychotherapy
is the treatment of choice for both AN and BN. For BN, the therapeutic approach
should be cognitive behavioral. For AN, the evidence of treatment effectiveness is
rather scarce. While previous studies show that CBT is effective in the treatment of
AN, at this stage of research it is not possible to conclude that CBT is superior to
other therapeutic approaches.
References
Agras, W. S., Walsh, T., Fairburn, C. G., Wilson, G. T., & Kraemer, H. C. (2000). A
multicenter comparison of cognitive-behavioral therapy and interpersonal psychotherapy
for bulimia nervosa. Archives of General Psychiatry, 57 , 459–466.
Alpers, G. W., & Tuschen-Caffier, B. (2001). Negative feelings and the desire to eat in bulimia
nervosa. Eating Behavior, 2, 339–352.
American Psychiatric Association. (2006). Practice guideline for the treatment of patients with
eating disorders (rev.). New York, NY: America Psychiatric Association.
Arcelus, J., Mitchell, A. J., Wales, J., & Nielsen, S. (2011). Mortality rates in patients with
anorexia nervosa and other eating disorders. A meta-analysis of 36 studies. Archives of
Beck, J. S. (2011). Cognitive behavior therapy: Basics and beyond (2nd ed.). New York, NY:
Guilford Press.
Blechert, J., Ansorge, U., & Tuschen-Caffier, B. (2010). A body-related saccade task reveals
distinct attentional patterns for bulimia nervosa and anorexia nervosa. Journal of Abnormal
Blechert, J., Feige, B., Hajcak, G., & Tuschen-Caffier, B. (2010). To eat or not to eat:
Availability of food modulates the electrocortical response to food pictures in restraint
eaters. Appetite, 54, 262–268.
Blechert, J., Feige, B., Joos, A., Zeeck, A., & Tuschen-Caffier, B. (2011). Electrocortical
processing of food and emotional pictures in anorexia nervosa and bulimia nervosa.
Psychosomatic Medicine, 73, 415–421.
Blouin, A. G., Zuro, C., & Blouin, J. H. (1990). Family environment in bulimia nervosa: The
role of depression. International Journal of Eating Disorders, 9, 649–658.
Bulik, C. M., Sullivan, P. F., Tozzi, F., Furberg, H., Lichtenstein, P., & Pedersen, N. L.
(2006). Prevalence, heritability, and prospective risk factors for anorexia nervosa. Archives
Bulik, C. M., Tozzi, F., Anderson, C., Mazzeo, S. E., Aggen, S., & Sullivan, P. F. (2003). The
relation between eating disorders and components of perfectionism. American Journal of
Button, E. J., Loan, P., Davies, J., & Sonuga-Barke, E. J. (1997). Self-esteem, eating problems,
and psychological well-being in a cohort of schoolgirls aged 15–16: A questionnaire and
interview study. International Journal of Eating Disorders, 21, 39–47.
Byely, L., Archibald, A. B., Graber, J., & Brooks-Gunn, J. (2000). A prospective study of
familial and social influences on girls’ body image and dieting. International Journal of
Eating Disorders, 28, 155–164.
Campbell-Sills, L., & Barlow, D. H. (2006). Incorporating emotion regulation into conceptu-
alizations and treatments of anxiety and mood disorders. In J. J. Gross (Ed.), Handbook
of emotion regulation (pp. 542–559). New York, NY: Guilford Press.
Cash, T. F., & Deagle, E. A., III, (1997). The nature and extent of body-image disturbances
in anorexia nervosa and bulimia nervosa: A meta-analysis. International Journal of Eating
Disorders, 22, 107–125.
Cash, T. F., & Pruzinsky, T. (Eds.). (2004). Body image. A handbook of theory, research, and
clinical practice. New York, NY: Guilford Press.
Cassin, S. E., & von Ranson, K. M. (2005). Personality and eating disorders: A decade in
review. Clinical Psychology Review, 25, 895–916.
Cattanach, L., Malley, R., & Rodin, J. (1988). Psychologic and physiologic reactivity to
stressors in eating disordered individuals. Psychosomatic Medicine, 50, 591–599.
Cools, J., Schotte, D. E., & McNally, R. J. (1992). Emotional arousal and overeating in
restrained eaters. Journal of Abnormal Psychology, 101, 348–351.
Cooper, P. J., & Fairburn, C. G. (1993). Confusion over the core psychopathology of bulimia
nervosa. International Journal of Eating Disorders, 13, 385–389.
Crisp, A. H., Hall, A., & Holland, A. J. (1985). Nature and nurture in anorexia nervosa:
A study of 34 pairs of twins, one pair of triplets, and an adoptive family. International
Journal of Eating Disorders, 4, 5–27.
Crow, S. J., Peterson, C. B., Swanson, S. A., Raymond, N. C., Specker, S., Eckert, E. D., &
Mitchell, J. E. (2009). Increased mortality in bulimia nervosa and other eating disorders.
Delinsky, S. S., & Wilson, D. M. (2010). Cognitive behavior therapy with body image exposure
for bulimia nervosa: A case example. Cognitive and Behavioral Practice, 17 , 270–277.
Delinsky, S. S., & Wilson, G. T. (2006). Mirror exposure for the treatment of body image
disturbance. International Journal of Eating Disorders, 39, 108–116.
DiMarco, I. D., Klein, D. A., Clark, V. L., & Wilson, G. T. (2009). The use of motivational
interviewing techniques to enhance the efficacy of guided self-help behavioral weight loss
treatment. Eating Behaviors, 10, 134–136.
Fairburn, C. G. (1993). Interpersonal psychotherapy for bulimia nervosa. In G. L. Klerman &
M. M. Weissman (Eds.), New applications of interpersonal psychotherapy (pp. 353–378).
Washington, DC: American Psychiatric Association.
Fairburn, C. G., Cooper, Z., & Shafran, R. (2003). Cognitive behaviour therapy for eating
disorders: A “transdiagnostic” theory and treatment. Behavior Research and Therapy, 41,
509–528.
Fairburn, C. G., Cowen, P. J., & Harrison, P. J. (1999). Twin studies and the etiology of
eating disorders. International Journal of Eating Disorders, 26, 349–358.
Fairburn, C. G., Jones, R., Peveler, R. C., Carr, S. J., Solomon, R. A., O’Connor, M. E., …
Hope, R. A. (1991). Three psychological treatments for bulimia nervosa. A comparative
Fairburn, C. G., Marcus, M. D., & Wilson, G. T. (Eds.). (1993). Cognitive-behavioral therapy
for binge eating and bulimia nervosa: A comprehensive treatment manual. New York, NY:
Guilford Press.
Fairburn, C. G., Shafran, R., & Cooper, Z. (1999). A cognitive behavioural theory of anorexia
nervosa. Behaviour Research and Therapy, 37 , 1–13.
Fairburn, C. G., Welch, S. L., Doll, H. A., Davies, B. A., & O’Connor, M. E. (1997). Risk
factors for bulimia nervosa. A community-based case–control study. Archives of General
Fichter, M. M., & Noegel, R. (1990). Concordance for bulimia nervosa in twins. International
Fichter, M. M., & Quadflieg, N. (2004). Twelve-year course and outcome of bulimia nervosa.
Fichter, M. M., Quadflieg, N., & Hedlund, S. (2006). Twelve-year course and outcome
predictors of anorexia nervosa. International Journal of Eating Disorders, 39, 87–100.
Franzen, S., & Florin, I. (1995). Familial transmission of restrained eating. Zeitschrift für
Klinische Psychologie, 24, 65–69.
Green, K. L., Cameron, R., Polivy, J., Cooper, K., Liu, L., Leiter, L., & Heatherton, T. (1997).
Weight dissatisfaction and weight loss attempts among Canadian adults. Canadian Heart
Health Surveys Research Group. Canadian Medical Association Journal, 157 (Suppl. 1),
S17–25.
Griffiths, J. A., & McCabe, M. (2000). The influence of significant others on disordered eating
and body dissatisfaction among early adolescent girls. European Eating Disorders Review,
8, 301–314.
Guyot, G. W., Fairchild, L., & Hill, M. (1981). Physical fitness, sport participation, body build,
and self-concept of elementary school children. International Journal of Sport Psychology,
12, 105–116.
Haedt-Matt, A. A., & Keel, P. K. (2011). Revisiting the affect regulation model of binge
eating: A meta-analysis of studies using ecological momentary assessment. Psychological
Bulletin, 137 , 660–681.
Hawkins, R. C., Turell, S., & Jackson, L. J. (1983). Desirable and undesirable masculine and
feminine traits in relation to students’ dieting tendencies and body image dissatisfaction.
Sex Roles, 9, 705–718.
Heatherton, T. F., & Baumeister, R. F. (1991). Binge eating as escape from self-awareness.
Heatherton, T. F., & Polivy, J. (1992). Chronic dieting and eating disorders: A spiral model. In
J. H. Crowther, D. Tennenbaum, S. E. Hobfoll, & M. A. P. Stephens (Eds.), The etiology
of bulimia nervosa: The individual and familial context (pp. 133–155). Washington, DC:
Hemisphere Publishing Corp.
Herman, C. P., & Mack, D. (1975). Restrained and unrestrained eating. Journal of Personality,
43, 647–660.
Herzog, D. B., Greenwood, D. N., Dorer, D. J., Flores, A. T., Ekeblad, E. R., Richards, A.,
… Keller, M. B. (2000). Mortality in eating disorders: A descriptive study. International
Hewig, J., Cooper, S., Trippe, R. H., Hecht, H., Straube, T., & Miltner, W. H. (2008). Drive
for thinness and attention toward specific body parts in a nonclinical sample. Psychosomatic
Medicine, 70, 729–736.
Hilbert, A., & Tuschen-Caffier, B. (2004). Body image interventions in cognitive-behavioural
therapy of binge-eating disorder: A component analysis. Behaviour Research and Therapy,
42, 1325–1339.
Hilbert, A., & Tuschen-Caffier, B. (2007). Maintenance of binge eating through nega-
tive mood: A naturalistic comparison of binge eating disorder and bulimia nervosa.
International Journal of Eating Disorders, 40, 521–530.
Hilbert, A., Tuschen-Caffier, B., & Vögele, C. (2002). Effects of prolonged and repeated body
image exposure in binge-eating disorder. Journal of Psychosomatic Research, 52, 137–144.
Holland, A. J., Sicotte, N., & Treasure, J. L. (1988). Anorexia nervosa: Evidence for a genetic
basis. Journal of Psychosomatic Research, 32, 561–571.
Jacobi, C., Hayward, C., de Zwaan, M., Kraemer, H. C., & Agras, W. S. (2004). Coming to
terms with risk factors for eating disorders: Application of risk terminology and suggestions
for a general taxonomy. Psychological Bulletin, 130, 19–65.
Jansen, A. (1994). The learned nature of binge eating. In C. R. Legg & D. A. Booth (Eds.),
Appetite: Neural and behavioural bases (pp. 193–211). New York, NY: Oxford University
Press.
Jansen, A. (1996). How restrained eaters perceive the amount they eat. British Journal of
Jansen, A., Nederkoorn, C., & Mulkens, S. (2005). Selective visual attention for ugly and
beautiful body parts in eating disorders. Behaviour Research and Therapy, 43, 183–196.
Keel, P. K., & Klump, K. L. (2003). Are eating disorders culture-bound syndromes? Implica-
tions for conceptualizing their etiology. Psychological Bulletin, 129, 747–769.
Keel, P. K., Mitchell, J. E., Miller, K. B., Davis, T. L., & Crow, S. J. (1999). Long-term
outcome of bulimia nervosa. Archives of General Psychiatry, 56, 63–69.
Kendler, K. S., MacLean, C., Neale, M., Kessler, R., Heath, A., & Eaves, L. (1991). The genetic
epidemiology of bulimia nervosa. American Journal of Psychiatry, 148, 1627–1637.
Key, A., George, C. L., Beattie, D., Stammers, K., Lacey, H., & Waller, G. (2002). Body image
treatment within an inpatient program for anorexia nervosa: The role of mirror exposure
in the desensitization process. International Journal of Eating Disorders, 31, 185–190.
Klump, K. L., Wonderlich, S., Lehoux, P., Lilenfeld, L. R., & Bulik, C. M. (2002). Does envi-
ronment matter? A review of nonshared environment and eating disorders. International
Laessle, R. G., Beumont, P. J., Butow, P., Lennerts, W., O’Connor, M., Pirke, K. M., …
Waadt, S. (1991). A comparison of nutritional management with stress management in
the treatment of bulimia nervosa. British Journal of Psychiatry, 159, 250–261.
LeGoff, D. B., Leichner, P., & Spigelman, M. N. (1988). Salivary response to olfactory food
stimuli in anorexics and bulimics. Appetite, 11, 15–25.
Mauler, B. I., Hamm, A. O., Weike, A. I., & Tuschen-Caffier, B. (2006). Affect regulation and
food intake in bulimia nervosa: Emotional responding to food cues after deprivation and
subsequent eating. Journal of Abnormal Psychology, 115, 567–579.
McClelland, L., Mynors-Wallis, L., Fahy, T., & Treasure, J. (1991). Sexual abuse, disordered
personality and eating disorders. British Journal of Psychiatry, Suppl. 10, 63–68.
Mills, J. S., & Palandra, A. (2008). Perceived caloric content of a preload and disinhibition
among restrained eaters. Appetite, 50, 240–245.
Mitchell, J. E., Hatsukami, D., Eckert, E. D., & Pyle, R. L. (1985). Characteristics of 275
patients with bulimia. American Journal of Psychiatry, 142, 482–485.
Moreno-Dom ı́nguez, S., Rodr ı́guez-Ruiz, S., Fernández-Santaella, M. C., Jansen, A., &
Tuschen-Caffier, B. (2012). Pure versus guided mirror exposure to reduce body dissatis-
faction: A preliminary study with university women. Body Image, 9, 285–288.
Murray, C., Waller, G., & Legg, C. (2000). Family dysfunction and bulimic psychopathol-
ogy: The mediating role of shame. International Journal of Eating Disorders, 28,
84–89.
National Institute for Health and Care Excellence. (2004). CG9 Eating disorders: NICE
guideline. Retrieved from http://www.nice.org.uk/CG009NICEguideline
Ogden, J., & Steward, J. (2000). The role of the mother–daughter relationship in explaining
weight concern. International Journal of Eating Disorders, 28, 78–83.
Palmer, R. L., Chaloner, D. A., & Oppenheimer, R. (1992). Childhood sexual experiences
with adults reported by female psychiatric patients. British Journal of Psychiatry, 160,
261–265.
Patton, G. C., Johnson-Sabine, E., Wood, K., Mann, A. H., & Wakeling, A. (1990). Abnormal
eating attitudes in London school girls: A prospective epidemiological study: Outcome at
twelve month follow-up. Psychological Medicine, 20, 383–394.
Pike, K. M., & Rodin, J. (1991). Mothers, daughters, and disordered eating. Journal of
Pike, K. M., Walsh, B. T., Vitousek, K., Wilson, G. T., & Bauer, J. (2003). Cognitive behavior
therapy in the posthospitalization treatment of anorexia nervosa. American Journal of
Psychiatry, 160, 2046–2049.
Pope, H. G., Jr., & Hudson, J. I. (1992). Is childhood sexual abuse a risk factor for bulimia
nervosa? American Journal of Psychiatry, 149, 455–463.
Pope, H. G., Jr., Mangweth, B., Negrao, A. B., Hudson, J. I., & Cordas, T. A. (1994).
Childhood sexual abuse and bulimia nervosa: A comparison of American, Austrian, and
Brazilian women. American Journal of Psychiatry, 151, 732–737.
Power, M. L., & Schulkin, J. (2008). Anticipatory physiological regulation in feeding biology:
Cephalic phase responses. Appetite, 50, 194–206.
Powley, T. L., & Berthoud, H. R. (1985). Diet and cephalic phase insulin responses. American
Journal of Clinical Nutrition, 42, 991–1002.
Rieger, E., Schotte, D. E., Touyz, S. W., Beumont, P. J., Griffiths, R., & Russell, J. (1998).
Attentional biases in eating disorders: A visual probe detection procedure. International
Rodin, J., Silberstein, L., & Striegel-Moore, R. (1984). Women and weight: A normative
discontent. Nebraska Symposium on Motivation, 32, 267–307.
Rosen, J. C. (1997). Cognitive behavioral body image therapy. In D. M. Garner & P.
Garfinkel (Eds.), Handbook of treatment for eating disorders (pp. 188–201). New York,
NY: Guilford Press.
Roty, M., Yager, J., & Rossotto, E. (1994). Childhood sexual, physical, and psychological abuse
and their relationship to comorbid psychopathology in bulimia nervosa. International
Rushford, N., & Ostermeyer, A. (1997). Body image disturbances and their change with
videofeedback in anorexia nervosa. Behaviour Research and Therapy, 35, 389–398.
Schotte, D. E., Cools, J., & McNally, R. J. (1990). Film-induced negative affect triggers
overeating in restrained eaters. Journal of Abnormal Psychology, 99, 317–320.
Shafran, R., Lee, M., Cooper, Z., Palmer, R. L., & Fairburn, C. G. (2007). Attentional bias in
eating disorders. International Journal of Eating Disorders, 40, 369–380.
Shisslak, C. M., Crago, M., Renger, R., & Clark-Wagner, A. (1998). Self-esteem and the
prevention of eating disorders. Eating Disorders: The Journal of Treatment & Prevention,
6, 105–118.
Stice, E. (2001). Risk factors for eating pathology: Recent advances and future directions. In
R. H. Striegel-Moore & L. Smolak (Eds.), Eating disorders: Innovative directions in
research and practice (pp. 51–73). Washington, DC: American Psychological
Association.
Striegel-Moore, R. H., Garvin, V., Dohm, F. A., & Rosenheck, R. A. (1999). Eating disorders
in a national sample of hospitalized female and male veterans: Detection rates and
psychiatric comorbidity. International Journal of Eating Disorders, 25, 405–414.
Striegel-Moore, R. H., Silberstein, L. R., & Rodin, J. (1986). Toward an understanding of risk
factors for bulimia. American Psychologist, 41, 246–263.
Strober, M., Freeman, R., Lampert, C., Diamond, J., & Kaye, W. (2000). Controlled family
study of anorexia nervosa and bulimia nervosa: Evidence of shared liability and transmission
of partial syndromes. American Journal of Psychiatry, 157 , 393–401.
Svaldi, J., Griepenstroh, J., Tuschen-Caffier, B., & Ehring, T. (2012). Emotion regulation
deficits in eating disorders: A marker of eating pathology or general psychopathology?
Psychiatry Research, 197 , 103–111.
Tata, P., Fox, J., & Cooper, J. (2001). An investigation into the influence of gender and
parenting styles on excessive exercise and disordered eating. European Eating Disorders
Review, 9, 194–206.
Thelen, M. H., Powell, A. L., Lawrence, C., & Kuhnert, M. E. (1992). Eating and body image
concerns among children. Journal of Clinical Child Psychology, 21, 41–46.
Trentowska, M., Bender, C., & Tuschen-Caffier, B. (2013). Mirror exposure in women with
bulimic symptoms: How do thoughts and emotions change in body image treatment?
Tuschen-Caffier, B., Pook, M., & Frank, M. (2001). Evaluation of manual-based cognitive-
behavioral therapy for bulimia nervosa in a service setting. Behaviour Research and Therapy,
39, 299–308.
Tuschen-Caffier, B., & Vögele, C. (1999). Psychological and physiological reactivity to stress:
An experimental study on bulimic patients, restrained eaters and controls. Psychotherapy
and Psychosomatics, 68, 333–340.
Tuschen-Caffier, B., Vögele, C., Bracht, S., & Hilbert, A. (2003). Psychological responses to
body shape exposure in patients with bulimia nervosa. Behaviour Research and Therapy,
41, 573–586.
Vitousek, K. B., & Hollon, S. D. (1990). The investigation of schematic content and processing
in eating disorders. Cognitive Therapy and Research, 14, 191–214.
Vocks, S., Busch, M., Schulte, D., Gronermeyer, D., Herpertz, S., & Suchan, B. (2010).
Effects of body image therapy on the activation of the extrastriate body area in anorexia
nervosa: An fMRI study. Psychiatry Research, 183, 114–118.
Vocks, S., Legenbauer, T., Wachter, A., Wucherer, M., & Kosfelder, J. (2007). What happens
in the course of body exposure? Emotional, cognitive, and physiological reactions to
mirror confrontation in eating disorders. Journal of Psychosomatic Research, 62, 231–239.
Vocks, S., Wachter, A., Wucherer, M., & Kosfelder, J. (2008). Look at yourself: Can body
image therapy affect the cognitive and emotional response to seeing oneself in the mirror
in eating disorders? European Eating Disorders Review, 16, 147–154.
Walsh, B. T., Wilson, G. T., Loeb, K. L., Devlin, M. J., Pike, K. M., Roose, S. P., … Waternaux,
C. (1997). Medication and psychotherapy in the treatment of bulimia nervosa. American
Welch, S. L., & Fairburn, C. G. (1994). Sexual abuse and bulimia nervosa: Three integrated
case control comparisons. American Journal of Psychiatry, 151, 402–407.
Welch, S. L., & Fairburn, C. G. (1996). Childhood sexual and physical abuse as risk factors for
the development of bulimia nervosa: A community-based case control study. Child Abuse
and Neglect, 20, 633–642.
Whittal, M. L., Agras, W. S., & Gould, R. A. (1999). Bulimia nervosa: A meta-analysis of
psychosocial and pharmacological treatments. Behavior Therapy, 30, 117–135.
Williams, G. J., Power, K. G., Millar, H. R., Freeman, C. P., Yellowlees, A., Dowds, T., …
Jackson, M. A. (1993). Comparison of eating disorders and other dietary/weight groups
on measures of perceived control, assertiveness, self-esteem, and self-directed hostility.
Williamson, D. A., White, M. A., York-Crowe, E., & Stewart, T. M. (2004). Cognitive-
behavioral theories of eating disorders. Behavior Modification, 28, 711–738.
Wilson, G. T., & Fairburn, C. G. (2002). Treatments for eating disorders. In P. E. Nathan
& J. M. Gorman (Eds.), A guide to treatments that work (2nd ed., pp. 559–592). New
Wilson, G. T., Fairburn, C. C., Agras, W. S., Walsh, B. T., & Kraemer, H. (2002). Cognitive-
behavioral therapy for bulimia nervosa: Time course and mechanisms of change. Journal
Wilson, G. T., Loeb, K. L., Walsh, B. T., Labouvie, E., Petkova, E., Liu, X., & Waternaux, C.
(1999). Psychological versus pharmacological treatments of bulimia nervosa: Predictors
and processes of change. Journal of Consulting and Clinical Psychology, 67 , 451–459.
26
Obesity
Simone Munsch
Fribourg University, Switzerland
Anita Jansen
University of Maastricht, The Netherlands
Introduction
Obesity, defined as a body mass index (BMI) equal to or greater than 30 kg/m2 , is
a major health problem that is increasing dramatically worldwide. Obesity is health-
threatening and brings about high medical costs and significant productivity losses as
a result of increased sick leave (Neovius, Neovius, Kark, & Rasmussen, 2010).
The ultimate cause of obesity, or excess body fat, is calorie intake exceeding
calorie output. Although it is quite easy to overeat and gain weight, it is extremely
difficult to reduce intake and lower body weight. Current knowledge about obesity
predominantly comes from biomedical, epidemiological, and public health studies and
recently also from the cognitive neuroscience field. Despite all this knowledge, long-
term effective treatments for obesity are not available, except for bariatric surgery.
Surgery is, however, risky (complications), invasive, and mostly irreversible, and
leads to inescapable lifelong abnormal eating. Hence there is a need for noninvasive
treatments that are effective in the long run. Genetic vulnerability is frequently used
as an argument against cognitive behavioral interventions. However, there are many
examples of genetically vulnerable people improving from cognitive behavioral therapy
(CBT); for example, individuals suffering from depression and anxiety disorders or
from conditions such as phenylketonuria, where sustained behavior change in terms
of dieting is maximally effective. The genetic contribution to obesity is mainly related
to the regulation of eating behavior. The most likely successful therapy for obesity
therefore targets pathways of the regulation of food intake.
In the present chapter an overview is given of the psychological mechanisms and
individual differences that determine food intake and body weight. Until now, psycho-
logical interventions to lose body weight—and to maintain this weight loss—have
been only partially successful. One of the claims in the present chapter is that

DOI: 10.1002/9781118528563.wbcbt26
obesity is predominantly a behavioral problem and that insights from clinical psy-
chology could contribute to the development of more effective interventions for
obesity.
Epidemiology, Phenomenology, and Etiology of Obesity
Epidemiology and Phenomenology

According to the World Health Organization (WHO, 2006), overweight and obesity
are among the most important problems of the twenty-first century. Worldwide,
about 23.2% of adults and 10% of children suffer from overweight, whereas 9.8% and
2.3% of all adults and children are obese (Kelly, Yang, Chen, Reynolds, & He, 2008).
In some Western countries overweight is more common than a healthy weight: in
the United States 67% of adults are overweight, of which 34% are obese. For the
United Kingdom these figures are 61% and 23% respectively. In Germany 67% of
adults are overweight and 13% of these are obese, and in the Netherlands 42% are
overweight, of which 10% are obese. In particular, overweight and obesity in children
is increasing: Between 1980 and 2010 child overweight in the Netherlands more
than doubled (from 6 to 14%), while prevalence rates of child obesity in Germany,
Austria, and Switzerland vary between 4 and 6.3%. The various health consequences
such as diabetes, correlates of coronary heart disease, or sleep disorders may already
be present during childhood. A major problem with early onset obesity is its strong
tendency to persist into adulthood (Lavie, Milani, & Ventura, 2009; WHO, 2006,
2009). In addition, psychological problems and in particular the prevalence of binge
eating disorder (BED) are significantly increased in obese children compared to
normal weight children (Tanofsky-Kraff et al., 2011). Although lay people often
stereotypically associate fatness with jolliness (e.g., Crisp & McGuiness, 1976), recent
epidemiological and treatment studies show the opposite: Overweight and obese
individuals are at increased risk of depression compared to normal weight people (see
A. Jansen, Havermans, Nederkoorn, & Roefs, 2008). A recent meta-analysis of 13
cross-sectional general population surveys including more than 60,000 participants
shows a modest but significant association between overweight/obesity and major
depressive disorder according to the DSM-IV diagnostic criteria (Scott et al., 2007). A
general and consensual finding is that in particular the obese suffering from BED show
an increased chance of being depressed, compared to the non-eating-disordered obese
(Dingemans, Bruna, & van Furth, 2002). In obese adults, BED prevalence is twice
as high compared to normal weight populations (Hudson, Hiripi, Pope, & Kessler,
2007). We should, however, note that mental health symptoms like depression might
be a consequence of the multiple somatic complaints of the obese. In sum, there is an
association between obesity in adulthood and mental disorders, but this association
might be due to the multiple somatic complaints associated with excessive body
weight (Baumeister & Härter, 2008).
Overweight and obesity are defined by an excess of the amount of body fat, which
is usually determined by using the BMI. The BMI correlates with the amount of
body fat. A higher BMI is associated with an increase in morbidity and mortality rate
Obesity 595
(WHO, 2009). Overweight and obesity are classified into different classes representing
increasing risk for various health consequences:
• BMI 18.5–24.9 kg/m2 : normal weight

• BMI 25–29.9 kg/m2 : overweight
• BMI 30–34.9 kg/m2 : obesity class I
• BMI 35.0–39.9 kg/m2 : obesity class II
• BMI >40 kg/m2 : extreme obesity, class III
A clear indication for treatment is given in individuals with a BMI over 30. If risk
factors such as abdominal fat distribution, hypercholesterolemia, diabetes, hypertonia,
and significant psychological suffering are given at present, treatment in overweight
(BMI 25–29.9 kg/m2 ) individuals is required (see also guidelines of the National
Heart Lung and Blood Institute, 2012).
Etiology
Overweight and obesity result from an ongoing positive energy balance due to
an excess of energy intake compared to energy use (Westerterp, 1993). Besides a
genetic predisposition, psychological, sociocultural, and environmental factors act as
determinants for energy intake and expenditure. To enhance prevention and treatment
effects it is especially important to identify the psychological factors contributing to
the maintenance of overweight and obesity.
Biological factors. Twin and adoption studies underline the importance of biological
factors, as approximately two-thirds of the variability in body weight is probably due
to genetic factors (Bouchard, 2007; Ravussin & Bogardus, 2000). Genetic factors
include alleles fostering the storing of energy in times when food is scarce (“thrifty
genotype”; Neel, Weder, & Julius, 1998). These alleles represent evolutionary mean-
ingful mechanisms but in today’s obesogenic environment they turn out to act as
genetically driven risk factors for certain individuals. Further maternal weight regu-
lation during the prenatal phase and an early obesity rebound between the ages of
4 and 6 represent genetically determined vulnerable phases for the development and
maintenance of overweight and obesity (Hebebrand, Sommerlad, Geller, Görg, &
Hinney, 2001).
However, the largest part of inherited body weight variability is supposed to
operate through effects on appetite-related traits. Specifically sensitivity to food cues
and experienced food reward show heritable influence (Wardle, Carnell, Haworth,
& Plomin, 2008). In recent years there have been substantial efforts to identify
specific candidate genes for obesity. Two appetitive phenotypes appear to be related
to obesity (Wardle & Carnell, 2009; Wardle et al., 2008): a phenotype that shows
decreased sensitivity to internal satiety cues, and a phenotype that is highly responsive
to external food cues. One of the most important candidates is the FTO-gene
(fat mass and obesity associated gene). People with the FTO-gene (AA alleles)
typically show difficulty in stopping or down-regulating eating. They are called
the “satiety insensitive phenotype” (Wardle et al., 2008). Genome-wide association
studies (GWAS) corroborate the existence of 32 loci altogether. These alleles explain
1.5% of the BMI variance, while 0.34% of the variance is explained by the FTO-gene.
The other phenotype is hyper-responsive to food cues. This phenotype is sensitive to
the rewarding effects of foods that are mediated by brain dopamine levels and typically
up-regulates intake with palatable food.
Although 67% of the variability in BMI is supposed to be genetically based, only
12% of genetic predisposition is related to metabolic rate. The largest part of inherited
body weight variability, about 40%, is thought to operate through effects on appetite-
related traits (Ravussin & Bogardus, 2000; Wardle & Carnell, 2009). The effects of
currently identified genes thus are marginal (Speliotes et al., 2010) and it was therefore
concluded by Ravussin and Bogardus (2000) that “the most likely successful therapy
for obesity may target pathways of the regulation of food intake” (p. 17).
Environmental factors: nutrition, eating style, and physical activity. Even though
there is a considerable genetically driven biological control of energy intake and body
weight, up to 40% of the variance of body weight is associated with environmental
factors such as nutritional habits, eating style, and physical activity patterns (Herpertz
et al., 2003). The worldwide increase in overweight and obesity prevalence rates is
associated with drastic changes in nutritional and physical activity habits during the
last 50 years. In today’s modern world, regular physical activity is no longer necessary
for survival and large amounts of palatable foods are always easily accessible for a
huge part of the population (Martinez-Gonzalez, Martinez, Hu, Gibney, & Kearney,
1999; Rolls, Roe, Beach, & Kris-Etherton, 2005).
Psychological factors: emotion and impulse regulation, and cognitive factors. The devel-
opment and maintenance of obesity is significantly influenced by psychological factors
such as deficient impulse and emotion regulation capacities. Several prospective stud-
ies reveal an association between depressive symptoms, oppositional defiant disorders,
and overweight or obesity (Goodman & Whitaker, 2002; Peisah, Brodaty, Lus-
combe, & Anstey, 2005; Pine, Goldstein, Wolk, & Weissman, 2001). In a cohort
study, depressive symptoms in 17-year-old adolescents were predictive for an increase
of body weight during the next 10 years (Hasler et al., 2004). Another recent
meta-analysis based on longitudinal studies found a bidirectional association between
depression and obesity. Clinically relevant depression predicted obesity, and depres-
sion influenced the development of obesity. These associations were most relevant for
Americans but were also found in samples from Europe (Luppino et al., 2010).
Psychological problems may have detrimental consequences for obese persons,
especially in childhood. Consequently, psychological well-being should be routinely
assessed in obese youth and adult patients. Table 26.1 summarizes instruments that
allow the identification of correlates of clinically significant mental health problems,
and BED in particular.
Emotion and impulse regulation. The obesogenic environment continuously exposes

individuals to a variety of palatable, calorie-dense food. This exposure likely promotes
food intake unrelated to hunger, but related to immediate conditions in certain
individuals (Stice, Spoor, Ng, & Zald, 2009). Personality characteristics such as
Table 26.1 Assessment of Eating Behavior and Mental Health
Instrument Age Construct
Eating Disorder Examination for Children 8–14 years 36 items, 4 subscales: restraint, eating concern,
(ChEDE; Bryant-Waugh, Cooper, Taylor, weight concern, shape concern; DSM-IV
& Lask, 1996) eating disorder diagnosis
Eating Disorder Examination-Questionnaire 12–14 years 28 items, 4 subscales: restraint, eating concern,
for Children (ChEDE-Q; TODAY Study weight concern, shape concern; measures
Group, 2007) diagnostic features of eating disorders
Schedule of Affective Disorders and 6–18 years Past and present DSM-IV mental disorders
Schizophrenia for School-age
Children—Present and Lifetime Version
(K-SADS-PL; Kaufman et al., 1997;
K-SADS; Puig-Antich & Chambers, 1978)
Eating in the Absence of Hunger for Children 6–19 years 14 items, 3 subscales: negative affect, external
and Adolescents (EAH-C; Tanofsky-Kraff, eating, fatigue/boredom; measures the
Ranzenhofer, et al., 2008) frequency of eating when one is not hungry
Eating Disorder Examination (EDE; Fairburn,
2008)
Eating Disorder Examination-Questionnaire 28 items, 4 scales: restraint scale, eating
(EDE-Q; Fairburn & Beglin, 1994) concern scale, weight concern scale, shape
concern scale
Basic Symptom Inventory (BSI; Derogatis, 53 items, 9 subscales, 3 global indexes
1993)
Instrument Age Construct
Symptom Checklist-90-Revised (SCL-90-R; 9 primary symptom dimensions: Somatization

Derogatis & Unger, 2010) (SOM), Obsessive-Compulsive (OBS),
Interpersonal Sensitivity (INT), Depression
(DEP), Anxiety (ANX), Hostility (HOS),
Phobic Anxiety (PHOB), Paranoid Ideation
(PAR), Psychoticism (PSY)
3 summary scores: Global Severity Index
(GSI), Positive Symptom Distress Index
(PSDI), Positive Symptom Total (PST)
Children’s Eating Behaviour Questionnaire 2–13 years 35 items, 8 scales: food responsiveness,
(CEBQ; Wardle, Guthrie, Sanderson, & enjoyment of food, emotional overeating,
Rapoport, 2001) desire to drink, satiety responsiveness,
slowness in eating, emotional undereating,
fussiness
Child Behavior Checklist (CBCL; Achenbach, 6–18 years 20 competence items and 118 items on
1991) behavior or emotional problems; measures
parent reports of children’s behavioral
problems and social competencies
Obesity 599
response inhibition abilities and reward sensitivity might determine one’s responses
to the abundance of food in contemporary societies. Obesity is associated with
insufficient inhibitory control and increased reward sensitivity (Nederkoorn, Braet,
Van Eijs, Tanghe, & Jansen, 2006; Nederkoorn, Smulders, Havermans, Roefs,
& Jansen, 2006). Response inhibition refers to the ability to overrule automatic
intentions to respond to (mostly tempting) stimuli. Studies using the Stop Signal
Task to measure one’s ability to inhibit show a clear difference between obese and
lean participants: Obese children and adults are less capable in stopping responses
than lean children and adults (A. Jansen et al., 2009; Nederkoorn, Braet, et al., 2006;
Nederkoorn, Smulders, et al., 2006). Reward sensitivity refers to an increased need
for large and quick rewards. Obese children and adults are more sensitive to rewards
than lean children and adults; for example, they gamble longer for rewards even
when this ends up in losses (Appelhans, 2009; Franken & Muris, 2005; Nederkoorn,
Smulders, et al., 2006).
Increased reward sensitivity and insufficient inhibitory control have been proposed
as a common pathway of attention-deficit/hyperactivity disorder (ADHD), obesity,
and BED, which may also explain the increased co-occurrence of ADHD and
obesity (Pagoto et al., 2009). Temperament characteristics such as decreased response
inhibition and increased reward sensitivity (sometimes referred to as impulsivity)
induce overeating (Guerrieri, Nederkoorn, Schrooten, Martijn, & Jansen, 2009;
Guerrieri et al., 2007) and may moderate the influence of negative affect on eating
behavior in obese individuals (Solanto et al., 2001; Stice et al., 2009).
Impulsivity might hinder treatment. In a sample of obese children (aged 8 to 12
years) treated with CBT, it appeared that BMI and impulsivity were correlated: Within
the obese sample the most obese children were the most impulsive ones (Nederkoorn,
Braet, et al., 2006). These most impulsive children lost the least amount of weight
during treatment (Nederkoorn, Jansen, Mulkens, & Jansen, 2007).
Another important and interconnected factor regarding the regulation of food
intake concerns emotion regulation. Responses to daily stressors depend on an
individual’s sensitivity toward emotions, the capability to correctly identify and
express emotions, and the ability to regulate one’s emotional response appropriately
(Gross, 2007; Haynos & Fruzzetti, 2011; Reicherts, Genoud, & Zimmermann,
2011). Difficulties with the regulation of emotions appear to be related to psy-
chopathology, as emotion regulation deficiencies are related to longer and more
severe periods of distress (Aldao, Nolen-Hoeksema, & Schweizer, 2010). Individuals
with poor emotion regulation capacities are further prone to turn to food to escape
or down-regulate their emotions, creating risk for excessive restriction or intake of
energy (Engler, Crowther, Dalton, & Sanftner, 2006; Munsch, Hasenboehler, &
Meyer, 2011; Munsch, Meyer, Quartier, & Wilhelm, 2011). In a laboratory study
it was found that an obese sample high in negative affect overate after negative
mood induction compared to an obese sample low in negative affect (A. Jansen,
Vanreyten, et al., 2008). A recent questionnaire-based study shows that obese
patients reveal difficulties in identifying and labeling emotions and rely more on
unhealthy strategies such as suppression compared to healthy controls. In particular
unhealthy emotion processing was associated with emotional eating (Zijlstra et al.,
2012).
Overall, impaired emotion and impulse regulation strategies seem to influence

energy intake. Future research should investigate the developmental trajectories of
emotion and impulse regulation deficits and focus on gender differences, as these fac-
tors might influence the efficacy of interventions focused on self-regulation capacities.
Obesity Treatment
It has been shown that a positive energy balance is responsible for the development
and maintenance of obesity. Consequently, current treatments include strategies
in order to change this energy balance by focusing on both energy intake and
physical activity behavior. In spite of substantial research efforts in the field of obesity
treatment, studies often do not indicate the strength of their treatment effects, and the
comparability of the efficacy of the different programs remains limited. The following
suggestions for effective treatment of obese adults are based on the guidelines of the
Cochrane Collaboration (Oude Luttikhuis et al., 2009) and the National Institute
for Health and Clinical Excellence (2012). Child-specific treatment suggestions are
discussed in the “Obesity in Childhood” section of this chapter.
Energy intake behavior. Interventions usually aim at a stepwise change toward a

calorie-reduced and balanced diet, even though different dietetic procedures seem
to result in similar effects regarding weight reduction. Current data regarding
interventions aiming at nutritional reduction are contradictory and reveal moderate
short-term efficacy. Initial weight reductions are usually reversed in the long
term. Further, these reductions might be statistically significant, but their clinical
significance is very modest.
Physical activity behavior. In order to lose weight, one’s amount of daily sedentary
behavior has to be reduced and the amount and frequency of physical activity have to
be increased. In general, 45–60 minutes of physical activity per day is recommended
in obese adults in order to foster weight reduction. For the maintenance of weight
losses, individuals are advised to be physically active for 90 minutes per day. An
increase of physical activity is associated with an increase of muscle mass and a
reduction of the health complications related to obesity (high blood pressure,
fasting serum glucose, etc.). Even though a substantial increase in physical activity is
needed, it should be kept in mind that only realistic, individually adapted goals foster
long-term behavioral change.
Psychological interventions. The aims of psychological interventions are twofold:

First, the interventions aim at changing eating behavior, and second, they intend
to induce behavior changes such as physical activity habits. Strategies focusing on
eating behavior foster a flexible and regular eating style and the relearning of hunger
and satiety regulation. Therefore, interventions such as self-monitoring, stimulus
control, motivational strategies, self-reinforcement, and cognitive techniques in order
to implement realistic goal setting are applied. Considering the chronic nature and
the high relapse rate of overweight and obesity, relapse prevention strategies such as
problem solving and stress management are also frequently taught.
Obesity 601
Efficacy of multimodular treatments. Multimodular treatments aiming at nutritional,

physical activity, and eating behavior changes are considered to be the most efficacious,
even though treatment effects are generally moderate, especially in the long term. The
most important issues for future research are the identification of reasons for early
dropout, low compliance, and attrition, as well as the identification of psychological
features associated with a negative or positive treatment course.
Setting (individual versus group treatment). Multimodular treatments in indi-

vidual and group settings are similarly efficacious. As the accessibility of treatments
needs to be increased, the efficacy and effectiveness of group settings and applications
such as Internet-based interventions, e-mailing, and the use of electronic devices
should be further investigated.
New Treatment Approaches

Emotion regulation. The effects of obesity treatments are moderate, and evidence
regarding their impact on psychological health is scarce. In eating disorders and other
mental disorders such as depression, anxiety, and somatoform disorders, there is some
evidence that additional treatment modules including emotion regulation strategies
can improve the effects of CBT programs (Berking et al., 2008). These interventions
provide training to improve the tolerance and acceptance of adverse emotional states
and to regulate negative emotions (Berking et al., 2008).
Further investigation is needed to establish whether specific training in impulse
regulation, such as the prevention of immediate reactions without premeditation
(inhibition training), and emotion regulation capacities, leads to enhanced treatment
effects in obese youth and adults.
Cognitive training. Given that CBT is one of the most effective treatment strategies
for many behavioral disorders, it seems likely that psychological treatment for obesity
will focus on CBT strategies (Carter & Jansen, 2012). However, results from a recent
CBT trial for weight loss and weight maintenance in obesity are disappointing (Cooper
et al., 2010). Some other studies, however, do suggest that a more intense focus on
cognitive interventions is needed for weight loss and weight loss maintenance (Stahre
& Hallstrom, 2005; Stahre, Tärnell, Håkanson, & Hällström, 2007; Werrij et al.,
2009). It has been suggested that cognitive restructuring might have a prophylactic
effect in helping to prevent relapse and maintain weight loss over the longer term
(Werrij et al., 2009).
Recent experimental pilot studies indicate that interventions aimed at the reduc-
tion of impulsive behaviors might be effective in the reduction of overeating. For
example, a training of inhibitory control was effective in the reduction of chocolate
intake (Houben & Jansen, 2011) and working memory training appeared to reduce
alcohol intake in problem drinkers (Houben, Wiers, & Jansen, 2011). Future studies
should find out whether new cognitive interventions that actually tackle maintain-
ing mechanisms—such as cognitive restructuring, training of inhibitory control, and
working memory training—are also effective in the long run, and can be implemented
in clinical practice.
Obesity in Childhood
Epidemiology and phenomenology. Obesity in childhood is an increasing worldwide
problem and children are becoming overweight and obese at a progressively younger
age (Ogden et al., 2006). Childhood overweight and obesity is not only known to
cause multiple health consequences but also shows a strong tendency to persist into
adulthood (Baker, Olsen, & Sørensen, 2007).
Moreover, obese children suffer from diverse psychological problems (Pitrou, Sho-
jaei, Wazana, Gilbert, & Kovess-Masfety, 2010; Roth, Munsch, Meyer, Isler, &
Schneider, 2008). These psychological problems encompass internalizing problems
(such as anxiety and depression, isolation and withdrawal) and externalizing problems
(such as hyperactivity, conduct problems, low self-esteem, and peer conflicts and
interaction problems) (Banis et al., 1988; Braet, Mervielde, & Vandereycken, 1997;
Drukker, Wojciechowski, Feron, Mengelers, & Van Os, 2009; Epstein, Klein, &
Wisniewski, 1994; Epstein, Myers, & Anderson, 1996; Lawlor et al., 2005; Lumeng,
Gannon, Cabral, Frank, & Zuckerman, 2003; Pitrou et al., 2010; Roth, Munsch,
Meyer, Winkler, et al., 2008; ter Bogt et al., 2006; Tershakovec, Weller, & Gallagher,
1994; Vila et al., 2004). Only a few studies used standardized diagnostic interviews
to assess mental disorders in obese children. Affective disorders, as well as anxiety
and conduct disorders and ADHD, were also frequently found (Mustillo et al.,
2003; Roth, Munsch, Meyer, Winkler, et al., 2008; Vila et al., 2004). It should be
noted that the degree of obesity is not systematically related to more psychological
problems, it is not systematically observed in all cross-sectional studies, and it is not
always independent of confounders such as socioeconomic status or lifestyle (Pitrou
et al., 2010). In general, the interrelatedness between weight gain and psycho-
logical problems might be bidirectional, in that clinically meaningful psychological
distress might foster weight gain and rapid weight gain may lead to psychosocial
problems.
The psychological consequences of obesity in childhood should be assessed as
carefully as the possible medical consequences. Besides self-report questionnaires such
as the Child Behavior Checklist (CBCL; Achenbach, 1991), specialized interviews
such as the Child Eating Disorder Examination (ChEDE; Bryant-Waugh, Cooper,
Taylor, & Lask, 1996) to assess the eating behavior of the child, or corresponding
questionnaire forms (ChEDE-Q; Bryant-Waugh et al., 1996), should be applied (for
further information, see Table 26.1).
As in the case of adults, the treatment of childhood obesity aims at changing
nutritional behavior and eating style, and increasing physical activity. Parents are
highly important when it comes to sustained behavior change in obese children and
thus should be included in treatment attempts. As measurement of BMI does not
reflect the status of overweight in children adequately, up to the age of 18 years BMI
percentiles are calculated taking into account age and gender (Kromeyer-Hauschild
et al., 2001). According to the criteria of the U.S. Centers for Disease Control and
Prevention (2012), children with a BMI over the 85th BMI percentile are classified
as overweight. Children with a BMI over the 95th BMI percentile are classified as
fulfilling the criteria for obesity even though this classification is, in a sense, arbitrary.
The natural course of BMI is age-dependent. After birth, BMI increases and reaches
Obesity 603
a peak at the age of 8 to 9 months. Thereafter BMI decreases until the age of 4.5
to 5 years. The second increase thereafter until puberty is called “obesity rebound.”
The risk of staying obese increases with age: Whereas a 3-year-old obese child has a
relatively low risk of being obese in adulthood, this risk increases up to 80% in a 10-
to 14-year-old adolescent. Furthermore, an early age of obesity rebound seems to be
predictive for later obesity (Baker et al., 2007).
Etiology. It is well known that biological, psychological, and psychosocial factors

are associated with the development and maintenance of obesity (WHO, 2006).
In children, the model behavior of the family plays an important role (Munsch,
Hasenboehler, & Meyer, 2011; Munsch et al., 2008). Increased prevalence rates of
childhood obesity interact through complex mechanisms and are probably related to
the cultural shift to a sedentary lifestyle, further characterized by a high daily intake
of fat (Laurson, Eisenmann, & Moore, 2008). Parental role modeling might be a
key issue in the maintenance of children’s energy intake and expenditure (Epstein,
Paluch, Gordy, & Dorn, 2000).
Familial factors. In children, family context, and familial eating behavior and its
transmission, have an important role with respect to the regulation of body weight
(Hasenboehler, Munsch, Meyer, Kappler, & Vögele, 2009; Munsch et al., 2007;
Zeller et al., 2007). In obese children, familial eating style is often transmitted by
specific instructions or reinforcements. A further important psychological correlate of
childhood obesity might be found in familial stress. Familial stress such as mental or
somatic illnesses of parents, or stress associated with low socioeconomic status, might
contribute to excessive energy intake. The underlying mechanism might be related to
shared genetic factors and the regulation within the neuroendocrine axis in response
to stress (Goodman & Whitaker, 2002; Hasler et al., 2005).
Psychological factors
Eating behavior. In obese children, studies report elevated scores of external and
emotional eating as well as engagement in restrained eating in an attempt to restrict
energy intake to achieve society’s aesthetic ideal of thinness (Braet & Van Strien,
1997; Nederkoorn, Braet, et al., 2006). Uncontrolled overeating might be driven by
a deficit in affect-regulation emotional eating as a response to an adverse arousal state
(Czaja, Rief, & Hilbert, 2009; E. Jansen, Mulkens, & Jansen, 2007) in combination
with engaging in strict dietary restraint.
There is increasing evidence that many obese children suffer regular binge eating,
with several important differences in phenomenology compared to adults with BED
(Ackard, Neumark-Sztainer, Story, & Perry, 2003; Decaluwé, Braet, & Fairburn,
2002; Goossens, Braet, & Decaluwé, 2007; Hilbert & Munsch, 2005; Marcus &
Kalarchian, 2003; Morgan et al., 2002; Tanofsky-Kraff, Marcus, Yanovski, & Yanovski,
2008; Tanofsky-Kraff et al., 2003). Children also binge eat during regular meals or at
parties. As in adults, the amount of energy intake seems to be less important for the
identification of binge-eating episodes than the subjective feeling of loss of control.
As only very few children seem to fulfill the adult research criteria for BED and thus
are diagnosed with EDNOS (eating disorder not otherwise specified), Marcus and
Kalarchian (2003) developed specific criteria to assess binge eating in children. They
suggest assessing the experience of “loss of control (LOC) eating,” defined as the
experience of loss of control independent of the amount of energy intake, rather
than the full-blown picture of adult BED (Tanofsky-Kraff, Marcus, et al., 2008).
LOC eating is associated with an increase in body fat mass of 15% over 4 years
(Tanofsky-Kraff et al., 2006).
Impulse and emotion regulation. A lack of self-regulatory competences in child-

hood are shown to be predictive for later overweight and obesity, as high emotionality,
intense expressions of anger and frustration, as well as decreased ability to delay grat-
ification related to food in toddlerhood has shown to be predictive for overweight
during middle childhood and adolescence (Agras, Hammer, McNicholas, & Kraemer,
2004; Duckworth, Tsukayama, & Geier, 2010; Francis & Susman, 2009; Seeyave
et al., 2009; Tsukayama, Toomey, Faith, & Duckworth, 2010). Laboratory studies
indicate that in childhood there is already a relationship between the amount of energy
intake and difficulties in inhibition of behavior and attentional deficits (Delgado-Rico,
Rio-Valle, Gonzalez-Jimenez, Campoy, & Verdejo-Garcia, 2012; Guerrieri, Ned-
erkoorn, & Jansen, 2008; A. Jansen et al., 2003; A. Jansen et al., 2009; E. Jansen,
Mulkens, Emond, & Jansen, 2008; Munsch, Meyer, et al., 2011). The influence of
impulsivity on treatment outcome is complex, as impulsivity traits might act most
negatively when it comes to long-term treatment outcome (Nederkoorn, Braet, et al.,
2006; Pauli-Pott, Albayrak, Hebebrand, & Pott, 2010).
Besides impulse regulation deficits, deficits in emotion regulation are already
present in childhood. In particular, depressive symptoms and anxiety are associated
with childhood obesity (Csabi, Tenyi, & Molnar, 2000; Drukker et al., 2009; Lamertz,
Jacobi, Yassouridis, Arnold, & Henkel, 2002; Pine et al., 2001; Pitrou et al., 2010; Vila
et al., 2004) and might follow from a vulnerability to interpretation bias (A. Jansen,
Smeets, et al., 2007). Longitudinal studies investigating the specific interrelatedness
of depressiveness and onset and course of obesity show that suffering from major
depression in childhood predicted adult BMI and was associated with a twofold
increased risk of becoming overweight (Pine et al., 2001). The inability to regulate
affect might explain the relationship between depressiveness and weight gain (the
affect regulation model) (Goossens, Braet, Van Vlierberghe, & Mels, 2009; Hasler
et al., 2005; Shomaker et al., 2009). This model postulates that emotional eating
works as a coping strategy to regulate and reduce negative emotions. Accordingly,
a positive relationship between anxiety or depression and excessive food intake in
children and adolescents has been confirmed by recent research (Goossens et al.,
2009).
Although the abovementioned studies indicate an association between obesity and
severe psychological problems, it is important to take into account that psychopathol-
ogy might not be solely due to an excess in body weight, but may also be transmitted
in families (Epstein, Klein, et al., 1994; Epstein et al., 1996).
Treatment of childhood obesity. In children, the model behavior of the family plays
an important role in the development of obesity (Golan & Crow, 2004; Munsch
et al., 2008). As the exclusive treatment of parents is comparably efficacious to
Obesity 605
combined parent–child treatment, it is suggested that parents should be the main

agents of change. Effects of obesity treatments in children are best when multimodular
behavioral change is induced (Oude Luttikhuis et al., 2009). The training of parents
includes information about the role of nutrition and eating style in the maintenance of
obesity and focuses on the reduction of sedentary behavior as well as on the increase
of familial activity. Further, parents should be taught strategies to support their child
when it comes to coping with teasing and low self-esteem. Another issue is how to
implement and motivate sustained behavior changes in the child. It is, for example,
possible to increase children’s liking of vegetables through flavor–flavor learning
(Havermans & Jansen, 2007) and to promote fruit consumption (E. Jansen, Mulkens,
& Jansen, 2010). Consequently, parents are trained in educational strategies in order
to support even small steps toward positive behavioral change (Epstein, Valoski, Wing,
& McCurley, 1994; Golan & Crow, 2004; E. Jansen, Mulkens, & Jansen, 2011; Jeor,
Perumean-Chaney, Sigman-Grant, Williams, & Foreyt, 2002; Moens, Braet, & Van
Winckel, 2010; Murtagh, Dixey, & Rudolf, 2006; Reinehr, Temmesfeld, Kersting,
de Sousa, & Toschke, 2007).
Treatment effects. Treatment effects in childhood obesity have increased but still
remain moderate, especially if long-term weight reduction, improvement of psycho-
logical problems, and dropout rates are considered (Oude Luttikhuis et al., 2009;
Wilfley et al., 2007). The inclusion of specialized modules aiming at the improvement
of social anxiousness, body image, and social competences result in a more profound
and sustained decrease in behavior problems (A. Jansen, Vanreyten, et al., 2008; E.
Jansen et al., 2011; Munsch et al., 2008; Roth, Munsch, & Meyer, 2011). Additional
booster sessions are shown to reduce weight regain, but there may be no time-limited
effective strategy to guarantee long-term weight stabilization in obese youth (Wilfley
et al., 2007).
Setting (individual versus group treatment). Treating obese children in groups

has several advantages. First, the group setting is attractive for children as they easily
learn through modeling and playing with other children. Further, socially anxious
children are given the possibility of positive experiences in terms of being accepted
and supported by others.
Case Reports
Erica
Erica is 36 years old (178 cm and 126 kg; BMI 39.8) and has been a fanatical
sportswoman. In her late twenties, she became less active and started to gain weight.
At the age of 28, after her first child was born, she was definitely obese. Since then,
she has tried continuously to lose weight, unfortunately without much success. Erica
has followed a range of popular diets, and although she frequently lost some pounds,
her weight loss never lasted. Usually, she ended up with a higher weight than before.
When she reached her highest ever weight, Erica decided that she needed professional
help.
Last month she started participating in CBT (following the Oxford manual; Cooper,
Fairburn, & Hawker, 2003) at the local mental health center. A physical examination
at the intake revealed type 2 diabetes, hypertension, and the beginnings of arthritis
in her knees. Erica also complains of fatigue and a loss of energy. A psychological
interview further underlined the presence of a mild depressive disorder. During the
interview it became clear that Erica’s self-worth decreases when gaining weight. She
lacks self-respect and is not able to accept herself.
Erica is highly motivated for treatment. She absolutely wants to regain control over
her eating and her weight. In response to the question “Why do you want to lose
weight?” Erica answers that she wants to feel better, and to improve her health and
her appearance.
During the behavioral analysis concerning Erica’s eating behavior, problems with
restricting energy intake in the late afternoon and evening became evident. Addition-
ally it revealed that Erica eats irregularly and that she has a preference for high-calorie
foods, in particular high-fat snacks. She starts the day without breakfast, as she does
not feel hungry early in the morning. At work she sometimes has a small lunch.
She usually feels quite exhausted and hungry when she goes home and she therefore
frequently buys high-calorie snacks on her way home from work. At that moment she
thinks of all the work at home—for example, preparing a meal for her husband and
two children—and concludes that she deserves a snack. At home, she is frequently
continuously grazing: she repeatedly eats small amounts of high-calorie tasty foods
(nuts, chips, chocolate, and so on) during the evening until she goes to bed. Next
morning she regrets having eaten all the high-calorie foods and not having adhered
to her dietary rules.
Erica tells the therapist that she has been trying to change her habits frequently,
she has been working hard to change, but she has always slipped back into bad habits.
The issue is, according to Erica, that the wrong food is everywhere. At nearly every
corner it is possible to buy cheap high-calorie sweets and snacks.
She has tried several diets. At the beginning of a diet, Erica usually loses weight, but
then it becomes more difficult, especially at times of sustained stress and when Erica
feels tired or emotional. She then gives in to temptations; at these moments she thinks
things like “I am craving it,” “It is unfair that I can’t eat this,” or “I am unhappy and
deserve it.” Overeating is the consequence, followed by shame and regret.
Erica also feels miserable about her body. She tells the therapist that looking at
herself or dressing makes her feel miserable. She avoids looking in the mirror, feels
ashamed about her body when naked; for example, when taking a shower. She never
goes to a swimming pool because she does not want to be seen in swimming clothes.
She is convinced that she will never look good as long as she is overweight. She does
not exercise anymore as she thinks that everybody will look at her and that everybody
will see her fat wobbling. Thinking about her body makes her feel sad, and when she
feels sad, she often starts snacking to cope with her feelings.
In treatment, a modest weight loss goal is set and Erica starts a 1,500-calorie diet.
It is expected that she will lose weight when consuming 1,500 kcal a day. Clear
advice is given about when to eat and what to eat. Erica monitors everything she
Obesity 607
eats and drinks. Close reviewing of the monitoring records enables the identification
of Erica’s high-risk situations. Skills are taught for coping with these situations.
Overall activity is intensified and appointments are made to do some formal exercise
(swimming during swimming hours for overweight people). Although it is not easy
for Erica, she succeeds in gradually changing her daily routine. Her motivation and
commitment are very high, which might foster success. Erica slowly loses weight
and she quickly feels much better. Cognitive interventions (Beck & Foss, 2007)
are started to change her ideas on her looks, and how to respond to sabotaging
thoughts. Although Erica still has a long way to go, she has made an excellent
start.
Sarah
Sarah is 9 years old (44 kg, 120cm, BMI-percentile >99). She has two brothers, who
are of a normal weight, but both her mother and her father are obese. When she was
3 years old, Sarah was already overweight and her weight increased significantly after
the age of 4.
Sarah has problems at school. She is easily distracted and reacts impulsively if she
feels attacked or provoked. She is teased because of her weight and shape at school
and suffers a lot from it. She tells us that she has no idea how to defend herself.
Her parents do realize that Sarah is not well and they feel very sorry for her as they
both remember having been teased because of their body weight. They try hard to
support Sarah in doing her homework as she needs a lot of structure. Lately, Sarah’s
pediatrician told them that he fears that Sarah’s weight will continue to increase.
Both parents try to offer healthy food, but as they are out at work during the day,
the children help themselves to items from the fridge until their parents return. In the
evening the parents usually serve the children cheese, butter, and cold meat.
Sarah tells us that she often eats more than her brothers and others at school. She
tells us that she hates herself for this. She also snacks frequently and she does not like
fruit or vegetables. She wants to lose weight and would like to be slimmer—like the
other girls at school. It makes her feel very sad if she is not invited to participate in
playing or sports. She is convinced that others laugh at her because of her body shape.
Sarah’s parents blame themselves for not being able to support their daughter.
Sarah’s father tells us that he is often exhausted at weekends and he then does not
feel prepared to go out and play with his children. The boys go out themselves, but
Sarah is often bored and stays inside the house.
Sarah and her parents are motivated to participate in a manualized CBT training for
obese children and their parents (Munsch et al., 2008). The psychological interview
does not reveal any mental disorders but the CBCL indicates an increased score
of attentional, impulsive symptoms, and a tendency to isolate from others. As the
pediatrician regularly sees Sarah, the medical investigation was not repeated. Due
to their work schedule the parents could not participate in a group program and
individual sessions were carried out. Sarah was regularly informed about the contents
of her parents’ training.
During the training, the maintaining factors of Sarah’s overweight were identified.
As a consequence, the parents helped the older brother and Sarah to prepare healthy
meals more regularly. Together with Sarah they developed nutritional and physical
activity goals. The nutritional goal included the eating of fruit three times a day and
waiting 5 minutes before a second serving of food. The physical activity goal was to
cycle on the playground near the house for 15 minutes per day. The parents agreed
to go shopping together once a week and to buy food they could easily allow their
children to eat (as the parents were trained to take responsibility for the food that is
offered, while the children are encouraged to eat until satisfied from what is being
served). They also involved their children in goal setting and in the reinforcement plan;
goals were fixed for all three children. The family soon realized that reinforcements
have to be feasible in the context of everyday life, such as, for example, being with
her mother in bed for five minutes, or playing football at weekends. Sarah’s brothers
were not happy to change their food preferences but they agreed in order to help
their sister. The parents trained Sarah in defending herself against being teased by
others. At the beginning it was difficult, as in particular Sarah’s mother could not
stand seeing her daughter suffering. It was important to train Sarah to defend herself
independently of her overweight. Also Sarah’s brothers helped and began to intervene
when Sarah was teased while they were present. Sarah’s parents contacted the teacher
and he agreed to intervene whenever he observed that anybody was teased because
of his or her shape or weight. The whole family found it very hard at the beginning
but the behavioral changes became part of the daily routine during the following 6
months. Sarah felt more capable of defending herself in front of others and succeeded
in asking others whether she could play with them. She started to develop a more
positive attitude toward herself. At the end of the treatment Sarah weighed about
41.8 kg with a height of 122 cm. She is doing very well but still wants to be slimmer.
The goal of regular monthly follow-up sessions is to motivate ongoing behavioral
change and to prepare Sarah for upcoming new developmental challenges during
early adolescence.
Outlook
It is extremely difficult to lower body weight successfully in the long run (Wing
& Hill, 2001). Many people try, but the majority of attempts to restrict intake are
unsuccessful. Most dieters regain more weight than they initially lost (Mann et al.,
2007) and it is estimated that less than 20% of obese individuals are capable of
achieving a normal weight (Wing & Phelan, 2005). Most studies point to a very
modest effect of long-term treatment when it comes to weight loss. For children,
results are slightly better, but child and adolescent interventions also show much
room for improvement.
One of the reasons for this low success rate in the psychological treatment of obesity
is a lack of knowledge of the mechanisms that maintain unhealthy eating and lifestyle
habits. Evidence is growing that cognitive and affective mechanisms play a critical
role in the maintenance of unhealthy eating, as well as personality characteristics
such as reward sensitivity. Effective behavioral interventions should try to tackle these
maintaining mechanisms and some experimental pilot studies are promising.
Obesity 609
References
Achenbach, T. M. (1991). Manual for the Child Behavior Checklist/4-18 and 1991 Profile.
Burlington, VT: University of Vermont, Department of Psychiatry.
Ackard, D. M., Neumark-Sztainer, D., Story, M., & Perry, C. (2003). Overeating among ado-
lescents: Prevalence and associations with weight-related characteristics and psychological
health. Pediatrics, 111, 67–74.
Agras, W. S., Hammer, L. D., McNicholas, F., & Kraemer, H. C. (2004). Risk factors for
childhood overweight: A prospective study from birth to 9.5 years. Journal of Pediatrics,
145, 20–25. doi:10.1016/j.jpeds.2004.03.023
Aldao, A., Nolen-Hoeksema, S., & Schweizer, S. (2010). Emotion-regulation strategies across
psychopathology: A meta-analytic review. Clinical Psychology Review, 30, 217–237.
doi:10.1016/j.cpr.2009.11.004
Appelhans, B. M. (2009). Neurobehavioral inhibition of reward-driven feeding: Implications
for dieting and obesity. Obesity, 17 , 640–647.
Baker, J. L., Olsen, L. W., & Sørensen, T. I. A. (2007). Childhood body-mass index and
the risk of coronary heart disease in adulthood. New England Journal of Medicine, 357 ,
2329–2337. doi:10.1056/NEJMoa072515
Banis, H. T., Varni, J. W., Wallander, J. L., Korsch, B. M., Jay, S. M., Adler, R., … Negrete, V.
(1988). Psychological and social adjustment of obese children and their families. Child:
Care, Health and Development, 14, 157–173.
Baumeister, H., & Härter, M. (2008). Overweight and obesity are associated with
psychiatric disorders: Are they? Psychosomatic Medicine, 70, 1060. doi:10.1097/
PSY.0b013e318190d803
Beck, J. S., & Foss, E. (2007). The Beck Diet Solution. Train your brain to think like a thin
person. Birmingham, AL: Oxmoor House.
Berking, M., Wupperman, P., Reichardt, A., Pejic, T., Dippel, A., & Znoj, H. (2008).
Emotion-regulation skills as a treatment target in psychotherapy. Behaviour Research and
Therapy, 46, 1230–1237.
Bouchard, C. (2007). The biological predisposition to obesity: Beyond the thrifty genotype
scenario. International Journal of Obesity, 31, 1337–1339.
Braet, C., Mervielde, I., & Vandereycken, W. (1997). Psychological aspects of childhood
obesity: A controlled study in a clinical and nonclinical sample. Journal of Pediatric
Braet, C., & Van Strien, T. (1997). Assessment of emotional, externally induced and restrained
eating behaviour in nine to twelve-year-old obese and non-obese children. Behaviour
Bryant-Waugh, R. J., Cooper, P. J., Taylor, C. L., & Lask, B. D. (1996). The use of the
eating disorder examination with children: A pilot study. International Journal of Eating
Disorders, 19, 391–397.
Carter, F. A., & Jansen, A. (2012). Improving psychological treatment for obesity.
Which eating behaviours should we target? Appetite, 58, 1063–1069. doi:10.1016/
j.appet.2012.01.016
Centers for Disease Control and Prevention. (2012). CDC Growth Charts. Retrieved from
http://www.cdc.gov/growthcharts/cdc_charts.htm
Cooper, Z., Doll, H. A., Hawker, D. M., Byrne, S., Bonner, G., Eeley, E., … Fairburn, C.
G. (2010). Testing a new cognitive behavioural treatment for obesity: A randomized
controlled trial with three-year follow-up. Behaviour Research and Therapy, 48, 706–713.
doi:10.1016/j.brat.2010.03.008
Cooper, Z., Fairburn, C. G., & Hawker, D. M. (2003). Cognitive-behavioral treatment of

obesity: A clinician’s guide. New York, NY: Guilford Press.
Crisp, A. H., & McGuiness, B. (1976). Jolly fat: Relation between obesity and psychoneurosis
in general population. BMJ , 1, 7–9. doi:10.1136/bmj.1.6000.7
Csabi, G., Tenyi, T., & Molnar, D. (2000). Depressive symptoms among obese children.
Eating and Weight Disorders, 5, 43–45.
Czaja, J., Rief, W., & Hilbert, A. (2009). Emotion regulation and binge eating in children.
International Journal of Eating Disorders, 42, 356–362. doi:10.1002/eat.20630
Decaluwé, V., Braet, C., & Fairburn, C. G. (2002). Binge eating in obese children and
adolescents. International Journal of Eating Disorders, 33, 78–84.
Delgado-Rico, E., Rio-Valle, J. S., Gonzalez-Jimenez, E., Campoy, C., & Verdejo-Garcia, A.
(2012). BMI predicts emotion-driven impulsivity and cognitive inflexibility in adolescents
with excess weight. Obesity. 20, 1604–1610. doi:10.1038/oby.2012.47
Derogatis, L. R. (1993). Brief Symptom Inventory: Administration, scoring, and procedures
manual. Minneapolis, MN: National Computer Systems.
Derogatis, L. R., & Unger, R. (2010). Symptom Checklist–90-Revised. In I. B. Weiner &
W. E. Craighead (Eds.), The Corsini encyclopedia of psychology. Chichester, England: John
Wiley & Sons, Ltd. doi:10.1002/9780470479216.corpsy0970
Dingemans, A. E., Bruna, M. J., & van Furth, E. F. (2002). Binge eating disorder: A review.
International Journal of Obesity and Related Metabolic Disorders, 26, 299–307.
Drukker, M., Wojciechowski, F., Feron, F. J., Mengelers, R., & Van Os, J. (2009). A com-
munity study of psychosocial functioning and weight in young children and adolescents.
International Journal of Pediatric Obesity, 4, 91–97.
Duckworth, A. L., Tsukayama, E., & Geier, A. B. (2010). Self-controlled children
stay leaner in the transition to adolescence. Appetite, 54, 304–308. doi:10.1016/
j.appet.2009.11.016
Engler, P. A., Crowther, J. H., Dalton, G., & Sanftner, J. L. (2006). Predicting eating disorder
group membership: An examination and extension of the sociocultural model. Behavior
Therapy, 37 , 69–79. doi:10.1016/j.beth.2005.04.003
Epstein, L. H., Klein, K. R., & Wisniewski, L. (1994). Child and parent factors that influence
psychological problems in obese children. International Journal of Eating Disorders, 15,
151–158.
Epstein, L. H., Myers, M. D., & Anderson, K. (1996). The association of maternal psy-
chopathology and family socioeconomic status with psychological problems in obese
children. Obesity Research, 4, 65–74.
Epstein, L. H., Paluch, R. A., Gordy, C. C., & Dorn, J. (2000). Decreasing sedentary behaviors
in treating pediatric obesity. Archives of Pediatrics & Adolescent Medicine, 154, 220–226.
doi:10.1001/archpedi.154.3.220
Epstein, L. H., Valoski, A., Wing, R. R., & McCurley, J. (1994). Ten-year outcomes of
behavioral family-based treatment for childhood obesity. Health Psychology, 13, 373.
Fairburn, C. G. (2008). Cognitive behavior therapy and eating disorders. New York, NY:
Guilford Press.
Fairburn, C. G., & Beglin, S. J. (1994). Assessment of eating disorders: Interview or self-report
questionnaire? International Journal of Eating Disorders, 16, 363–370.
Francis, L. A., & Susman, E. J. (2009). Self-regulation and rapid weight gain in children
from age 3 to 12 years. Archives of Pediatrics & Adolescent Medicine, 163, 297–302.
doi:10.1001/archpediatrics.2008.579
Franken, I. H. A., & Muris, P. (2005). Individual differences in reward sensitivity are related
to food craving and relative body weight in healthy women. Appetite, 45, 198–201.
doi:10.1016/j.appet.2005.04.004
Obesity 611
Golan, M., & Crow, S. (2004). Targeting parents exclusively in the treatment of childhood
obesity: Long-term results. Obesity, 12, 357–361.
Goodman, E., & Whitaker, R. C. (2002). A prospective study of the role of depression in the
development and persistence of adolescent obesity. Pediatrics, 110, 497–504.
Goossens, L., Braet, C., & Decaluwé, V. (2007). Loss of control over eating in obese
youngsters. Behaviour Research and Therapy, 45, 1–9. doi:10.1016/j.brat.2006.01.006
Goossens, L., Braet, C., Van Vlierberghe, L., & Mels, S. (2009). Loss of control over eating in
overweight youngsters: The role of anxiety, depression and emotional eating. European
Eating Disorders Review, 17 , 68–78. doi:10.1002/erv.892
Gross, J. J. E. (2007). Handbook of emotion regulation. New York, NY: Guilford Press.
Guerrieri, R., Nederkoorn, C., & Jansen, A. (2008). The interaction between impulsivity and
a varied food environment: Its influence on food intake and overweight. International
Journal of Obesity (London), 32, 708–714. doi:10.1038/sj.ijo.0803770
Guerrieri, R., Nederkoorn, C., Schrooten, M., Martijn, C., & Jansen, A. (2009). Inducing
impulsivity leads high and low restrained eaters into overeating, whereas current dieters
stick to their diet. Appetite, 53, 93–100.
Guerrieri, R., Nederkoorn, C., Stankiewicz, K., Alberts, H., Geschwind, N., Martijn, C., …
Jansen, A. (2007). The influence of trait and induced state impulsivity on food intake in
normal-weight healthy women. Appetite, 49, 66–73.
Hasenboehler, K., Munsch, S., Meyer, A. H., Kappler, C., & Vögele, C. (2009). Family struc-
ture, body mass index and eating behaviour. International Journal of Eating Disorders,
42, 332–338.
Hasler, G., Pine, D. S., Gamma, A., Milos, G., Ajdacic, V., Eich, D., … Angst, J. (2004).
The associations between psychopathology and being overweight: A 20-year prospective
study. Psychological Medicine, 34, 1047–1057. doi:10.1017/S0033291703001697
Hasler, G., Pine, D. S., Kleinbaum, D. G., Gamma, A., Luckenbaugh, D., Ajdacic, V., …
Angst, J. (2005). Depressive symptoms during childhood and adult obesity: The Zurich
Cohort Study. Molecular Psychiatry, 10, 842–850. doi:10.1038/sj.mp.4001671
Havermans, R. C., & Jansen, A. (2007). Increasing children’s liking of vegetables through
flavour–flavour learning. Appetite, 48, 259–262. doi:10.1016/j.appet.2006.08.063
Haynos, A. F., & Fruzzetti, A. E. (2011). Anorexia nervosa as a disorder of emotion
dysregulation: Evidence and treatment implications. Clinical Psychology: Science and
Practice, 18, 183–202.
Hebebrand, J., Sommerlad, C., Geller, F., Görg, T., & Hinney, A. (2001). The genetics of
obesity: Practical implications. International Journal of Obesity and Related Metabolic
Herpertz, S., Kielmann, R., Wolf, A. M., Langkafel, M., Senf, W., & Hebebrand, J. (2003).
Does obesity surgery improve psychosocial functioning? A systematic review. International
Journal of Obesity and Related Metabolic Disorders, 27 , 1300–1314.
Hilbert, A., & Munsch, S. (2005). “Binge-Eating”-Störung bei Kindern und Jugendlichen
[Binge eating disorder in children and adolescents]. Kindheit und Entwicklung, 14,
209–221.
Houben, K., & Jansen, A. (2011). Training inhibitory control: A recipe for resisting sweet
temptations. Appetite, 56, 345–349. doi:10.1016/j.appet.2010.12.017
Houben, K., Wiers, R. W., & Jansen, A. (2011). Getting a grip on drinking behavior.
Psychological Science, 22, 968–975. doi:10.1177/0956797611412392
Hudson, J. I., Hiripi, E., Pope, H. G., Jr., & Kessler, R. C. (2007). The prevalence and
correlates of eating disorders in the National Comorbidity Survey Replication. Biological
Psychiatry, 61, 348–358. doi:10.1016/j.biopsych.2006.03.040
Jansen, A., Havermans, R., Nederkoorn, C., & Roefs, A. (2008). Jolly fat or sad fat? Subtyping
non-eating disordered overweight and obesity along an affect dimension. Appetite, 51,
635–640. doi:10.1016/j.appet.2008.05.055
Jansen, A., Nederkoorn, C., van Baak, L., Keirse, C., Guerrieri, R., & Havermans, R. (2009).
High-restrained eaters only overeat when they are also impulsive. Behaviour Research and
Therapy, 47 , 105–110. doi:10.1016/j.brat.2008.10.016
Jansen, A., Smeets, T., Boon, B., Nederkoorn, C., Roefs, A., & Mulkens, S. (2007). Vulner-
ability to interpretation bias in overweight children. Psychology & Health, 22, 561–574.
doi:10.1080/14768320600941012
Jansen, A., Theunissen, N., Slechten, K., Nederkoorn, C., Boon, B., Mulkens, S., & Roefs,
A. (2003). Overweight children overeat after exposure to food cues. Eating Behaviors, 4,
197–209. doi:10.1016/S1471-0153(03)00011-4
Jansen, A., Vanreyten, A., van Balveren, T., Roefs, A., Nederkoorn, C., & Havermans, R.
(2008). Negative affect and cue-induced overeating in non-eating disordered obesity.
Appetite, 51, 556–562. doi:10.1016/j.appet.2008.04.009
Jansen, E., Mulkens, S., Emond, Y., & Jansen, A. (2008). From the Garden of Eden to the
land of plenty: Restriction of fruit and sweets intake leads to increased fruit and sweets
consumption in children. Appetite, 51, 570–575. doi:10.1016/j.appet.2008.04.012
Jansen, E., Mulkens, S., & Jansen, A. (2007). Do not eat the red food! Prohibition of
snacks leads to their relatively higher consumption in children. Appetite, 49, 572–577.
doi:10.1016/j.appet.2007.03.229
Jansen, E., Mulkens, S., & Jansen, A. (2010). How to promote fruit con-
sumption in children: Visual appeal versus restriction. Appetite, 54, 599–602.
doi:10.1016/j.appet.2010.02.012
Jansen, E., Mulkens, S., & Jansen, A. (2011). Tackling childhood overweight: Treating parents
exclusively is effective. International Journal of Obesity, 35, 501–509.
Jeor, S. T. S., Perumean-Chaney, S., Sigman-Grant, M., Williams, C., & Foreyt, J. (2002).
Family-based interventions for the treatment of childhood obesity. Journal of the American
Dietetic Association, 102, 640–644.
Kaufman, J., Birmaher, B., Brent, D., Rao, U. M. A., Flynn, C., Moreci, P., … Ryan, N.
(1997). Schedule for Affective Disorders and Schizophrenia for School-Age Children-
Present and Lifetime Version (K-SADS-PL): Initial reliability and validity data. Journal of
the American Academy of Child & Adolescent Psychiatry, 36, 980–988.
Kelly, T., Yang, W., Chen, C. S., Reynolds, K., & He, J. (2008). Global burden of obesity in
2005 and projections to 2030. International Journal of Obesity (London), 32, 1431–1437.
doi:10.1038/ijo.2008.102
Kromeyer-Hauschild, K., Wabitsch, M., Kunze, D., Geller, F., Geiss, H. C., Hesse, V., … Hebe-
brand, J. (2001). Perzentile für den Body-mass-index für das Kinder- und Jugendalter
unter Heranziehung verschiedener deutscher Stichproben. Monatsschrift Kinderheilkunde,
149, 807–818.
Lamertz, C. M., Jacobi, C., Yassouridis, A., Arnold, K., & Henkel, A. W. (2002). Are obese
adolescents and young adults at higher risk for mental disorders? A community survey.
Obesity Research, 10, 1152–1160. doi:10.1038/oby.2002.156
Laurson, K., Eisenmann, J. C., & Moore, S. (2008). Lack of association between television
viewing, soft drinks, physical activity and body mass index in children. Acta Pædiatrica,
97 , 795–800. doi:10.1111/j.1651-2227.2008.00713.x
Lavie, C. J., Milani, R. V., & Ventura, H. O. (2009). Obesity and cardiovascular disease: Risk
factor, paradox, and impact of weight loss. Journal of the American College of Cardiology,
53, 1925–1932. doi:S0735-1097(09)00746-3
Obesity 613
Lawlor, D. A., Mamun, A. A., O’Callaghan, M. J., Bor, W., Williams, G. M., & Najman, J. M.
(2005). Is being overweight associated with behavioural problems in childhood and
adolescence? Findings from the Mater-University study of pregnancy and its outcomes.
Archives of Disease in Childhood, 90, 692–697.
Lumeng, J. C., Gannon, K., Cabral, H. J., Frank, D. A., & Zuckerman, B. (2003). Association
between clinically meaningful behavior problems and overweight in children. Pediatrics,
112, 1138–1145.
Luppino, F. S., de Wit, L. M., Bouvy, P. F., Stijnen, T., Cuijpers, P., Penninx, B. W. J.
H., & Zitman, F. G. (2010). Overweight, obesity, and depression: A systematic review
and meta-analysis of longitudinal studies. Archives of General Psychiatry, 67 , 220–229.
doi:10.1001/archgenpsychiatry.2010.2
Mann, T., Tomiyama, A. J., Westling, E., Lew, A. M., Samuels, B., & Chatman, J. (2007).
Medicare’s search for effective obesity treatments: Diets are not the answer. American
Marcus, M. D., & Kalarchian, M. A. (2003). Binge eating in children and adolescents.
International Journal of Eating Disorders, 34 (Suppl.), S47–57. doi:10.1002/eat.10205
Martinez-Gonzalez, M. A., Martinez, J. A., Hu, F. B., Gibney, M. J., & Kearney, J. (1999).
Physical inactivity, sedentary lifestyle and obesity in the European Union. International
Journal of Obesity and Related Metabolic Disorders, 23, 1192–1201.
Moens, E., Braet, C., & Van Winckel, M. (2010). An 8-year follow-up of treated obese
children: Children’s process and parental predictors of successful outcome. Behaviour
Research and Therapy, 48, 626–633. doi:10.1016/j.brat.2010.03.015
Morgan, C. M., Yanovski, S. Z., Nguyen, T. T., McDuffie, J., Sebring, N. G., Jorge, M. R., …
Yanovsky, J. A. (2002). Loss of control over eating, adiposity, and psychopathol-
ogy in overweight children. International Journal of Eating Disorders, 31, 430–441.
doi:10.1002/eat.10038
Munsch, S., Hasenboehler, K., & Meyer, A. H. (2011). Is amount of food intake in overweight
and obese children related to their psychopathology and to maternal eating behavior?
Journal of Psychosomatic Research, 70, 362–367. doi:10.1016/j.jpsychores.2010.12.007
Munsch, S., Hasenboehler, K., Michael, T., Meyer, A. H., Roth, B., Biedert, E., & Margraf, J.
(2007). Restrained eating in overweight children: Does eating style run in families?
International Journal of Pediatric Obesity, 2, 97–103.
Munsch, S., Meyer, A. H., Quartier, V., & Wilhelm, F. H. (2011). Binge eating in binge
eating disorder: A breakdown of emotion regulatory process? Psychiatry Research. 195,
118–124. doi:10.1016/j.psychres.2011.07.016
Munsch, S., Roth, B., Michael, T., Meyer, A. H., Biedert, E., Roth, S., … Margraf, J.
(2008). Randomized controlled comparison of two cognitive behavioral therapies for
obese children: Mother versus mother-child cognitive behavioral therapy. Psychotherapy
and Psychosomatics, 77 , 235–246. doi:10.1159/000129659
Murtagh, J., Dixey, R., & Rudolf, M. (2006). A qualitative investigation into the levers and
barriers to weight loss in children: Opinions of obese children. Archives of Disease in
Childhood, 91, 920–923. doi:10.1136/adc.2005.085712
Mustillo, S., Worthman, C., Erkanli, A., Keeler, G., Angold, A., & Costello, E. J. (2003).
Obesity and psychiatric disorder: developmental trajectories. Pediatrics, 111, 851–859.
National Heart Lung and Blood Institute. (2012). Clinical guidelines on the identifica-
tion, evaluation, and treatment of overweight and obesity in adults. Retrieved from
http://www.nhlbi.nih.gov/guidelines/obesity/
National Institute for Health and Clinical Excellence. (2012). NICE guidance. Retrieved from
http://guidance.nice.org.uk/
Nederkoorn, C., Braet, C., Van Eijs, Y., Tanghe, A., & Jansen, A. (2006). Why obese
children cannot resist food: The role of impulsivity. Eating Behaviors, 7 , 315–322.
doi:10.1016/j.eatbeh.2005.11.005
Nederkoorn, C., Jansen, E., Mulkens, S., & Jansen, A. (2007). Impulsivity predicts treat-
ment outcome in obese children. Behaviour Research and Therapy, 45, 1071–1075.
doi:10.1016/j.brat.2006.05.009
Nederkoorn, C., Smulders, F. T. Y., Havermans, R. C., Roefs, A., & Jansen, A. (2006).
Impulsivity in obese women. Appetite, 47 , 253–256.
Neel, J. V., Weder, A. B., & Julius, S. (1998). Type II diabetes, essential hypertension,
and obesity as “syndromes of impaired genetic homeostasis”: The “thrifty geno-
type” hypothesis enters the 21st century. Perspectives in Biology and Medicine, 42,
44–74.
Neovius, K., Neovius, M., Kark, M., & Rasmussen, F. (2010, July). Association between weight
status and sick-leave: Nationwide cohort study. Paper presented at the 11th International
Congress on Obesity, Stockholm, Sweden.
Ogden, C. L., Carroll, M. D., Curtin, L. R., McDowell, M. A., Tabak, C. J., & Flegal, K. M.
(2006). Prevalence of overweight and obesity in the United States, 1999–2004. JAMA,
295, 1549–1555. doi:10.1001/jama.295.13.1549
Oude Luttikhuis, H. B. L., Jansen, H., Shrewsbury, V. A., O’Malley, C., Stolk, R. P., &
Summerbell, C. D. (2009). Interventions for treating obesity in children. Cochrane
Database of Systematic Reviews, 21, CD001872.
Pagoto, S. L., Curtin, C., Lemon, S. C., Bandini, L. G., Schneider, K. L., Bodenlos, J. S., & Ma,
Y. (2009). Association between adult attention deficit/hyperactivity disorder and obesity
in the U.S. population. Obesity (Silver Spring), 17 , 539–544. doi:10.1038/oby.2008.587
Pauli-Pott, U., Albayrak, O., Hebebrand, J., & Pott, W. (2010). Does inhibitory con-
trol capacity in overweight and obese children and adolescents predict success in a
weight-reduction program? European Child and Adolescent Psychiatry, 19, 135–141.
doi:10.1007/s00787-009-0049-0
Peisah, C., Brodaty, H., Luscombe, G., & Anstey, K. J. (2005). Children of a cohort of
depressed patients 25 years on: Identifying those at risk. Australian and New Zealand
Journal of Psychiatry, 39, 907–914. doi:10.1111/j.1440-1614.2005.01663.x
Pine, D. S., Goldstein, R. B., Wolk, S., & Weissman, M. M. (2001). The association
between childhood depression and adulthood body mass index. Pediatrics, 107 , 1049–
1056.
Pitrou, I., Shojaei, T., Wazana, A., Gilbert, F., & Kovess-Masfety, V. (2010). Child overweight,
associated psychopathology, and social functioning: A French school-based survey in 6-
to 11-year-old children. Obesity, 18, 809–817.
Puig-Antich, J., & Chambers, W. (1978). The Schedule for Affective Disorders and Schizophrenia
for school-aged children [Unpublished interview schedule]. New York, NY: New York State
Psychiatric Institute.
Ravussin, E., & Bogardus, C. (2000). Energy balance and weight regulation: Genetics versus
environment. British Journal of Nutrition, 83, 17–20.
Reicherts, M., Genoud, P. A., & Zimmermann, G. (2011). Emotionale Offenheit. Ein neues
Model in Forschung und Praxis. Bern, Switzerland: Hogrefe Huber.
Reinehr, T., Temmesfeld, M., Kersting, M., de Sousa, G., & Toschke, A. M. (2007). Four-year
follow-up of children and adolescents participating in an obesity intervention program.
International Journal of Obesity, 31, 1074–1077.
Rolls, B. J., Roe, L. S., Beach, A. M., & Kris-Etherton, P. M. (2005). Provision of foods
differing in energy density affects long-term weight loss. Obesity, 13, 1052–1060.
Obesity 615
Roth, B., Munsch, S., & Meyer, A. H. (2011). Long-term evaluation of a psychological
training for obese children and their parents (TAKE). Praxis der Kinderpsychologie und
Kinderpsychiatrie, 60, 304–321.
Roth, B., Munsch, S., Meyer, A., Isler, E., & Schneider, S. (2008). The association between
mothers’ psychopathology, childrens’ competences and psychological well-being in obese
children. Eating and Weight Disorders—Studies on Anorexia, Bulimia and Obesity, 13,
129–136.
Roth, B., Munsch, S., Meyer, A., Winkler, C., Isler, E., Steinhausen, H. C., … Schneider,
S. (2008). Die psychische Befindlichkeit übergewichtiger Kinder. Zeitschrift für Kinder-
und Jugendpsychiatrie, 36, 163–176.
Scott, K. M., Bruffaerts, R., Simon, G. E., Alonso, J., Angermeyer, M., de Girolamo, G., …
Von Korff, M. (2007). Obesity and mental disorders in the general population:
Results from the world mental health surveys. International Journal of Obesity, 32,
192–200.
Seeyave, D. M., Coleman, S., Appugliese, D., Corwyn, R. F., Bradley, R. H., Davidson, N.
S., … Lumeng, J. C. (2009). Ability to delay gratification at age 4 years and risk of
overweight at age 11 years. Archives of Pediatric and Adolescent Medicine, 163, 303–308.
Shomaker, L. B., Tanofsky-Kraff, M., Elliott, C., Wolkoff, L. E., Columbo, K. M., Ranzenhofer,
L. M., … Yanovsky, J. A. (2009). Salience of loss of control for pediatric binge episodes:
Does size really matter? International Journal of Eating Disorders. 143, 707–716.
doi:10.1002/eat.20767
Solanto, M. V., Abikoff, H., Sonuga-Barke, E., Schachar, R., Logan, G. D., Wigal, T., …
Turkel, E. (2001). The ecological validity of delay aversion and response inhibition as
measures of impulsivity in AD/HD: A supplement to the NIMH multimodal treatment
study of AD/HD. Journal of Abnormal Child Psychology, 29, 215–228.
Speliotes, E. K., Willer, C. J., Berndt, S. I., Monda, K. L., Thorleifsson, G., Jackson, A. U., …
Loos, L. J. (2010). Association analyses of 249,796 individuals reveal 18 new loci
associated with body mass index. Nature Genetics, 42, 937–948.
Stahre, L., & Hallstrom, T. (2005). A short-term cognitive group treatment program gives
substantial weight reduction up to 18 months from the end of treatment: A randomized
controlled trial. Eating and Weight Disorders, 10, 51–58.
Stahre, L., Tärnell, B., Håkanson, C.-E., & Hällström, T. (2007). A randomized con-
trolled trial of two weight-reducing short-term group treatment programs for obesity
with an 18-month follow-up. International Journal of Behavioral Medicine, 14, 48–55.
doi:10.1007/bf02999227
Stice, E., Spoor, S., Ng, J., & Zald, D. H. (2009). Relation of obesity to con-
summatory and anticipatory food reward. Physiology & Behavior, 97 , 551–560.
doi:10.1016/j.physbeh.2009.03.020
Tanofsky-Kraff, M., Cohen, M. L., Yanovski, S. Z., Cox, C., Theim, K. R., Keil, M.,
… Yanovsky, J. A. (2006). A prospective study of psychological predictors of body
fat gain among children at high risk for adult obesity. Pediatrics, 117 , 1203–1209.
doi:10.1542/Peds.2005-1329
Tanofsky-Kraff, M., Marcus, M. D., Yanovski, S. Z., & Yanovski, J. A. (2008). Loss of control
eating disorder in children age 12 years and younger: Proposed research criteria. Eating
Behaviors, 9, 360–365. doi:10.1016/j.eatbeh.2008.03.002
Tanofsky-Kraff, M., Morgan, C. M., Yanovski, S. Z., Marmarosh, C., Wilfley, D. E., & Yanovski,
J. A. (2003). Comparison of assessments of children’s eating-disordered behaviors by
interview and questionnaire. International Journal of Eating Disorders, 33, 213–224.
doi:10.1002/eat.10128
Tanofsky-Kraff, M., Ranzenhofer, L. M., Yanovski, S. Z., Schvey, N. A., Faith, M., Gustafson,
J., & Yanovsky, J. A. (2008). Psychometric properties of a new questionnaire to assess
eating in the absence of hunger in children and adolescents. Appetite, 51, 148–155.
doi:10.1016/j.appet.2008.01.001
Tanofsky-Kraff, M., Shomaker, L. B., Olsen, C., Roza, C. A., Wolkoff, L. E., Columbo,
K. M., … Yanovsky, J. A. (2011). A prospective study of pediatric loss of control
eating and psychological outcomes. Journal of Abnormal Psychology, 120, 108–118.
doi:10.1037/a0021406
ter Bogt, T. F., van Dorsselaer, S. A., Monshouwer, K., Verdurmen, J. E., Engels, R. C., &
Vollebergh, W. A. (2006). Body mass index and body weight perception as risk factors for
internalizing and externalizing problem behavior among adolescents. Journal of Adolescent
Health, 39, 27–34.
Tershakovec, A. M., Weller, S. C., & Gallagher, P. R. (1994). Obesity, school performance and
behaviour of black, urban elementary school children. International Journal of Obesity
and Related Metabolic Disorders, 18, 323–327.
TODAY Study Group. (2007). Treatment options for type 2 diabetes in adolescents and
youth: A study of the comparative efficacy of metformin alone or in combination with
rosiglitazone or lifestyle intervention in adolescents with type 2 diabetes. Pediatric
Diabetes, 8, 74–87.
Tsukayama, E., Toomey, S. L., Faith, M. S., & Duckworth, A. L. (2010). Self-
control as a protective factor against overweight status in the transition from child-
hood to adolescence. Archives of Pediatric and Adolescent Medicine, 164, 631–635.
Vila, G., Zipper, E., Dabbas, M., Bertrand, C., Robert, J. J., Ricour, C., & Mouren-Siméoni,
M. C. (2004). Mental disorders in obese children and adolescents. Psychosomatic Medicine,
66, 387–394.
Wardle, J., & Carnell, S. (2009). Appetite is a heritable phenotype associated with adiposity.
Annals of Behavioral Medicine, 38, 25–30. doi:10.1007/s12160-009-9116-5
Wardle, J., Carnell, S., Haworth, C. M., & Plomin, R. (2008). Evidence for a strong genetic
influence on childhood adiposity despite the force of the obesogenic environment.
American Journal of Clinical Nutrition, 87 , 398–404.
Wardle, J., Guthrie, C. A., Sanderson, S., & Rapoport, L. (2001). Development of the
Children’s Eating Behaviour Questionnaire. Journal of Child Psychology and Psychiatry
and Allied Disciplines, 42, 963–970.
Werrij, M. Q., Jansen, A., Mulkens, S., Elgersma, H. J., Ament, A. J. H. A., &
Hospers, H. J. (2009). Adding cognitive therapy to dietetic treatment is associ-
ated with less relapse in obesity. Journal of Psychosomatic Research, 67 , 315–324.
doi:10.1016/j.jpsychores.2008.12.011
Westerterp, K. (1993). Food quotient, respiratory quotient, and energy balance. American
Journal of Clinical Nutrition, 57 , 759S–764S.
Wilfley, D. E., Stein, R. I., Saelens, B. E., Mockus, D. S., Matt, G. E., Hayden-Wade, H. A., …
Epstein, L. H. (2007). Efficacy of maintenance treatment approaches for childhood
overweight. JAMA, 298, 1661–1673. doi:10.1001/jama.298.14.1661
Wing, R. R., & Hill, J. O. (2001). Successful weight loss maintenance. Annual Review of
Nutrition, 21, 323–341.
Wing, R. R., & Phelan, S. (2005). Long-term weight loss maintenance. American Journal of
Clinical Nutrition, 82, 222–225.
World Health Organization (2006). Obesity and overweight. Fact sheet no. 311. Retrieved
from http://www.who.int/mediacentre/factsheets/fs311/en/
Obesity 617
World Health Organization (2009). Childhood overweight and obesity. Retrieved from
http://www.who.int/dietphysicalactivity/childhood/en/
Zeller, M., Reiter-Purtill, J., Modi, A., Gutzwiller, J., Vannatta, K., & Davies, W. (2007).
Controlled study of critical parent and family factors in the obesigenic environment.
Obesity, 15, 126–136.
Zijlstra, H., van Middendorp, H., Devaere, L., Larsen, J. K., van Ramshorst, B.,
& Geenen, R. (2012). Emotion processing and regulation in women with mor-
bid obesity who apply for bariatric surgery. Psychology & Health, 27 , 1375–1387
doi:10.1080/08870446.2011.600761
27
Women’s Sexual Difficulties
Lori A. Brotto and Morag A. Yule
As a result of studying over 700 couples engaged in solitary and partnered sexual
activity in their St Louis, Missouri clinic, Masters and Johnson (1966) forwarded
a four-stage sexual response cycle that consisted of linear stages of excitement,
plateau, orgasm, and resolution, which reflected progressively increasing levels of
physiological sexual arousal. Within the next decade, Kaplan (1977, 1979) and Lief
(1977) independently added a sexual desire phase to the beginning of the sexual
response cycle. The resulting “triphasic model of sexual response” (see Figure 27.1)
predominated clinical practice and research of sexual response from that time until
the present.
Masters and Johnson’s work had important implications for sex therapy and for
the development and widespread implementation of behavior-based psychological
therapy. First, in contrast to the previous work of Freud in Three Essays on the
Theory of Sexuality (1905), Masters and Johnson believed that there was no separate
vaginal orgasm, which meant that subsequent behavior-based treatments focused on
teaching women to experience clitoral orgasm. Second, they noted that women had
a capacity for multiple orgasms without a refractory period (unlike men). They also
acknowledged the enormous individual variability across women, unlike men who
appeared to have a more predictable, linear progression of sexual response. Finally,
their work emphasized the need for sex therapy to be focused on the couple as a
sexual unit, rather than the individual.
In 1977 Bancroft summarized the key elements of behavior sex therapy and these
included (a) systematic desensitization, (b) shaping of fantasies, (c) operant methods,
and (d) role rehearsal. The assumption among early behavioral sex therapists was that
changes in behavior would lead to changes in beliefs and attitudes since cognitive

DOI: 10.1002/9781118528563.wbcbt27
Orgasm
excitement
Sexual
Arousal
Resolution
Desire
Time
Figure 27.1 Triphasic model of human sexual

response.
dissonance would ensure that cognitions would be congruent with behavior. Sensate
focus was developed by Masters and Johnson (1970) and became a primary treatment
approach for a variety of sexual difficulties in both men and women. There were
three stages to sensate focus: Stage 1 focused on sequential touching of one partner
and then the other, excluding the breasts and genitals, during which the giver of
the touch was guided by his own curiosity, not by what he believed his partner
liked. The recipient of the touch provided verbal feedback to the toucher about
the qualities of the touch. After approximately 15 minutes, roles were reversed
and the toucher now became the touchee. There was a focus on sensual, rather
than erotic, pleasure, and overt sexual activity was often prohibited during the
period of sensate focus practice. Stage 2 now included breast and genital touch
and the goal remained to learn about the other partner’s body, rather than the
overt creation of pleasure. Stage 3 involved mutual touching with the progressive
reintroduction of intercourse. The therapist sought to monitor the couple’s responses
to prescribed homework activities, and would emphasize positive reinforcers while
removing negative reinforcers.
The outcomes of Masters and Johnson’s sex therapy, which included sensate focus,
sexual communication, and education, were evaluated, and using a single therapist-
derived endpoint of improved versus not improved, Masters and Johnson found
success rates in the range of 72–98% following their daily therapy which took place
over 2 weeks, and only a 5% relapse rate after 5 years (1970). Although modifications
of their intensive daily behavior-based therapy have been attempted (see Table 27.1),
other researchers have never been able to replicate the very high rates that Masters
and Johnson achieved.
Before long, behavioral sex therapists recognized that improvements in sexual
response would not take place with behavioral change alone; rather, beliefs and
attitudes needed to be targeted as well. In their behavior-based therapy, Mas-
ters and Johnson recognized the importance of exploring fantasies, which revealed
beliefs and attitudes—of which negative ones were identified and challenged. This
gave rise to the development of cognitive behavioral therapy (CBT) for sexual
dysfunction.
Women’s Sexual Difficulties 621
Table 27.1 Summary of Behavior-Based Psychological Therapies for Sexual Dysfunction
Reference Sample Therapy Outcomes Follow-up
Masters & 790 men and Daily sex therapy 72–98% rated as a 5% relapse at 5 years
Johnson women for 2–3 weeks “success”
(1970) by male–female
team
Hawton, 140 couples Weekly couple 61% completed 76% of original sample
Catalan, therapy for 15 treatment; 26% completed
Martin, & weeks by single had complete follow-up; 75% had
Fagg (1986) therapist resolution of continuing
problem; 50% difficulties but only
had partial 34% were concerned
resolution
Sarwer & 365 married Weekly sex 65% rated as a Less than 50% of
Durlak couples therapy for 7 “success” responders
(1997) weeks completed 3-month
follow-up; 74% of
those maintained
treatment gains
General Principles of Cognitive Behavioral Therapy in the

Treatment of Women’s Sexual Difficulties
The objective of CBT is to resolve problems stemming from dysfunctional thoughts

(cognitions), behaviors, and feelings (emotions), through a methodical, goal-oriented
approach focused on the current presentation of a problem, rather than on its source.
The core CBT model has been adapted for use in treating an increasingly wide range
of mental health problems, including sexual dysfunction, and there is a moderate
amount of empirical evidence supporting its effectiveness in many of these (Butler,
Chapman, Forman, & Beck, 2006).
Early researchers of sexuality identified anxiety surrounding sexual performance,
perhaps arising from an inward focus on one’s abilities and appearance, as being one of
the most important immediate causes of sexual dysfunction (Kaplan, 1974; Masters &
Johnson, 1970). According to Masters and Johnson, spectatoring is a process by which
an individual feels overly self-conscious during sexual activity, and instead of focusing
on the sensory aspects of the experience, is evaluating and monitoring his or her own
performance. This results in sexual spectators being distracted by thoughts about their
performance, disrupting the flow of sexual functioning and hindering sexual arousal
and orgasm (Dove & Wiederman, 2000; Masters & Johnson, 1970). Such cognitive
interference, which distracts the person from focusing on the erotic experience, can
also lead to activation of the autonomic nervous system (the part of the nervous system
responsible for anxiety, or “fight or flight” response), which produces a negative
emotional state that is not synonymous with sexual arousal or pleasure. In fact, an
individual experiencing sexual difficulties might experience this autonomic arousal as
anxiety, whereas someone without sexual concerns may experience the same arousal as
sexual excitement. This anxiety creates further cognitive interference, perhaps giving
rise to thoughts such as “I am a failure” or “I will never be able to experience desire,”
which in turn may lead to decreased sexual ability. The individual may begin to
avoid sexual situations in the future, or develop the tendency to experience anxiety
immediately upon, or perhaps even before, entering a sexual situation.
Barlow (1986) took this idea of spectatoring one step further and, in a series of
experiments, demonstrated that anxiety and cognitive interference interact to produce
sexual dysfunction. According to Barlow, problems in sexual functioning are caused
by the inability of the spectator to decode sexual cues properly. Instead of erotic cues
activating sexual arousal, they activate performance anxiety for the spectator, which
immediately causes a shift in attention from potentially rewarding arousal properties
to more intimidating consequences, such as failure or embarrassment. This, in turn,
can lead to deterioration of sexual performance. Barlow emphasized the similarity
between this process and other performance anxieties, such as that experienced by
those with social phobia.
Most of the research on sexual spectatoring has focused on men; however, there
is evidence that cognitive distraction during sexual activity does have a negative
impact on women’s sexual esteem, sexual satisfaction, and orgasm consistency. Sexual
satisfaction in particular was influenced by distracting thoughts while being sexual
with a partner (Dove & Wiederman, 2000), and sexual arousal has also been shown
to be negatively impacted by cognitive distraction (Adams, Haynes, & Brayer, 1985;
Elliott & O’Donohue, 1997; Koukounas & McCabe, 1997). More recently, Nobre
and Pinto-Gouveia conducted a series of studies investigating the role of cognitive
and emotional factors on sexual dysfunction, and determined that women with sexual
dysfunction hold stronger beliefs surrounding the influence of age and body image on
sexuality, and this makes them more vulnerable to activation of negative self-schemas
(specifically those of incompetence) when confronted with an unsuccessful sexual
situation (Nobre & Pinto-Gouveia, 2008b). These self-critical schemas then trigger
a system of negative automatic thoughts, preventing the woman from focusing on
sexual stimuli and promoting negative emotions, which further impairs sexual response
(Nobre & Pinto-Gouveia, 2006, 2008a). These models of sexual dysfunction have
important treatment implications, in that they suggest targeting problematic thoughts
and shifting attention allocation through performance-based exercises. These are
precisely the targets of CBT.
CBT as a treatment for sexual dysfunction has been in widespread use for nearly
four decades, although it has been tested empirically on a more limited scale. For
example, Morokoff and Heiman (1980) examined the effect of CBT for women
with and without sexual difficulties on subjective (self-report) and genital measures
of sexual arousal. Before treatment both groups had similar levels of genital arousal;
however, the nonclinical women reported higher levels of subjective sexual arousal
than the women with sexual difficulties. Following therapy, genital arousal remained
comparable across the two groups, but subjective sexual arousal in the clinical
group had increased and was equivalent to that of the nonclinical group. The
authors interpreted their findings as indicating that women with and without sexual
dysfunction differ in their awareness or interpretation of physiological genital arousal,
such that women with sexual arousal difficulties may not be attending to genital
changes, and so do not feel sexually aroused as a result. This led the authors to
suggest that future treatment for low sexual arousal should focus on cognitive and
affective processes, rather than on improving physiological sexual response directly.
That a woman may show a robust genital arousal response in the complete
absence of subjective sexual arousal is a common finding in this area of research
(Chivers & Bailey, 2005; Chivers, Seto, Lalumière, Laan, & Grimbos, 2010). There
is often a marked discrepancy between subjective and genital measures of sexual
arousal, such that a woman will usually always show pronounced genital arousal using
laboratory measures such as the vaginal photoplethysmograph, but may report a level
of subjective sexual arousal that is either much less than the physical response, or
even absent altogether (Chivers & Bailey, 2005). Such “discordance” suggests that
treatments focused on strengthening the physiological sexual response may do nothing
to alter a woman’s reported sexual difficulties. It is perhaps not surprising, therefore,
that all proposals to the Food and Drug Administration (FDA) for pharmaceutical
products to treat women’s sexual dysfunction have been rejected on the grounds
of inadequate efficacy data (as well as questionable long-term safety data). Because
sexual dysfunction in women is often the result of cognitive interference and anxiety,
CBT could be considered a front-line treatment.
What Is Unique about Cognitive Behavioral

Therapy for Sexual Problems?
CBT for sexual difficulties is different from CBT for more conventional psychological
difficulties by virtue of the fact that it is often targeted at the couple, not at the
individual. When sex therapy was carried out only with an individual (the “presenting
patient”), there were often two key issues guiding treatment: (a) how do nonsexual
problems in a relationship affect the sexual functioning of the individual?; and (b) how
do changes brought about from therapy play out in the relationship? (Lief & Friedman,
2006). Masters and Johnson dealt with this dilemma by insisting on only seeing
couples in their treatment. Even when the nonidentified patient did not experience any
of his or her own sexual difficulties (which was the case in only 50% of their patients),
relationship factors often interacted with the sexual complaints and influenced the
process of therapy. A therapist could elicit nonsexual problems such as those related to
power, intimacy, communication, respect, and role conflict and discover the negative
reinforcers used by the couple as they completed homework assignments. Sensate
focus often led couples to overcome negative affect such as shame, anxiety, and anger
and change attitudes by rewarding positive responses to increasing sensual and erotic
pleasure by encouraging words from the therapists (Lief & Friedman, 2006).
Therapists were doing “double duty” by administering sex therapy and couple
therapy, and in the early days of sex therapy, most training programs offered training
in one or the other, but rarely both, leading therapists to acquire these skills on their
own. Couple sex therapy, unlike individual therapy, requires therapists to be proficient
in sex therapy, couples therapy, assessment of the individual, assessment of a couple,
assessment of sexual factors, and implementation of a treatment plan targeting the
couple (McCarthy & Thestrup, 2008).
Another facet of couple sex therapy that differs from individual CBT relates to
the fact that the therapist must provide adequate education and information about
available sexual norms. This is made difficult by the fact that norms rarely exist for such
a highly subjective experience as sexual response and behavior, yet, at the same time,
the therapist’s ability to provide data often normalizes and destigmatizes individuals’
concerns. For example, conveying to a 21-year-old woman who is highly distressed
at her anorgasmia during intercourse that many (if not most) women are unable to
experience orgasm through vaginal penetration alone, and that often clitoral orgasms
come about with less effort, can be highly therapeutic. Another guiding principle is
that a woman’s sexual response, including orgasm, is often much more variable than
the experience of a man. However, just as there are between-gender differences, there
are enormous within-gender differences (Meana, 2010).
Thus, CBT for sexual problems includes therapy directed at both partners’ sexual
and nonsexual complaints, education about available norms, attention to nonverbal
communication in session, and as much careful attention to process as there is to
content. Unfortunately, the number of sex therapists is decreasing, not increasing,
particularly as the vigorous search for a pharmaceutical panacea has driven treatment
practices (Binik & Meana, 2009). However, given the failure of any pharmaceutical
products to receive FDA approval for women’s sexual ailments, it seems that there
continues to be a role for the cognitive behavioral therapist in the treatment of low
desire, arousal, orgasm, and genital pain difficulties. We will now review the literature
on each of these domains in turn.
Cognitive Behavioral Therapy for Low Desire in Women
Unfortunately there are very few empirical studies examining CBT for low sexual
desire, the most common sexual complaint in women and the leading reason why
women seek sex therapy. Moreover, it has long been recognized that sexual desire
problems are the most difficult to treat and are the most resistant to change (Beck,
1995). The Diagnostic and Statistical Manual of Mental Disorders (4th ed., text
rev.; DSM-IV-TR; American Psychiatric Association [APA], 2000) defines hypoactive
sexual desire disorder (HSDD) as absent or deficient sexual fantasies and desire for
sexual activity with accompanying distress. Recent population-based data from the
“Prevalence of Female Sexual Problems Associated with Distress and Determinants of
Treatment Seeking” (PRESIDE) trial, gathered on 31,581 American women, suggest
that approximately 22% of women aged 18 to 44 reported low sexual desire, whereas
this number was reduced to 9% when distress over the low desire was included
(Shifren, Monz, Russo, Segreti, & Johannes, 2008). Low desire was found in 39%
of 45- to 64-year-old women (with 12% reporting low desire plus distress), and the
figures were 75% for women more than 65 years old (with 7% having low desire
plus distress). In a structured cognitive behavioral marital therapy for women seeking
treatment for low desire, 55 women were randomized to either standard CBT with or
without orgasm consistency training. Their treatment included sensate focus, directed
masturbation, and the coital alignment technique—more behavior-based elements.
After eight 2-hour sessions (plus an additional 30–45 minutes for those in the orgasm
consistency training group), women in both groups had a significant increase in sexual
desire and arousal, and improvements were retained at 6-month follow-up (Hurlbert,
1993). In a more recent controlled trial, 74 couples, in which the female partner met
criteria for HSDD, were randomized to couple CBT versus wait-list control (Trudel
et al., 2001). The 12 weekly 2-hour sessions consisted of psychoeducation, couple
exercises, sensate focus, communication and emotional training, mutual reinforcement
training, cognitive challenging, and sexual fantasy training, with between-session
reading and homework activities. At the end of treatment 74% of the women no
longer met criteria for HSDD and 64% maintained this at 1-year follow-up.
Dutch researchers developed a CBT bibliotherapy that was meant to be a minimal
intervention approach. It consisted of a bibliotherapy manual of 266 pages that
had three introductory chapters followed by specific chapters that focused on
different aspects of sexual dysfunction, and a chapter focused on communication
problems. Participants with a wide array of sexual difficulties were randomized either
to the bibliotherapy group or a wait-list control group (van Lankveld, Everaerd,
& Grotjohann, 2001). The manual contained educational information, a list of
individual and partner exercises that generally followed sensate focus instructions,
and some “rational-emotive self-analysis.” Participants were also invited to contact
the investigator about any questions or concerns. A total of 53 women with HSDD
were randomized to the CBT bibliotherapy group and 44 women with HSDD to the
control group. Overall, there was not a strong effect of bibliotherapy on the women
with HSDD, suggesting that, perhaps, bibliotherapy techniques may not adequately
capture the complexity of desire dysfunction.
Most recently, a three-session mindfulness-based CBT group treatment for women
with low sexual desire has been developed and found to significantly improve
sexual desire, sex-related distress, and perceptions of genital tingling (Brotto,
Basson, & Luria, 2008). Mindfulness is an ancient Eastern practice that embodies
present-moment, nonjudgmental awareness. It made its debut in Western health care
in the 1970s through treatment of chronic pain and the work of Kabat-Zinn (1990).
Since then, it has been found to be effective for a large range of psychological and
health-related conditions. Because women with sexual desire complaints might be
characterized as experiencing normal genital arousal in the absence of mental sexual
excitement, mindfulness-based strategies which aim to cultivate active awareness of
the body have been postulated to be ideally suited to deal with complaints related
to sexual desire (Brotto & Heiman, 2007; Brotto, Seal, & Rellini, 2012). Future
research must focus on randomized controlled trials of mindfulness-based CBT for
this population of women.
Sexual Arousal
Unfortunately, sexual arousal complaints independent of other sexual complaints have

not been examined in the context of psychological treatments. This is despite the
frequent complaints of female sexual arousal disorder (FSAD), which is defined as
“persistent or recurrent inability to attain or maintain until completion of the sexual
activity, an adequate lubrication or swelling response” (APA, 2000, p. 544). In the
PRESIDE study, sexual arousal complaints increased with age and ranged from 10%
(18- to 44-year-old women) to 65% (women aged 65 and over). The prevalence
of arousal difficulties plus distress ranged from 3 to 6% across these age groups.
Notably, in the clinical setting, complaints of reduced genital sensations and lack of
excitement appear to be more prevalent than the complaint of insufficient lubrication,
calling into question the existing definition of HSDD (Graham, 2010b). This has
also been a sexual concern that has been the focus of intense pharmaceutical efforts
to find a “female Viagra”; however, to date, there is no evidence of any effective
pharmacological treatment for FSAD.
In a study comparing eight 55-minute sessions of individual CBT versus oral ginkgo
biloba extract (versus placebo) in women with FSAD, treatment was aimed at increas-
ing women’s focus on their sexual pleasure and physiological sexual arousal response
during sexual activity (Meston, Rellini, & Telch, 2008). There was no significant
impact of the CBT treatment on genital sexual response (as measured by a vaginal
photoplethysmograph) when women were exposed to erotic films in a controlled
laboratory environment. However, the CBT did significantly increase women’s sub-
jective sexual arousal to these erotic films. Treatment also resulted in a trend toward
increased concordance between self-reported and physiologically measured sexual
arousal. Treatment also significantly enhanced sexual activity-related desire, arousal,
lubrication, and orgasm ratings, whereas responses were not significantly improved
with gingko biloba treatment. Although the focus of this study was not on CBT (but
rather gingko biloba), the findings suggest that CBT may be effective in improving
arousal-related concerns.
In another uncontrolled study of gynecologic cancer survivors with the primary
complaint of FSAD, Brotto and colleagues tested a three-session individually admin-
istered mindfulness-based CBT on the primary outcomes of sexual arousal measured
with self-report questionnaires as well as in response to laboratory-evoked erotic
stimuli (Brotto, Heiman, et al., 2008). Treatment involved a combination of edu-
cation, cognitive strategies aimed at challenging cancer-related maladaptive beliefs
about women’s incapacity for sexual arousal, behavioral strategies involving exposure
to arousal-enhancing tools, and mindfulness meditation exercises that were to be
practiced daily between sessions. Women’s perception of their genital arousal during
an erotic film significantly increased with treatment, even though their actual levels
of physiologically measured sexual response did not. Moreover, their self-reported
sexual arousal during sexual activity significantly increased following treatment, as
did self-reports of desire, orgasm, and sexual satisfaction. Although the absence of
a control group makes it difficult to delineate the precise mechanisms by which
this mindfulness-based CBT was effective, there is converging evidence across studies
(Brotto, Basson, & Luria, 2008; Brotto, Heiman, et al., 2008) that such psychological
techniques may be effective for women’s complaints of low desire and arousal.
Anorgasmia
Female orgasmic disorder (FOD) is the second most frequently reported female sexual
problem, affecting 10% (in women aged 18 to 44 years) to 55% (in women aged 65
and over) of women assessed in the large PRESIDE study (Shifren et al., 2008). The
DSM-IV-TR defines it as a “persistent or recurrent delay in, or marked absence of,
orgasm” that causes marked distress or interpersonal difficulty (APA, 2000, p. 549).
According to the definition of FOD, a diagnosis should be made only when the
lack of orgasm occurs following a normal sexual excitement phase; however, it is
not uncommon for women seeking treatment for anorgasmia also to report marked
difficulties in becoming sexually aroused and excited (Graham, 2010a).
Much remains unknown about the definition of orgasm and the factors that
contribute to FOD (Graham, 2010a; Meston, Hull, & Levin, 2004; Meston, Levin,
Sipski, Hull, & Heiman, 2004), making it even more difficult to quantify. Subjective
descriptions of orgasm are varied, and orgasms are experienced in diverse ways,
perhaps depending on numerous contextual factors. Compared to other aspects of
women’s sexual response (e.g., desire and arousal), there is a much greater literature
evaluating psychological treatments, and in particular CBT, for FOD.
Anorgasmia is often associated with anxiety, and for this reason, historical treatments
have tended also to include elements of anxiety reduction. As discussed in previous
sections, anxiety can disrupt the flow of the sexual response cycle by removing focus
from erotic cues, and placing it instead on distracting thoughts such as performance
concerns, embarrassment, guilt, or body image (Meston, Levin, et al., 2004). This
makes it very difficult for orgasm to occur, as not enough pleasure is experienced
to allow the woman to reach the threshold required for orgasm. It is important to
assess whether the anorgasmia is global (occurring in all situations) or is situational
(occurring only in specific circumstances). A woman complaining of anorgasmia may
experience orgasm during masturbation, foreplay, and/or oral sex, but be unable to
reach orgasm during intercourse alone. It is also important to determine whether the
anorgasmia is primary (i.e., she has never experienced an orgasm), or if it is acquired
(i.e., the problem arose following a period of orgasmic ability, as is often the case in
medication-induced anorgasmia).
CBT for orgasmic difficulties in women focuses on decreasing anxiety, changing
thoughts and attitudes surrounding sexuality, promoting positive associations between
emotions and sexual behavior, and increasing satisfaction from and ability to orgasm
(Meston, 2006). It has been used to treat anorgasmia effectively via various treatment
modalities, such as bibliotherapy, and group, individual, and couples therapy, and
is composed typically of various homework exercises that focus on visual and tactile
exploration and awareness of the body, as well as body acceptance. While many of the
techniques employed are arguably physiological (e.g., using guided masturbation or
sexual touch to allow the woman to learn how to experience orgasm), significant cog-
nitive changes are promoted simultaneously (Heiman, 2002). Cognitive techniques
for anorgasmia focus on psychosexual education and communication skills training,
encouraging changes in attitude and sexually relevant thoughts.
Behavioral techniques such as directed masturbation, sensate focus, and systematic
desensitization target anxiety reduction (Meston, Levin, et al., 2004; ter Kuile,
Both, & van Lankveld, 2010). Directed masturbation has been shown to be an
empirically valid, effective treatment for women with primary anorgasmia, and may
be beneficial to women with acquired anorgasmia (Meston, Levin, et al., 2004).
Sensate focus is primarily a couples’ skill-learning process that was summarized earlier.
Systematic desensitization uses progressive relaxation training, hierarchy construction,

and exposure exercises to reduce anxiety (Anderson, 1983).
Finally, behavioral techniques focused on increasing stimulation and awareness of
pleasure can also be used. Kegel exercises (in which an individual, through structured
contraction and relaxation of the pelvic floor, may gain greater control over these
muscles), for example, provide an increased awareness of sensations in the genitals.
Ensuring the woman is receiving sufficient stimulation during sexual activity is also
important, and the coital alignment technique has been found to be particularly useful
in the treatment of anorgasmia. Introduced by Eichel, Eichel, and Kule (1988), the
coital alignment technique involves a specific physical alignment and movement of
partners during sexual intercourse that allows constant clitoral stimulation during
vaginal penetration, resulting in intense and consistent orgasms. This has been shown
to create a mutually satisfying sexual experience (Pierce, 2000).
Several aspects of treatment have been found to be particularly helpful for the
management of anorgasmia. Group treatment is effective in normalizing the problem,
and decreasing feelings of isolation, which are important therapeutic factors. A
focus on arousal and pleasure during sexual activity can reduce goal orientation
and decrease anxiety, while giving permission to experience pleasure. Assertiveness
training is beneficial for sexual functioning, in that the woman feels more able to
identify and ask for what she likes. Finally, a self-centered treatment model (in which
masturbation and responsibility for one’s own sexuality and orgasm are emphasized)
has been shown to increase both individual sexual responsiveness and with a partner.
It has also been suggested that some partner participation in the treatment process
is helpful, both in terms of increasing orgasm response, and in strengthening the
partner relationship (Kuriansky & Sharpe, 1981).
Dyspareunia
Dyspareunia is defined in the DSM-IV-TR as “recurrent or persistent genital pain

associated with sexual intercourse” that causes significant distress or interpersonal dif-
ficulty (APA, 2000, p. 556). The most common reason for dyspareunia is a condition
called “provoked vestibulodynia” (PVD), which is characterized by sharp, stinging,
burning pain around the opening of the vagina and which affects approximately
12–20% of reproductive-aged women (Harlow, Wise, & Stewart, 2001; Landry &
Bergeron, 2009). Because the woman’s pain interferes with sexual activity and rela-
tionship intimacy, PVD can have distressing consequences for psychosocial well-being
and sexual satisfaction (Gates & Galask, 2001; Meana, Binik, Khalifé, & Cohen,
1997; Wikman, Sjöberg, & Danielsson, 2000). The etiology of PVD is multifactorial
and involves pathophysiological changes in pain regulatory pathways, pelvic floor
muscles, and psychological and sexual function (Damsted-Peterson, Boyer, & Pukall,
2009). Because of the long history of the usefulness of CBT in the treatment of non-
sexual chronic pain, and because of the significant anxiety that characterizes women
with PVD (Desrochers, Bergeron, Khalifé, Dupuis, & Jodoin, 2009), this provides
a strong rationale for the use of CBT. The development of validated questionnaires
specifically to address the cognitions characteristic of women with PVD, such as the
Vaginal Penetration Cognition Questionnaire (Klaassen & ter Kuile, 2009), can be an
important method of capturing improvements with CBT in this patient population.
Specifically, penetration-related maladaptive beliefs in women with PVD have been
categorized as control cognitions (e.g., “I am afraid that I will panic during pene-
tration”), catastrophic and pain cognitions (e.g., “I think about everything that can
go wrong and fail with penetration”), self-image cognitions (e.g., “I feel guilty when
penetration is not possible”), positive cognitions (e.g., “penetration is a moment of
intimacy with my partner”), and genital incompatibility cognitions (e.g., “I am afraid
that my vagina is too narrow for penetration”). The vast array of maladaptive beliefs
held by women with PVD suggests that the cognitive challenging strategies within
CBT may be an ideal treatment approach.
Table 27.2 summarizes the existing studies testing CBT for women with dys-
pareunia; in most cases, women had a diagnosis of PVD. Treatment usually always
has a component of education explaining what is known about the pathophysiology
involved in this condition. Cognitive restructuring is aimed at the catastrophizing and
hypervigilance to pain that usually accompanies PVD. In the study reported earlier
which involved randomizing couples in which the female partner experienced a sexual
dysfunction to either 10 weeks of CBT bibliotherapy and minimal therapist support
by telephone or wait-list control (van Lankveld et al., 2001), CBT was not found
to be statistically effective among the women with dyspareunia whereas women with
vaginismus did significantly benefit.
In one of the most widely cited studies showing the effectiveness of CBT for PVD,
Bergeron et al. (2001) randomized 78 women to either vestibulectomy (surgery to
remove the area of the vestibular tissue that was painful), pelvic floor physiotherapy
including biofeedback, or group CBT. They found that participants in all conditions
significantly improved but the surgery group had significantly greater reductions in
genital pain. However, the fact that seven participants dropped out of the surgery
arm while no participants dropped out of the CBT arm suggests that the study may
have been biased in favor of the surgery condition. When women were assessed 2.5
years later, women in the CBT condition maintained the gains achieved immediately
posttreatment whereas women in the vestibulectomy group had lost some of their
improvements on pain during intercourse (Bergeron, Khalifé, Glazer, & Binik,
2008).
In a study on group CBT similar that carried out by Bergeron et al. (2001), Dutch
researchers were primarily interested in mediating factors that predicted patient
outcomes (ter Kuile & Weijenborg, 2006). A total of 76 women with PVD (mean
age 25 years, mean duration of symptoms 4.1 years) participated in 12 biweekly
2-hour group sessions taking place over a period of 6 months. There was a significant
reduction in pain with intercourse, sexual dissatisfaction, vestibular pain, and vaginal
muscle tension. Success of treatment was mediated by improvements in vestibular pain,
sexual dissatisfaction, and vaginal muscle tension. Moreover, changes in vestibular
pain and sexual dissatisfaction during treatment predicted long-term treatment success
at 3-month follow-up. Interestingly, none of the pretreatment scores examined by the
authors, including age, relationship duration, pain duration, treatment expectation,
marital dissatisfaction, psychological distress, vestibular pain, vaginal muscle tension,
or perceived pain control, predicted treatment outcome at follow-up.
Table 27.2 Studies Testing Cognitive Behavioral Therapy in the Treatment of Provoked
Vestibulodynia
Van Lankveld 26 women with 10 weeks of No significant effect of Not effective

et al. (2001) dyspareunia bibliotherapy bibliotherapy on
CBT vs. outcomes
wait-list
control
Bergeron et al. 78 women 10 weeks group Pain reduction with Reductions in
(2001) CBT vs. pelvic vestibular pain index: pain were
floor CBT 28.6%, maintained
physiotherapy vestibulectomy 70%, from 6
with biofeedback 23.7% months post-
biofeedback Reduction in pain treatment to
vs. vestibulec- with intercourse: CBT 2.5-year
tomy 37.5%, vestibulectomy follow-up
52.5%, biofeedback
35%
ter Kuile & 76 women Group CBT Significant reduction in Not reported
Weijenborg taking place pain with intercourse,
(2006) biweekly; 12, vestibular pain, and
2-hour vaginal muscle
sessions over 6 tension; significant
months; no improvements in
control group overall sexual
functioning and
perceived pain control
Brown et al. 43 women Self-manage- All groups effective with None assessed
(2009) ment CBT vs. stronger effects in
oral CBT group (though
amitriptyline study was
vs. topical underpowered)
triamcinolone
plus oral
amitriptyline
Masheb et al. 50 women Individual CBT Both treatments Gains were
(2009) vs. individual significantly effective maintained
supportive Nearly half had at 1-year
psychotherapy clinically significant follow-up
improvements with some
CBT group more women
effective on continuing
cotton-swab ratings of to improve
vestibular pain
Bergeron, 97 women Group CBT vs. Significant pain CBT group

Khalifé, & medical reduction and had greater
Dupuis management improvement in global improve-
(2008) (i.e., localized sexual functioning in ments at
application of both groups 6-month
a cortico- follow-up in
steroid cream, pain, sexual
water-based functioning,
lubricant catastrophiz-
during ing scores,
intercourse, and
and treatment
education) satisfaction
More recently, Brown, Wan, Bachmann, and Rosen (2009) randomized 43 women
to either self-management with CBT, oral amitriptyline, or topical triamcinolone plus
oral amitriptyline for 12 weeks. The CBT arm included group education, physical
therapy, and sex education. There was a significant reduction in pain in the CBT
group and effects appeared to have been stronger than the two medication arms;
however, the lack of power led to nonsignificant group differences.
Masheb, Kerns, Lozano, Minkin, and Richman (2009) more recently compared 42
women who were randomized to either 10 weeks of individual CBT or supportive
psychotherapy. The CBT condition included motivational enhancement, role playing,
problem solving, and contingent reinforcement. The control condition did not
include any elements of behavioral interventions or problem solving. Both treatments
were equally effective on all measures and 42% had a clinically significant reduction in
pain. The CBT group had significantly greater improvements on pain elicited during
a physician cotton swab testing, and on measures of sexual functioning. Continued
improvements in pain severity were observed when women were assessed one year
later. Unfortunately, the absence of a control group means that the mechanisms
underlying improvements, particularly since the support group therapy arm improved,
are unknown.
In the only available study that compared CBT with medical management, Berg-
eron, Khalifé, and Dupuis (2008) randomized women to either 13 weeks of group
CBT or medical management which was comprised of topical application of a cor-
ticosteroid analgesic cream. The group CBT arm consisted of 10 90-minute group
CBT sessions identical to the treatment reported on by Bergeron et al. (2001). Par-
ticipants in both arms reported a significant reduction in pain and an improvement in
their global sexual functioning that was retained at 6 months. At follow-up, however,
women in the CBT group reported significantly more improvement in pain and sexual
functioning, lower catastrophizing, and higher treatment satisfaction. In examining
predictors of treatment outcome, catastrophizing-magnification and pain self-efficacy
functioning significantly predicted pain severity at follow-up for the medical manage-
ment group (Desrochers, Bergeron, Khalifé, Dupuis, & Jodoin, 2010). In the CBT
arm, pain self-efficacy was the single most important predictor of pain intensity at
follow-up.
Vaginismus
Vaginismus is a recurrent or persistent involuntary contraction of the muscles in

the pelvic floor, interfering with vaginal penetration, and causing marked distress
or interpersonal difficulty. Subtypes of vaginismus include lifelong (the woman
has never been able to achieve comfortable penetration) or acquired (penetration
was previously possible, but is now impeded), and generalized (occurring in any
situation) or situational (occurring in specific situations only; e.g., with intercourse
only). According to the DSM-IV-TR, even the anticipation of vaginal insertion may
trigger muscle tightness (APA, 2000). The prevalence of vaginismus is unknown, as
there are no epidemiologically sound estimates available (Reissing, Binik, & Khalifé,
2011). Women with vaginismus have a high rate of comorbid anxiety disorders (van
Lankveld et al., 2010), and associated factors include negative attitudes toward sex
(Basson, 1996), aversion and disgust (Borg, de Jong, & Schultz, 2011), conservative
moral values, childhood sexual trauma (Reissing, Binik, Khalifé, Cohen, & Amsel,
2003), religious orthodoxy, and environmental factors (Stanley, 1981), among other
psychological correlates (Reissing et al., 2011).
Nonsurgical treatments for vaginismus, focusing on the muscle tightness, are
carried out by specialized pelvic floor physiotherapists, and include the use of
progressive vaginal dilation to desensitize the woman to penetration of the vagina
(see Figure 27.2). Dilators are graduated inserts made of plastic, silicon, rubber, or
wax, and range in size from the width of the small finger to the size of an erect
penis. Women are taught to apply lubricant to the dilator, to insert it to a depth of
approximately 10 cm (the length of the unaroused vagina), and to keep the dilator
in place for approximately 10 minutes during which the woman is encouraged to
relax. These insertion exercises ideally take place two or three times a week. Dilator
practice can also be combined with Kegel exercises (to increase control of the vaginal
Figure 27.2 Vaginal dilators. Reproduced by permission of Bruce Watt, Soul Source
Enterprises.
musculature) (Kaplan, 1974), education to normalize and reduce negative beliefs

surrounding sexuality, and psychotherapy targeting phobic avoidance, feelings of
guilt, and fear of pain (Reissing et al., 2011). Physiotherapy that includes biofeedback
of the pelvic floor muscles has also been an important component of treatment, and
is often combined with psychotherapy (Schultz et al., 2005).
It has long been suggested that the vaginal muscle tone inherent in vaginismus is
a phobic reaction to a fear of pain (Walthard, 1909), resulting from real or imagined
negative experiences with sexuality and penetration, or orgasmic difficulties (Masters
& Johnson, 1970; Reissing et al., 2011). Involuntary muscle contraction occurs due
to fear and anxiety about anticipated penetration. According to Wijma and Wijma
(1997), at the beginning of the experience of vaginismus, pain or fear was associated
with penetration, triggering the vaginal muscles to contract reflexively. After a period
of time, the situation in which penetration occurs, or even thoughts of penetration,
can activate the same reflexive muscle contraction, which increases pain, setting
off a vicious cycle. Thus, anxiety plays a significant role in the development and
maintenance of vaginismus, and the tensing of the vaginal muscles is thought to be a
conditioned fear response to sexual stimuli (ter Kuile et al., 2007).
Because of the proposed model of maintenance, psychological treatment has been
the favored treatment for vaginismus, rather than earlier solutions such as surgical
intervention (Reissing et al., 2011). Recently, treatment programs have also included
exposure techniques to allow the woman gradually to decrease her anxiety in situations
where vaginal penetration will be attempted. Fear of vaginal penetration is maintained
through avoidance behavior, which prevents opportunities to disconfirm irrational
beliefs (Leiblum, 2000; e.g., “I cannot handle the pain, intercourse is impossible”).
Therefore, CBT directly targets avoidance behaviors so that associated maladaptive
beliefs can be challenged and disconfirmed, and the conditioned fear response can be
overcome. Studies have found that focusing on explicit and systematic exposure to
stimuli during penetration increases the ability to engage in sexual intercourse (ter
Kuile et al., 2007).
Rosenbaum (2011) developed a series of graduated exposures designed to prepare
a client, physically and emotionally, for vaginal penetration (including genital self-
examination, pelvic examination, finger and dilation insertion, and sexual intercourse).
Through a series of six steps, which range from lying fully dressed and covered by a
sheet on an examination table, to lying uncovered on the same table undressed and
without underwear, the woman is given the instruction to experience and control her
anxiety, with the understanding that she can always go back a step to a place where
she feels more secure. The theory behind this method is that the woman learns to
have greater control over the exposure process, and rather than viewing anxiety as
an uncontrollable entity, she will begin to recognize and accept anxiety as something
that can be controlled. As the exposure stages progress, the anxiety is experienced as
less and less intense, finally fading away altogether. Similar techniques can be applied
for gradually increasing the use of a dilator, either on her own, or with a partner.
The duration of this exposure process depends entirely on the woman, and can range
from one therapy visit up to six. Rosenbaum (2011) notes that failure to progress
along these steps warrants a referral to the client’s psychotherapist, where additional
CBT techniques, such as challenging specific thoughts surrounding penetration, can

be addressed.
The series of gradual exposures just described fits nicely into the therapeutic process
of CBT. While it may be difficult to implement such a regimen of in vivo exposures in
session, imaginal exposures can be utilized to allow the woman to become used to the
idea of progressing through the stages. Thought challenging can be very useful to facil-
itating this process, in that it allows the woman to reconceptualize beliefs that maintain
the fear of penetration. A major goal of CBT for genital pain is to reconceptualize the
pain as being a multidimensional problem that is influenced by a number of factors,
including thoughts, emotions, behaviors, and relationship factors (Bergeron & Lord,
2003). Gradual exposures, such as those just described, are nearly always combined
with some form of applied relaxation (ter Kuile, Bulte, Weijenborg, Beekman, &
Melles, 2009). Additional CBT techniques include psychoeducation on genital pain
and its impact on sexuality, pain monitoring, distraction techniques (meant to focus
attention on sexual stimuli, rather than on pain), and communication skills training.
Negative beliefs surrounding sexuality can influence interpretations of sexual sit-
uations in such a way that distortions in cognitive processing are induced. These
distortions, along with behavioral responses to negative thoughts, may contribute
to the maintenance of vaginismus and sexual pain, and can be targeted using CBT
techniques such as behavioral experiments and exposure (Borg et al., 2011). As
mentioned above, women with vaginismus have more conservative moral values than
women without, and it has been speculated that the perceived immorality of sex and
sexual stimuli might play an active role in the defensive contraction of the pelvic
floor muscles. These strong negative values and thoughts surrounding vaginismus
are ideal targets for CBT in that alternate perspectives can be explored with the
client to determine whether there might be different ways to evaluate sexual sit-
uations. Table 27.3 summarizes the existing studies testing CBT for women with
vaginismus.
Case Example
Presenting Complaint
Veronica is a 48-year-old woman who has been married for 21 years. She presented
for treatment with the primary complaint of infrequent sexual intercourse. Veronica
is a perimenopausal woman who is the senior librarian at a university library. She and
her husband, Bob, have two children, aged 16 and 9, both of whom live with the
couple. Veronica noted that sexual intercourse took place once every 3 or 4 months,
typically late at night, and tended to consist of limited to no intercourse followed by
a quick intromission period that ended in her husband reaching ejaculation after only
a few minutes.
During sexual activity, Veronica said that her mind was focused on wondering
when sex would be over. She described significant concerns about her body, and
being distracted by the fact that she had still not lost the 60 pounds she gained
while pregnant with her second child. Because of her body image concerns, she
Table 27.3 Studies Testing Cognitive Behavioral Therapy in the Treatment of Vaginismus
ter Kuile et al. 117 women 3 months of group or bibliotherapy Increased frequency of Not reported
(2007) with lifelong CBT vs. wait-list control intercourse, decreased fear of
vaginismus coitus, and an enhancement of
non-coital penetrative behavior.
Intercourse frequency was partially
mediated by changes in fear of
coitus and avoidance behavior.
No treatment predictors were
detected.
van Lankveld 117 women 3 months of group or bibliotherapy 18% of CBT participants had CBT participants were able to engage in
et al. (2006) CBT vs. wait-list control successfully attempted penile-vaginal intercourse at follow-up
penile-vaginal intercourse, (27% at 3 months, 28% at 12 months)
compared with none in the
control group.
ter Kuile et al. 10 women 3 therapist-aided exposure sessions 90% of participants were able to Results remained at 1-year follow-up
(2009) over 1 week, plus 2 follow-up engage in intercourse following
sessions, single-case A-B design treatment.
Level of fear and pain beliefs
surrounding penetration
decreased.
Seo, Choe, & 12 women 8 weeks of functional electrical All women could engage in None assessed
Lee (2005) stimulation biofeedback (to train satisfactory vaginal
the women to gain control over intercourse.
their vaginal musculature, such that
they could learn to relax the pelvic
muscle contractions that compose
vaginismus) along with CBT
The re-education and reactivation
of the ability to control the
pelvic floor muscles through
biofeedback seems to be an
effective tool in the treatment
of vaginismus.
This technique is acceptable to
women suffering from
vaginismus and provides
strong motivation to
continue with treatment.
Engman, 44 women 14 sessions of CBT Not assessed At a mean of 39 months posttreatment,
Wijma, & 81% maintained the ability to engage
Wijma in intercourse, and 61% reported
(2010) reduced pain with intercourse.
The authors cited a noteworthy
increase in participants’ subjective
self-worth as women and as human
beings.
insisted that they have sexual intercourse with the lights completely off, and she
did not allow Bob to caress her body with his hands. During sexual activity she
also remained hypervigilant to any sounds from outside the room, and reported
being fearful that one of their children would walk in and see them having
sex. Because of this, Veronica kept her vocalizations during love-making deliber-
ately minimal. Veronica reported having desire “out of the blue” approximately
once or twice a year, typically during their vacations, and she would occasion-
ally masturbate, but mostly as a means of falling asleep. Veronica reported only a
minimal genital arousal response during sex, and denied ever having an orgasm
in her life. However, intercourse was not painful. She indicated that she has
never really craved sexual activity, but that her current absence of any desire has
been especially pronounced for the last few years as her responsibilities with work
increased.
Prior to seeking treatment, Veronica and Bob had experimented with different
sexual positions (at Bob’s suggestion) in hopes of creating more pleasure. They
had also tried a course of androgel (50 mg), which she applied to her abdomen
four hours before sexual activity, prescribed by Veronica’s primary care physician.
Neither of these interventions was helpful. Their current request for treatment was
prompted by Bob’s increasing frustration at their infrequent sexual activity, which
was creating tension in their relationship. Whereas their communication, in general,
was good, the topic of sexuality made Veronica anxious as she believed that Bob was
truly unhappy in their marriage and would leave unless their sexual frequency
improved.
Assessment
During her individual interview, Veronica described some discomfort about sexual
topics that she related to her early childhood when her parents warned her against
the dangers of sex. Veronica had had a few sex partners prior to Bob, and although
there was some desire during the first few months of those relationships, it faded
as the relationships progressed and became more serious. Veronica felt that she was
completely responsible for the failure of those relationships and attributes this to her
sexual problems. To this day, she reported believing that the success of her marriage
will depend on whether her sexual difficulties can improve, and carried significant
guilt around this belief.
A brief psychiatric examination was performed. Veronica had no history of major
depressive episodes, though she had suffered from dysthymia for most of her life.
Anxiety was a more pronounced symptom for her. She described having a hard time
relaxing, which was difficult for Bob, who enjoyed spending time away from work
watching movies or taking naps. She denied any history of childhood or adult sexual
abuse.
Veronica’s health was excellent. She exercised regularly and did not smoke or
consume alcohol. She was not using any medications although she did suffer from
migraine headaches (once a month) for which she used Tylenol-3 with adequate
effectiveness. She had no history of endocrine problems and her surgical history
included two cesarean sections.
Formulation
Veronica did not have sexual thoughts, fantasies, or desire for sexual activity. However,
on most occasions of sexual activity, she did experience some pleasure and sexual desire
after sex began, though it was short-lived because of Bob’s rapid ejaculation. She met
criteria for HSDD according to the DSM-IV-TR. On the basis of her brief medical
history, it is unlikely that there was a significant medical and/or hormonal component
to Veronica’s reduced sexual desire. She did not feel that perimenopause contributed
to her loss of sexual interest given that it had been much more long standing.
Veronica had several problematic automatic thoughts. Among them was the belief
that her children might hear them having sex, that masturbation is wrong, and that
it is inappropriate for Bob to caress her body. She was also very preoccupied with
her negative body image and believed that Bob found her body repulsive, which led
her to avoid sex even more. Veronica had sex solely out of a sense of obligation, she
resented being asked for sex by Bob, and she experienced guilt for her low desire.
Her behaviors included avoidance of talking about her low desire, deliberately going
to bed after Bob, and thinking about other obligations on her to-do list during
sex. Each of these cognitions, emotions, and behaviors led to a cascade of other
thoughts, feelings, and behaviors; thus, a tightly woven vicious circle was spun around
Veronica’s sexual activity and low desire.
A CBT approach was adopted. Treatment focused on identifying, challenging,
and replacing her automatic thoughts related to sex. It was helpful for Veronica to
complete a thought record to see the range of her automatic thoughts and how they
gave rise to a host of negative emotions and problematic behaviors. Given Veronica’s
significant distractibility, multitasking, and anxiety proneness, a mindfulness-based
cognitive behavioral intervention was also added. Over time, this allowed Veronica to
have more compassion for herself and treat her body image related concerns during sex
to be viewed simply as “mental events” which, over time, were less likely to provoke
anxiety and guilt. We also normalized her age and relationship-related changes in
sexual desire, and instead worked together to cultivate sexual pleasure during the
sexual interaction, given that this was often associated with triggering desire for her.
It was also important that Bob’s early ejaculation be explored by his primary care
provider given that the wakening of Veronica’s sexual response was usually shortened
due to Bob’s ejaculating too quickly. Over the course of 6 months, Veronica learned
to accept her problematic thoughts as just thoughts, she learned methods of relaxation
and mindfulness to remain more present during sexual encounters, and she began to
challenge some of her more problematic beliefs about the children hearing her during
sex, leading to a gradual improvement in her feelings of sexual pleasure during sex
and a corresponding increase in the frequency of their planned sexual interactions.
Future Directions in Cognitive Behavioral Therapy and

Women’s Sexual Difficulties
Taken together, although there is evidence for the beneficial effect of CBT on
women’s sexual difficulties, the majority of this research was carried out prior to 1995
and there is little current research evaluating CBT in this domain. This may partially
be attributable to the boom in scientific research seeking a pharmaceutical product
to cure women’s sexual difficulties. The lack of any FDA-approved medication for
women’s sexual difficulties, however, suggests that there remains work to be done
for sex researchers in the area of evidence-based psychological therapies (Rowland,
2007). There is growing, but insufficient, evidence that CBT works to improve
women’s sexual difficulties; however, there is also recent evidence that medications
thought to be on a clear pathway to FDA approval for improving sexual dysfunction
in women are about as effective as a placebo pill (BioSante Pharmaceuticals, 2011).
This is a crucial time for sex therapy and research to use this pendulum shift
to further develop and test CBT treatments for sexual dysfunction in women. A
growing body of literature showing the benefits of mindfulness-based CBT in other
domains of health (Grossman, Niemann, Schmidt, & Walach, 2004) also supports
recent efforts to develop and test similar interventions for women with sexual
complaints.
References
Adams, A. E., III., Haynes, S. N., & Brayer, M. A. (1985). Cognitive distraction in female
sexual arousal. Psychophysiology, 22, 689–696. doi:10.111/j.1469-8986.1985.tb01669.x
Anderson, B. L. (1983). Primary orgasmic dysfunction: Diagnostic considerations and review
of treatment. Psychological Bulletin, 93, 105–136.
Bancroft, J. (1977). The behavioral approach to treatment. In J. Money & H. Musaph (Eds.),
Handbook of sexology (pp. 1197–1225). North Holland, The Netherlands: Elsevier
Science.
Barlow, D. H. (1986). Causes of sexual dysfunction: The role of anxiety and cognitive inter-
ference. Journal of Consulting and Clinical Psychology, 54, 140–148. doi:10.1037/0022-
006X.54.2.140
Basson, R. (1996). Lifelong vaginismus: A clinical study of 60 consecutive cases. Journal of the
Society of Obstetrics and Gynecology Canada, 3, 551–561. doi:10.2217/whe.10.46
Beck, J. G. (1995). Hypoactive sexual desire disorder: An overview. Journal of Consulting and
Bergeron, S., Binik, Y. M., Khalifé, S., Pagidas, K., Glazer, H. I., Meana, M., & Amsel, R.
(2001). A randomized comparison of group cognitive-behavioral therapy, surface elec-
tromyographic biofeedback, and vestibulectomy in the treatment of dyspareunia resulting
from vulvar vestibulitis. Pain, 91, 297–306. doi:10.1016/S0304-3959(00)00449-8
Bergeron, S., Khalifé, S., & Dupuis, M. (2008, February). Provoked vestibulodynia: A random-
ized comparison of cognitive-behavioral therapy and medical management. Paper presented
at the Annual Meeting of the International Society for the Study of Women’s Sexual
Health, San Diego, CA.
Bergeron, S., Khalifé, S., Glazer, H. I., & Binik, Y. M. (2008). Surgical and behavioral treat-
ments for vestibulodynia: Two-and-one-half year follow-up and predictors of outcome.
Obstetrics & Gynecology, 111, 159–166. doi:10.1097/01.AOG.0000295864.76032.a7
Bergeron, S., & Lord, M. (2003). The integration of pelvi-perineal re-education and cognitive-
behavioural therapy in the multidisciplinary treatment of the sexual pain disorders. Sexual
and Relationship Therapy, 18, 135–141. doi:10.1080/1468199031000099406
Binik, Y. M., & Meana, M. (2009). The future of sex therapy: Specialization or marginalization?
Archives of Sexual Behaviour, 38, 1016–1027. doi:10.1007/s10508-009-9475-9
BioSante Pharmaceuticals. (2011). News Release: BioSante Pharmaceuticals announces results
from LibiGel® efficacy trials. Retrieved from http://www.biosantepharma.com/News-
Releases.php?ID=121411
Borg, C., de Jong, P. J., & Schultz, W. W. (2011). Vaginismus and dyspareunia: Relationship
with general and sex-related moral standards. Journal of Sexual Medicine, 8, 223–231.
doi:10.1111/j.1743-6109.2010.02080.x
Brotto, L. A., Basson, R., & Luria, M. (2008). A mindfulness-based group psychoeducational
intervention targeting sexual arousal disorder in women. Journal of Sexual Medicine, 5,
1646–1659. doi:10.1111/j.1743-6109.2008.00850.x
Brotto, L. A., & Heiman, J. R. (2007). Mindfulness in sex therapy: Applications for women
with sexual difficulties following gynecologic cancer. Sexual & Relationship Therapy, 22,
3–11. doi:10.1080/14681990601153298
Brotto, L. A., Heiman, J., Goff, B., Greer, B., Lentz, G., Swisher, E., … Van Blaricom,
A. (2008). A psychoeducational intervention for sexual dysfunction in women with
gynecologic cancer. Archives of Sexual Behavior, 37 , 317–329. doi:10.1007/s10508-
007-9196-x
Brotto, L. A., Seal, B. N., & Rellini, A. (2012). Pilot study of a brief cognitive behav-
ioral versus mindfulness-based intervention for women with sexual distress and a
history of childhood sexual abuse. Journal of Sex & Marital Therapy, 38, 1–27.
doi:10.1080/0092623X.2011.569636
Brown, C. S., Wan, J., Bachmann, G., & Rosen, R. (2009). Self-management, amitriptyline,
and amitriptyline plus triamcinolone in the management of vulvodynia. Journal of Women’s
Health, 18, 163–169. doi:10.1089/jwh.2007.0676
17–31. doi:10.1016/j.cpr.2005.07.003
Chivers, M. L., & Bailey, J. M. (2005). A sex difference in features that elicit genital response.
Biological Psychology, 70, 115–120. doi:10.1016/j.biopsycho.2004.12.002
Chivers, M. L., Seto, M. C., Lalumière, M. L., Laan, E., & Grimbos, T. (2010). Agreement of
self-reported and genital measures of sexual arousal in men and women: A meta-analysis.
Archives of Sexual Behavior, 39, 5–56. doi:10.1007/s10508-009-9556-9
Damsted-Petersen, C., Boyer, S. C., & Pukall, C. F. (2009). Current perspectives in vulvodynia.
Women’s Health, 5, 423–436. doi:10.2217/whe.09.30
Desrochers, G., Bergeron, S., Khalifé, S., Dupuis, M. J., & Jodoin, M. (2009). Fear avoidance
and self-efficacy in relation to pain and sexual impairment in women with provoked vestibu-
lodynia. Clinical Journal of Pain, 25, 520–527. doi:10.1097/AJP.0b013e31819976e3
Desrochers, G., Bergeron, S., Khalifé, S., Dupuis, M., & Jodoin, M. (2010). Provoked vestibu-
lodynia: Psychological predictors of topical and cognitive-behavioral treatment outcome.
Dove, N. L., & Wiederman, M. W. (2000). Cognitive distraction and women’s sexual function-
ing. Journal of Sex and Marital Therapy, 26, 67–78. doi:10.1080/009262300278650
Eichel, W., Eichel, M. A., & Kule, S. (1988). The technique of coital alignment and its relation
to female orgasmic response and simultaneous orgasm. Journal of Sex and Marital
Therapy, 14, 129–141. doi:10.1080/00926238808403913
Elliott, A. N., & O’Donohue, W. T. (1997). The effects of anxiety and distraction on sexual
arousal in a nonclinical sample of heterosexual women. Archives of Sexual Behavior, 26,
607–624. doi:10.1023/A:1024524326105
Engman, M., Wijma, K., & Wijma, B. (2010). Long-term coital behaviour in women treated
with cognitive behaviour therapy for superficial coital pain and vaginismus. Cognitive
Behaviour Therapy, 39, 193–202. doi:10.1080/16506070903571014
Freud, S. (1905). Three essays on the theory of sexuality (J. Strachey, Trans.). New York, NY:
Basic Books.
Gates, E. A., & Galask, R. P. (2001). Psychological and sexual functioning in women with
vulvar vestibulitis. Journal of Psychosomatic Obstetrics and Gynaecology, 22, 221–228.
doi:10.3109/01674820109049977
Graham, C. A. (2010a). The DSM diagnostic criteria for female orgasmic disorder. Archives of
Sexual Behaviour, 39, 256–270. doi:10.1007/s10508-009-9542-2
Graham, C. A. (2010b). The DSM diagnostic criteria for female sexual arousal disorder.
Archives of Sexual Behavior, 39, 240–255. doi:10.1007/s10508-009-9535-1
35–43. doi:10.1016/S0022-3999(03)00573-7
Harlow, B. L., Wise, L. A., & Stewart, E. G. (2001). Prevalence and predictors of chronic lower
genital tract discomfort. American Journal of Obstetrics and Gynecology, 185, 545–550.
doi:10.1067/mob.2001.116748
Hawton, K., Catalan, J., Martin, P., & Fagg, J. (1986). Long-term outcome of sex therapy.
Behaviour Research and Therapy, 24, 665–675. doi:10.1016/0005-7967(86)90062-8
Heiman, J. (2002). Psychologic treatments for female sexual dysfunction: Are they
effective and do we need them? Archives of Sexual Behavior, 31, 445–450.
doi:10.1023/A:1019848310142
Hurlbert, D. (1993). A comparative study using orgasm consistency training in the treatment
of women reporting hypoactive sexual desire. Journal of Sex & Marital Therapy, 19,
49–55. doi:10.1080/00926239308404887
Kabat-Zinn, J. (1990). Full-catastrophe living. New York, NY: Dell.
Kaplan, H. S. (1974). The new sex therapy: Active treatment of sexual dysfunctions. New York,
NY: Brunner & Mazel.
Kaplan, H. S. (1977). Hypoactive sexual desire. Journal of Sex & Marital Therapy, 3, 3–9.
doi:10.1080/00926237708405343
Kaplan, H. S. (1979). Disorders of sexual desire. New York, NY: Brunner & Mazel.
Klaassen, M., & ter Kuile, M. M. (2009). Development and initial validation of the Vaginal
Penetration Cognition Questionnaire (VPCQ) in a sample of women with vaginismus
and dyspareunia. Journal of Sexual Medicine, 6, 1617–1627. doi:10.1111/j.1743-
6109.2009.01217.x
Koukounas, E., & McCabe, M. P. (1997). Sexual and emotional variables influencing sexual
response to erotica. Behaviour Research and Therapy, 35, 221–231. doi:10.1016/S0005-
7967(96)00097-6
Kuriansky, J. B., & Sharpe, L. (1981). Clinical and research implications of the evaluation of
women’s group therapy for anorgasmia: A review. Journal of Sex & Marital Therapy, 7 ,
268–277. doi:10.1080/00926238108405428
Landry, T., & Bergeron, S. (2009). How young does vulvo-vaginal pain begin? Prevalence
and characteristics of dyspareunia in adolescents. Journal of Sexual Medicine, 6, 927–935.
doi:10.1111/j.1743-6109.2008.01166.x
Leiblum, S. R. (2000). Vaginismus: A most perplexing problem. In S. R. Leiblum & R. C.
Rosen (Eds.), Principles and practices of sex therapy (3rd ed., pp. 181–202). New York,
NY: Guilford Press.
Lief, H. I. (1977). Inhibited sexual desire. Medical Aspects of Human Sexuality, 7 , 94–95.
Lief, H. I., & Friedman, R. C. (2006). History of psychologic treatments. In I. Goldstein, C.

M. Meston, S. R. Davis, & A. M. Traish (Eds.), Women’s sexual function and dysfunction:
Study diagnosis and treatment. London, England: Taylor & Francis.
Masheb, R. M., Kerns, R. D., Lozano, C., Minkin, M. J., & Richman, S. (2009). A
randomized clinical trial for women with vulvodynia: Cognitive-behavioral therapy vs.
supportive psychotherapy. Pain, 141, 31–40. doi:10.1016/j.pain.2008.09.031
Masters, W. H., & Johnson, V. E. (1966). Human sexual response. Boston, MA: Little Brown
Company.
Masters, W. H., & Johnson, V. E. (1970). Human sexual inadequacy. Boston, MA: Little
Brown Company.
McCarthy, B., & Thestrup, M. (2008). Integrating sex therapy interventions with couple
therapy. Journal of Contemporary Psychotherapy, 38, 139–149. doi:10.1007/s10879-
008-9083-3
Meana, M. (2010). Elucidating women’s (hetero)sexual desire: Definitional challenges
and content expansion. Journal of Sex Research, 47 , 104–122. doi:10.1080/
00224490903402546
Meana, M., Binik, Y. M., Khalifé, S., & Cohen, D. R. (1997). Biopsychosocial profile of
women with dyspareunia. Obstetrics and Gynecology, 90, 583–589. doi:10.1016/S0029-
7844(98)80136-1
Meston, C. M. (2006). Female orgasmic disorder: Treatment strategies and outcome results. In
I. Goldstein, C. M. Meston, S. R. Davis, & A. M. Traish (Eds.), Women’s sexual function
and dysfunction: Study, diagnosis and treatment (pp. 449–461). London, England: Taylor
& Francis.
Meston, C. M., Hull, E., & Levin, R. J. (2004). Disorders of orgasm in women. Journal of
Sexual Medicine, 1, 66–68. doi:10.1111/j.1743-6109.2004.10110.x
Meston, C. M., Levin, R. J., Sipski, M. L., Hull, E. M., & Heiman, J. R. (2004b). Women’s
orgasm. Annual Review of Sex Research, 15, 181–265.
Meston, C. M., Rellini, A., & Telch, M. (2008). Short- and long-term effects of ginkgo biloba
extract on sexual dysfunction in women. Archives of Sexual Behavior, 37 , 530–547.
doi:10.1007/s10508-008-9316-2
Morokoff, P. J., & Heiman, J. R. (1980). Effects of erotic stimuli on sexually functional and
dysfunctional women: Multiple measures before and after sex therapy. Behaviour Research
and Therapy, 18, 127–137. doi:10.1016/0005-7967(80)90107-2
Nobre, P., & Pinto-Gouveia, J. (2006). Emotions during sexual activity: Differences between
sexually functional and dysfunctional men and women. Archives of Sexual Behavior, 35,
491–499. doi:10.1007/s10508-006-9047-1
Nobre, P. J., & Pinto-Gouveia, J. (2008a). Differences in automatic thoughts presented during
sexual activity between sexually functional and dysfunctional men and women. Journal of
Cognitive Therapy and Research, 32, 37–49. doi:10.1007/s10608-007-9165-7
Nobre, P. J., & Pinto-Gouveia, J. (2008b). Cognitive and emotional predictors of female sexual
dysfunctions: Preliminary findings. Journal of Sex & Marital Therapy, 34, 325–342.
doi:10.1080/00926230802096358
Pierce, A. P. (2000). The coital alignment technique (CAT): An overview of studies. Journal
of Sex & Marital Therapy, 26, 257–268. doi:10.1080/00926230050084650
Reissing, E. D., Binik, Y. M., & Khalifé, S. (2011). Does vaginismus exist? A critical review of
the literature. Journal of Nervous & Mental Disease, 187 , 261–274.
Reissing, E. D., Binik, Y. M., Khalifé, S., Cohen, D., & Amsel, R. (2003). Etiological
correlates of vaginismus: Sexual and physical abuse, sexual knowledge, sexual self-
schema, and relationship adjustment. Journal of Sex and Marital Therapy, 29, 47–59.
doi:10.1080/713847095
Rosenbaum, T. Y. (2011). Addressing anxiety in vivo in physiotherapy treatment of women

with severe vaginismus: A clinical approach. Journal of Sex & Marital Therapy, 37 , 89–93.
doi:10.1080/0092623X.2011.547340
Rowland, D. L. (2007). Will medical solutions to sexual problems make sexologi-
cal care and science obsolete? Journal of Sex & Marital Therapy, 33, 385–397.
doi:10.1080/00926230701477022
Sarwer, D. B., & Durlak, J. A. (1997). A field trial of the effectiveness of behavioral
treatment for sexual dysfunctions. Journal of Sex and Marital Therapy, 23, 87–97.
doi:10.1080/00926239708405309
Schultz, W., Basson, R., Binik, Y., Eschenbach, D., Wesselmann, U., & van Lankveld,
J. (2005). Women’s sexual pain and its management. Journal of Sexual Medicine, 2,
301–316. doi:10.1111/j.1743-6109.2005.20347.x
Seo, J., Choe, J. H., & Lee, W. S. (2005). Efficacy of functional electrical stimulation-
biofeedback with sexual cognitive-behavioral therapy as a treatment for vaginismus.
Urology, 66, 77–81. doi:10.1080/00926239708405309
Shifren, J. L., Monz, B. U., Russo, P. A., Segreti, A., & Johannes, C. B. (2008). Sexual
problems and distress in United States women: Prevalence and correlates. Obstetrics and
Gynecology, 112, 970–978. doi:10.1097/AOG.0b013e3181898cdb
Stanley, E. (1981). Vaginismus. British Medical Journal, 282, 1435–1437.
ter Kuile, M. M., Both, S., & van Lankveld, J. J. D. M. (2010). Cognitive behavioral therapy
for sexual dysfunctions in women. Psychiatric Clinics of North America, 33, 595–610.
doi:10.1016/j.psc.2010.04.010
ter Kuile, M. M., Bulte, I., Weijenborg, P. T. M., Beekman, A., & Melles, R. (2009). Therapist-
aided exposure for women with lifelong vaginismus: A replicated single-case design.
Journal of Consulting and Clinical Psychology, 77 , 149–159. doi:10.1037/a0014273
ter Kuile, M. M., van Lankveld, J., de Groot, H. E., Melles, R., Neffs, J., & Zand-
bergen, M. (2007). Cognitive-behavioral therapy for women with lifelong vaginis-
mus: Process and prognostic factors. Behavior Research and Therapy, 45, 359–373.
doi:10.1016/j.brat.2006.03.013
ter Kuile, M. M., & Weijenborg, P. T. (2006). A cognitive-behavioral group program for
women with vulvar vestibulitis syndrome (VVS): Factors associated with treatment success.
Journal of Sex and Marital Therapy, 32, 199–213. doi:10.1080/00926230600575306
Trudel, G., Marchand, A., Ravart, M., Aubin, S., Turgeon, L., & Fortier, P. (2001). The effect
of a cognitive behavioral treatment group program on hypoactive sexual desire in women.
Sexual and Relationship Therapy, 16, 145–164. doi:10.1080/14681990120040078
van Lankveld, J. J. D. M., Everaerd, W., & Grotjohann, Y. (2001). Cognitive-behavioral
bibliotherapy for sexual dysfunctions in heterosexual couples: A randomized waiting-
list controlled clinical trial in the Netherlands. Journal of Sex Research, 38, 51–67.
doi:10.1080/00224490109552070
van Lankveld, J. J., Granot, M., Weijmar Schultz, W. C., Binik, Y. M., Wesselmann, U., Pukall,
C. F., … Achtrari, C. (2010). Women’s sexual pain disorders. Journal of Sexual Medicine,
7 , 615–631. doi:10.1111/j.1743-6109.2009.01631.x
van Lankveld, J. J. D. M., ter Kuile, M. M., de Groot, H. E., Melles, R., Nefs, J., & Zand-
bergen, M. (2006). Cognitive-behavioral therapy for women with lifelong vaginismus:
A randomized waiting-list controlled trial of efficacy. Journal of Consulting and Clinical
Psychology, 74, 168–178. doi:10.1037/0022-006X.74.1.168
Walthard, M. (1909). Die psychogene aetiologie und die psychotherapie des vaginismus.
Muench Med Wochensch, 56, 1997–2000.
Wijma, K., & Wijma, B. (1997). Posttraumatic stress disorder after childbirth: A cross sectional
study. Journal of Anxiety, 11, 587–597. doi:10.1016/S0887-6185(97)00041-8
Wikman, M., Sjöberg, I., & Danielsson, I. (2000). Vulvar vestibulitis: Medical, psychosexual and
psychosocial aspects, a case–control study. Acta Obstetricia et Gynecologica Scandinavica,
79, 872–872. doi:10.1034/j.1600-0412.2000.079010872.x
28
Male Sexual Dysfunctions
Pedro Nobre
Universidade do Porto, Portugal
Introduction
Male sexual dysfunctions are highly prevalent clinical conditions with strong negative
impact on men’s well-being and life satisfaction (Laumann, Paik, & Rosen, 1999). In
this chapter we will review the description and classification of sexual dysfunctions,
present findings on prevalence and comorbidity, discuss the psychological etiology and
conceptual models of sexual dysfunction, describe the assessment process, and present
the main components of cognitive behavioral treatments for male sexual dysfunction.
Classification and Description of Sexual Dysfunctions

The consecutive revisions of the Diagnostic and Statistical Manual of Mental Dis-
orders (DSM; American Psychiatric Association [APA], 2000) and the International
Classification of Diseases (ICD; World Health Organization, 1992) have demon-
strated the historical evolution of the concepts of sexual normality/pathology. The
DSM-II (APA, 1968) was the first edition to include a category for genital-urinary
disorders, which would be the precursor of sexual disorders. Later, the DSM-III
(APA, 1980) constituted a crucial turning point, with the classification of sexual
disorders relying on the pioneer studies of Masters and Johnson (1966, 1970)
and the subsequent developments proposed by Kaplan (1979). Since then, sex-
ual dysfunction has been conceptualized as a difficulty in one or more of the
sexual response cycle phases. The DSM-IV-TR (APA, 2000) classifies sexual dys-
functions according to four phases: sexual desire, sexual arousal, orgasm, and
resolution. Besides these phases, the DSM-IV-TR (APA, 2000) adds a specific
category for disorders associated with sexual pain (see Table 28.1). Whenever a
disorder is observed in more than one of the categories, this should be identified

DOI: 10.1002/9781118528563.wbcbt28
Table 28.1 Categories of Male Sexual Dysfunction as Proposed by

the DSM-IV-TR
Response cycle phase Male sexual disorders
Desire Hypoactive sexual desire disorder

Sexual aversion
Arousal Male erectile disorder
Orgasm Male orgasmic disorder
Premature ejaculation
Pain Dyspareunia
by reporting as many diagnoses as observed. However, special attention should

be addressed to differential diagnosis as well as to principal diagnosis (the main
complaint presented, which should be the principal target of therapy). Addition-
ally, the diagnosis of sexual dysfunction should be complemented with indications
regarding the associated onset (lifelong or acquired), context (generalized or situ-
ational), and etiological factors (due to psychological factors or due to combined
factors).
Sexual desire disorders. The majority of the classification systems consider two clinical
diagnoses of sexual desire disorders: hypoactive sexual desire disorder and sexual
aversion. Deficiency or absence of sexual fantasies and desire to engage in sexual
activity characterize the first dysfunction, while the second is best described by
the aversive and avoidance response to any sexual contact with a partner (APA,
2000).
Male erectile disorder. Male erectile disorder is defined by the DSM-IV-TR (APA,
2000) as the persistent or recurrent inability to attain, or to maintain until completion
of sexual activity, an adequate erection (criterion A), causing marked distress or
interpersonal difficulties (criterion B). Erectile difficulties may occur regardless of
sexual activities, partners, or stimulation types (generalized type), or be present in
determined specific situations (e.g., sexual intercourse vs. masturbation) or with
specific partners (usual sexual partner vs. occasional partner) (APA, 2000). In the two
last examples etiology is mainly psychological, while the first example suggests further
inquiry regarding the potential role of organic factors.
Orgasmic disorders. Orgasmic disorders are described as difficulties related to orgasmic

response, which constitutes the climax of sexual activity and is characterized by a set of
physiological (rhythmic contraction of the perineal muscles) and subjective responses
(climax sensations or tension relief). This diagnostic group includes two different
clinical manifestations. Male orgasmic disorder is defined by the DSM-IV-TR (APA,
2000) as the persistent or recurrent delay or absence of orgasm after a “normal” sexual
Male Sexual Dysfunctions 647
excitement phase (criterion A) causing marked distress or interpersonal difficulties

(criterion B). Premature ejaculation is defined as the persistent or recurrent onset of
orgasm and ejaculation with minimum stimulation before or shortly after penetration,
and before the subject wishes it (criterion A), causing marked distress or interpersonal
difficulties (criterion B) (APA, 2000).
Sexual pain disorders. Sexual pain disorders include two different clinical manifesta-
tions: dyspareunia, which consists in the experience of pain associated with sexual
activity (usually before, during, or after intercourse), and vaginismus, which is char-
acterized by the involuntary contraction of the muscles surrounding the outer third
of the vagina interfering with sexual intercourse (APA, 2000). Dyspareunia could
be diagnosed to both men and women, although its presence is significantly higher
among women (Masters & Johnson, 1970), while vaginismus is exclusive to the
female population. In men, sexual pain is usually associated with medical conditions
such as Peyronie disease or urinary infections.
New classification proposals. The DSM classification of sexual disorders has been the
object of criticism, and some alternative classification systems have been developed
(National Institutes of Health Impotence, 1993; Lue et al., 2004). The main
objections have been related to the terminology and inconsistency of the definitions,
lack of objective and quantified criteria, and lack of scientific evidence. Currently,
the DSM-5 work group for sexual dysfunctions is proposing a new classification,
taking into account some of the most common criticisms of the DSM-IV as well
as a thorough review of evidence-based literature in the field. The DSM-5 work
group is suggesting changes in the terminology of some clinical conditions (e.g., male
orgasmic disorder is substituted by delayed ejaculation, and premature ejaculation is
now termed early ejaculation). Moreover, temporal criteria are now included, with
a minimum of 6 months of persistent or recurrent difficulties as the threshold for
assigning a clinical diagnosis. Additionally, severity and frequency of the symptoms
are introduced as important markers, with clinical diagnosis being assigned only when
the symptoms occur on at least 75% of sexual occasions. Finally, a list of specifiers
is suggested for inclusion in the diagnosis (e.g., partner factors, relationship factors,
individual vulnerability factors, cultural/religious factors) (Segraves, 2010a, 2010b,
2010c).
Prevalence of Male Sexual Dysfunction

Studies regarding the prevalence of sexual dysfunction have been increasing in the
last two decades. Simons and Carey (2001), in a review of the literature, identified
52 empirical studies published during the 1990s. Despite the disparity of the results,
most studies indicate high prevalence levels of sexual dysfunctions in the general
population. Laumann et al. (1999), in one of the most cited epidemiological studies
conducted in a probability based sample of the United States, indicated cumulative
percentages of sexual dysfunctions of 43% in women and 31% in men, suggesting that
sexual dysfunction is an important public health concern. Additionally, in a recent
literature review, Lewis et al. (2004) indicated that 20–30% of adult men experienced
at least one sexual dysfunction at the time of the study. In this review, early ejaculation
was the most common clinical complaint with estimates ranging from 9 to 31% in the
different epidemiological studies. The prevalence of erectile dysfunction was estimated
between 1 and 9% in younger men (under 40 years of age) increasing to 50–75% in
men older than 70. Delayed orgasm prevalence rates were estimated to range between
1 and 8%. Finally, sexual desire disorder was the less common complaint and mostly
present in older men (Lewis et al., 2004). However, recent studies based on national
probability samples in the United Kingdom and Australia have found low sexual
interest as the most prevalent complaint among men in the general population. In the
National Survey of Sexual Attitudes and Lifestyles in Britain (Mercer et al., 2003),
17.1% of the male participants reported lack of interest in sex during at least one
month in the previous year. Additionally, Richters et al. (2003) found lack of interest
to be the most common sexual difficulty among 24.9% of the 8,517 interviewed
Australian men.
Besides epidemiological studies, there are some data published on the prevalence
rates of sexual dysfunction in clinical settings. Interestingly, findings from clinical
samples indicate a different prevalence pattern. While the majority of the population-
based studies indicate premature ejaculation as the most common sexual problem,
the most frequent complaint in clinical settings by far is erectile dysfunction (see
Simons & Carey, 2001, for a review).
Comorbidity and Patterns of Association among Sexual Dysfunctions

Studies regarding comorbidity have shown a considerable overlap among sexual
disorders. In men, clinical observations suggest a strong association between erectile
dysfunction and both hypoactive sexual desire disorder and premature ejaculation
(American Psychiatric Association, 2000; Rosen, 2000). Epidemiological studies
support clinical observations indicating high correlations between erectile dysfunction
and premature ejaculation (Laumann et al., 2005) and low sexual desire (Fugl-
Meyer & Fugl-Meyer, 1999).
Moreover, recent findings using structural equation models in a sample of 406
Portuguese men with sexual difficulties indicated an overlap between sexual desire,
erectile function, and orgasmic function (Carvalho, Vieira, & Nobre, 2011). Results
suggested that sexual functioning in men with sexual difficulties was best characterized
by a two-factor structure: (a) a general sexual function factor (including sexual desire,
erectile function, and orgasmic function), and (b) premature ejaculation. These results
corroborate the strong association between erectile functioning and sexual desire, and
suggest that premature ejaculation is a distinct dimension despite the high comorbidity
with erectile dysfunction.
Psychological Etiology of Sexual Dysfunction
Studies on the role of psychological factors on sexual dysfunction have resulted in a

better understanding of their role in the last few decades. Among the most studied
variables are dispositional variables such as personality, affect, and sexual inhibition
(Bancroft & Janssen, 2000; Barlow, 2002), sexual beliefs (Baker & de Silva, 1988;
Nobre & Pinto-Gouveia, 2006a), cognitive schemas (Andersen, Cyranowski, &
Espindle, 1999; Nobre & Pinto-Gouveia, 2009b), automatic thoughts (Nobre &
Pinto-Gouveia, 2008), and emotions (Mitchell, DiBartolo, Brown, & Barlow, 1998;
Nobre & Pinto-Gouveia, 2006b; Nobre et al., 2004).
Personality and Trait-Affect

Barlow (2002) proposed a triple vulnerability model for emotional disorders (includ-
ing sexual dysfunction) in which he he hypothesized that neuroticism and negative
affect predict anxiety-related disorders. Moreover, studies conducted in men and
women with and without sexual dysfunction have indicated that negative trait-affect
and neuroticism were significantly higher in clinical samples compared to controls
(Oliveira & Nobre, 2012; Quinta Gomes & Nobre, 2011).
Bancroft and Janssen (2000) developed a theoretical model based on the dual
control of sexual response (sexual inhibition/sexual excitation), postulating that
individuals have a propensity for both mechanisms and that the balance between
them predicts sexual response. Studies have partially corroborated this hypothesis
indicating that sexual inhibition is strongly correlated to impaired erectile response in
men (Bancroft, Graham, Janssen, & Sanders, 2009; Bancroft & Janssen, 2000).
Sexual Beliefs
Regarding the role of sexual beliefs and myths on sexual functioning, Zilbergeld
(1999) stated that men with erectile disorders present a set of myths and erroneous
beliefs about sexuality that work as a vulnerability factor to the development of
their difficulties. Additionally, Wincze and Barlow (1997) identified a set of sexual
myths underlying male sexual dysfunctions with emphasis on excessively high sex-
ual performance beliefs, and erroneous ideas about sexual response and women’s
sexual satisfaction. Besides the male myths, Hawton (1989) called attention to a
set of female beliefs that reflect the double standard, permissive but demanding for
men, and repressive for women. Heiman and LoPiccolo (1988) further included
dimensions related to the role of age and physical appearance, and beliefs about
performance demands in women. Besides these data from clinical observations, Baker
and de Silva (1988) found that men with sexual dysfunction present significantly
higher beliefs in Zilbergeld’s myths compared with a group of sexually functional
individuals.
Moreover, Nobre and Pinto-Gouveia (2006a) found that men and women with
sexual dysfunction reported having higher scores on a scale of dysfunctional sexual
beliefs (Nobre, Pinto-Gouveia, & Gomes, 2003) when compared to sexually healthy
men and women (Nobre & Pinto-Gouveia, 2006a). Men in the clinical sample were
more likely to present beliefs related to excessive sexual performance demands (e.g.,
“A real man has sexual intercourse very often”; “In sex, getting to the climax is the
most important”; “Sex without orgasm can’t be good”), and beliefs about women’s
sexual satisfaction and their reaction to men’s failure (e.g., “The quality of the erection
is what most satisfies women”; “A woman may have doubts about a man’s virility
when he fails to get an erection during sexual activity”; “A man who doesn’t sexually
satisfy a woman is a failure”) (Nobre & Pinto-Gouveia, 2006a).
The authors hypothesized that these dysfunctional sexual beliefs would play an
important role as vulnerability factors for the development of sexual dysfunction.
Sexual beliefs may be conceptualized as conditional beliefs or rules that can be
transformed into an “if … then” format, stipulating conditions for the way individuals
interpret their sexual events. If we take as an example the “macho” belief, “A man
who doesn’t get a firm and rigid erection is a failure,” it is understandable that a
man who holds such a belief will tend to react in a more negative way if, on occasion,
his erectile response is not so high or rigid. In other words, sexual beliefs might
work as lenses that magnify the negative aspects of sexual experience and make some
individuals more prone to further develop sexual problems.
Cognitive Schemas
Studies assessing the role of cognitive schemas on sexual dysfunction are scarce.
Despite the extensive scientific literature on the implication of cognitive structures
on several psychological disorders, there are only a few studies in the field of
sex research (Andersen et al., 1999; Nobre & Pinto-Gouveia, 2009a, 2009b).
Nobre and Pinto-Gouveia (2009b) found that both men and women with sexual
difficulties, when exposed to negative sexual events, tend to activate significantly
more negative self-schemas when compared to individuals without sexual problems.
More specifically, both men and women with sexual dysfunction tend to interpret
unsuccessful events as a sign of failure and personal incompetence: “I’m incompetent,”
“I’m weak,” “I’m a failure.” This activation of negative schemas might be related
to the tendency shown by individuals with sexual dysfunction to present attributions
of an internal, stable, and global nature to negative sexual experiences (Weisberg,
Brown, Wincze, & Barlow, 2001). Nobre (2009, 2010) hypothesized that these
negative self-schemas activated by individuals during exposure to sexual situations
are strongly linked to the type of sexual beliefs they present with. Specifically,
individuals with dysfunctional sexual beliefs (as described above) would be more
vulnerable to activate negative self-schemas whenever an unsuccessful sexual event
occurs. The negative event would act as a precipitant for the activation of negative self-
schemas (mainly self-incompetence schemas), with sexual beliefs playing a moderator
role.
Automatic Thoughts and Emotions

Studies on the content of automatic thoughts during sexual activity indicated that
men with sexual dysfunction presented more automatic thoughts related to erection
and sexual intercourse, failure anticipation thoughts, and lack of erotic thoughts
(Nobre & Pinto-Gouveia, 2008). Nobre (2010) hypothesized that these negative
automatic thoughts presented during sexual activity are the result of the previous
activation of negative self-schemas described above, and that they play an important
role as maintaining factors for sexual dysfunction.
Regarding the role of emotions in sexual dysfunctional processes, research consis-

tently suggests that depressive affect is negatively related to sexual arousal. (Mitchell
et al., 1998; Nobre et al., 2004). Studies conducted on the content of the emotional
response during sexual activity (Nobre & Pinto-Gouveia, 2006b) indicated that men
with sexual dysfunction had significantly more emotions of sadness, disillusion, and
fear, and less pleasure and satisfaction, compared to sexually healthy individuals.
Overall, these data seem to suggest that depressed mood (lack of pleasure, sadness,
disillusion) is strongly associated with sexual dysfunction. The authors hypothesized
that this depressed mood during sexual activity is strongly linked with the nega-
tive self-schemas activated by individuals with sexual dysfunction, impairing sexual
response and playing an important role as maintaining factors of sexual dysfunction
(Nobre & Pinto-Gouveia, 2006b).
Conceptual Models of Sexual Dysfunction
Based on the research findings on psychological etiology of sexual dysfunction

presented above, some authors have developed theoretical models that attempt to
integrate the accumulated knowledge. David Barlow played a major role in this
regard. Not only he was one of the pioneers in the study of cognitive factors of sexual
problems, but he was also involved in most of the research conducted on this topic
(Bach, Brown, & Barlow, 1999; Barlow, Sakheim, & Beck, 1983, Mitchell et al.,
1998, Weisberg et al., 2001) and developed conceptual models of sexual dysfunction
(Barlow, 1986; Sbrocco & Barlow, 1996; Wiegel, Scepkowski, & Barlow, 2007).
Moreover, Nobre and colleagues have been conducting research and developing and
testing conceptual psychological models of sexual dysfunction (Carvalho & Nobre,
2011, Nobre, 2009, 2010; Soares & Nobre, 2013).
Nobre’s Cognitive-Emotional Model

Based on the research conducted in the last 10 years, Nobre and colleagues have
developed and tested conceptual models of sexual dysfunction in men and women
(Nobre, 2009, 2010). The structure of the models is based on the principles of
cognitive theory. At a central level are the cognitive schemas (or core beliefs),
composed of ideas we have about ourselves, others, and the future that are responsible
for the meaning assigned to events (Beck, 1967, 1996). Nobre and colleagues
were particularly interested in the activation of self-schemas when facing sexually
unsuccessful situations. Using the definition of schema, its activation guides the
interpretation and the meaning assigned to a particular situation, mobilizing a set
of coherent cognitive (automatic thoughts) and emotional responses and influencing
behavioral reactions. According to the findings described previously, the model
postulates that individuals with sexual dysfunction tend to activate more negative
self-schemas when exposed to negative sexual situations (specifically incompetence
schemas) (Nobre & Pinto-Gouveia, 2009b).
Sexual beliefs constitute another central component of the model, consisting of
ideas subjects have about sexuality that are based on earlier life experiences and
learning processes. In this particular study, sexual beliefs are conceptualized as

conditional rules (Beck, 1996) presented on an “if … then” basis. These conditional
rules play a central role, since they stipulate the conditions necessary for the activation
of the cognitive schemas. Whenever a sexual event fulfills the rules defined by the
sexual belief, congruent cognitive schemas are activated. Therefore, sexual beliefs
play a central role as vulnerability factors for the development of sexual dysfunction.
Individuals presenting with rigid, inflexible, and dysfunctional sexual beliefs are more
prone to catastrophize negative sexual events and to activate negative self-schemas
(mainly incompetence schemas: “I am incompetent, I am a failure”) (Nobre &
Pinto-Gouveia, 2006a).
Besides sexual beliefs, the model postulates the existence of two more general
vulnerability factors for sexual dysfunction: personality and trait-affect (Oliveira &
Nobre, 2012; Quinta Gomes & Nobre, 2011). Specifically, the model suggests that
neuroticism, low positive trait-affect, and high negative trait-affect constitute risk
factors for the development of sexual problems. These more general vulnerability
factors, which were also found to be associated with most anxiety and depressive
disorders, are thought to interact with the dysfunctional sexual beliefs and moderate
the process of meaning assignment to sexual situations, particularly the negative events
(Soares & Nobre, 2013).
In addition to these more central components, the model is also composed of
cognitive and emotional responses resulting from the activation of cognitive schemas.
Using the same example presented above, the activation of the cognitive schema
“I’m a failure” would drive the development of automatic thoughts oriented to
stimuli associated with failure and its possible negative consequences (e.g., failure
anticipation and disengagement thoughts, lack of erotic thoughts), decreasing the
focus on erotic stimuli, as well as negative emotional responses (sadness, lack of
pleasure and satisfaction) (Nobre & Pinto-Gouveia, 2006b, 2008). It is also important
to emphasize that these two components work in an interactional fashion, influencing
each other and determining the sexual response. These automatic thoughts and
negative emotions would also work as maintaining factors of the sexual problem,
since they prevent people from focusing attention on erotic cues and pleasurable
sensations associated with sex.
In summary, sexual dysfunction would result from the integrated influence of the
above mentioned psychological variables. However, it is also important to emphasize
the fact that the model is not unidirectional. Sexual functioning also influences the
activation of cognitive schemas in future sexually unsuccessful situations. The lower
the sexual functioning, the greater the probability of negative schema activation in
future situations, feeding back the cycle (see Figure 28.1).
The structure and assumptions of this model were tested specifically for male
erectile disorder and female desire disorder using path analyses (Nobre, 2009, 2010).
Moreover, recent studies further examined the impact of the main cognitive predictors
on sexual functioning and satisfaction, in interaction with other major predictors of
sexual response (e.g., medical factors, relationship factors, psychopathology). Findings
supported the central role of the cognitive variables as mediators and moderators of
the relation between medical and relationship factors and sexual functioning in men
and women (Carvalho & Nobre, 2010, 2011; Vilarinho & Nobre, 2008).
Low positive
Neuroticism Negative
trait-affect
trait-affect
Dysfunctional
sexual beliefs
Negative Activation of
sexual event incompetence
schemas
Negative emotions Negative thoughts

sadness failure anticipation
lack of pleasure lack of erotic thoughts
and satisfaction
Low sexual
response
Figure 28.1 Schematic structure of the cognitive-emotional model. Adapted from Soares
& Nobre (2013), p. 290. Copyright 2013 from The cultural context of sexual pleasure and
problems: Psychotherapy with diverse clients edited by K. Hall and C. Graham. Reproduced
by permission of Taylor and Francis Group, LLC, a division of Informa plc.
Assessment of Sexual Dysfunction
An adequate and complete assessment process is a central prerequisite for successful

treatment. This importance results not only from the possibility of a correct identifi-
cation of the sexual difficulties presented (and the subsequent assignment of clinical
diagnoses), but also from the promotion of a comprehensive formulation of the
predisposing, precipitant, and maintaining factors involved, as well as the planning of
an efficacious intervention.
The main goals of an assessment process include the following aspects:
Definition of the nature of the problem and assignment of a correct clinical diagnosis.
Both the formulation of etiological hypotheses and the adequacy of the treatment plan
rely on this goal. Whenever a sexual dysfunction is identified, differential diagnosis
should be taken into consideration (e.g., hypoactive sexual desire due to major
depression), as well as the different subtypes regarding the onset (lifelong/acquired
type), context (generalized/situational type), and etiology (psychological/combined
factors). Besides, it is also important to assess the possible implications of etiological
factors of an organic nature, in which case a decision has to be made about whether
these biological factors are sufficient to explain the onset of the dysfunction (sexual
dysfunction due to a general medical condition, or substance-induced) or not. If an
exclusively organic etiology is found, a medical approach should be considered.
Identification of the predisposing, precipitant, and maintaining factors of sexual diffi-
culties. The importance of this goal results from the adequate formulation of causal
hypotheses and individual case conceptualization. According to Carey, Wincze, and
Meisler (1993), the accomplishment of this goal should be based not only on the
causal-temporal analysis mentioned above, but also on a systemic analysis involving
the biopsychosocial dimensions. Thus, a specific clinical case might involve predis-
posing, precipitant, and maintaining factors of diverse biopsychosocial origins. As
predisposing factors, organic factors such as diabetes and psychological factors such
as sexual erroneous beliefs might coexist. As precipitant factors, simple occasional
sexual failure (psychological factor), relationship conflicts (interpersonal factor), or
hormonal problems (organic factor) might be involved. Finally, as maintaining fac-
tors, phenomena such as performance demands (psychological) or use of hypertensive
medication may be present.
Treatment planning. This goal is a consequence of the first two, and its adequacy
depends of the accuracy of the clinical diagnosis, and the adequacy of the case
formulation.
Assessment of the clients’ goals and their motivation for change. This aspect is of
critical importance since clients’ goals do not necessarily match therapists’ purposes.
Therefore, it is necessary to clarify clients’ objectives, as well as to assess their feasibility,
since most present unrealistic expectancies about treatment gains and human sexual
response. Besides, it is also important to assess clients’ motivation for change, a
variable which is strongly associated with their involvement in the treatment process
and success.
Establishment of the therapeutic relationship. Taking into consideration the fact that the
therapeutic relationship is one of the factors most strongly associated with treatment
outcome, the establishment of an empathic environment during the assessment
process deserves serious attention. The development of a professional and open
atmosphere facilitates the establishment of a confidence relationship and the decrease
of social and cultural constraints.
Determination of a pretreatment baseline. The identification of the initial client
position regarding a set of variables associated with sexual difficulties facilitates an
accurate assessment of the severity of the problem and allows the measurement
of progress during treatment. This baseline may include: physiological measures
(penile circumference changes during exposure to sexually explicit material), medical
measures (e.g., testosterone), or self-reported measures (e.g. sexual functioning,
sexual satisfaction).
Provide feedback to the client. Feedback assumes special relevance since it allows the
clarification of eventual misunderstandings and provides a comprehensive formulation
of the factors involved in the predisposition, precipitation, and maintenance of sexual
difficulties, as well as information regarding the treatment plan.
Clinical Interview
The clinical interview constitutes the central method of assessment of sexual dysfunc-
tion. According to Hawton (1989), a clinical interview should cover the following set
of issues:
1. Nature and development of sexual dysfunction. This phase is predominantly

oriented to the study of the sexual difficulties, and should be essentially focused on
the nature of the problem, its onset and development, and factors contributing to
its maintenance. With the goal of assigning an accurate diagnosis, the classification
criteria should be carefully taken into consideration with special emphasis on the
differential diagnosis.
2. Early sexual development and experience. Sexual development and early experiences
influence sexual life and might contribute to the development of sexual difficulties.
Therefore, the clinical interview should assess aspects such as age of puberty,
unwanted sexual experiences, girlfriends/boyfriends, early sexual experiences,
sexual orientation, and so on.
3. Sexual information and erroneous beliefs. The transmission of inadequate sexual
information to adolescents constitutes a core factor in the development of
erroneous beliefs about sexuality and should be carefully assessed.
4. Relationship satisfaction. A couple’s relationship is another important area to
assess, since it may constitute an important precipitant or maintaining factor for
sexual difficulties and is crucial for treatment planning.
5. Religious beliefs. The religious beliefs of each partner should be assessed, along
with their compatibility, their interference with the couple’s relationship, and
their role in the development of erroneous sexual beliefs.
6. Psychiatric history. There should also be an assessment of the history of mental
diseases with a known impact on sexual functioning (e.g., depressive disorders,
psychotic disorders, alcoholism, substance abuse).
Self-Report Questionnaires
The use of self-report questionnaires is a very important complement to clinical
interviews and allows the assessment of a variety of factors associated with sexual
difficulties as well as the measurement of progress over the course of treatment. A list
of relevant measures according to specific dimensions is presented below.
Sexual functioning.
International Index of Erectile Function. The International Index of Erectile
Function (IIEF; Rosen et al, 1997) is a 15-item, brief, self-administered measure of
erectile function, evaluating five domains of male sexual function: erectile function,
orgasmic function, sexual desire, intercourse satisfaction, and overall satisfaction.
Psychometric studies have supported its validity and reliability as well as its sensitivity
to treatment changes.
Relationship factors.
Dyadic Adjustment Scale. The Dyadic Adjustment Scale (DAS; Spanier, 1976)
is a 32-item scale specifically oriented to assess the quality of a couple’s interaction
in nonsexual areas. Moreover, psychometric studies have supported its validity and
reliability.
Medical factors.
Medical History Form. The Medical History Form (MHF; Wincze & Carey, 2001)
assesses dimensions such as medical history (including relevant diseases, treatments,
operations, and hospitalizations), medication, medical family history, and the use of
alcohol, tobacco, and other drugs.
Cognitive-emotional factors.
Sexual Self Schema. The Sexual Self Schema (SSS, male version; Andersen et al.,
1999) assesses cognitive generalizations about sexual aspects of oneself that are
responsible for guiding sexual behavior. The male version is composed of 45
items assessing three different dimensions: passionate-loving, powerful-aggressive,
and open-minded-liberal. The SSS presents good psychometric characteristics.
Questionnaire of Cognitive Schema Activation in Sexual Context. The Ques-
tionnaire of Cognitive Schema Activation in Sexual Context (QCSASC, male version;
Nobre & Pinto-Gouveia, 2009a) is a 28-item instrument that assesses cognitive
schemas presented by individuals when facing negative sexual situations. A principal
component analysis identified five factors: undesirability/rejection, incompetence,
self-deprecation, difference/loneliness, and helplessness.
Sexual Dysfunctional Beliefs Questionnaire. The Sexual Dysfunctional Beliefs
Questionnaire (SDBQ; Nobre, Pinto-Gouveia, & Gomes, 2003) is a 40-item ques-
tionnaire assessing sexual beliefs associated with male sexual dysfunctions. A principal
component analysis identified six factors (Nobre, Pinto-Gouveia, & Gomes, 2003):
sexual conservatism, female sexual power, “macho” beliefs, beliefs about women’s
sexual satisfaction, restricted attitude toward sexual activity, and sex as an abuse of
men’s power.
Sexual Modes Questionnaire. The Sexual Modes Questionnaire (SMQ; Nobre &
Pinto-Gouveia, 2003) is a measure aimed at assessing automatic thoughts, emotions,
and sexual responses during sexual activity. A principal component analysis of the
automatic thoughts subscale identified five factors: failure anticipation thoughts,
erection concern thoughts, age related thoughts, negative thoughts toward sex, and
erotic thoughts.
Sexual Inhibition/Excitation Scales. The Sexual Inhibition/Excitation Scales
(SIS/SES; Janssen, Vorst, Finn, & Bancroft, 2002) assess an individual’s propensity
for sexual inhibition or sexual excitation. The SES is a 20-item scale that assesses four
dimensions: social interactions, visual stimulation, sexual thoughts and fantasies, and
nonspecific sexual stimuli.
Integration of assessment information. Since the assessment of sexual dysfunction

implies a diversity of methods and a multidisciplinary approach, the process of
integrating the different data assumes an important role. As previously mentioned,
one of the main purposes of the assessment is to develop a case formulation that
facilitates the planning of an appropriate therapeutic intervention. In this regard
the integration of the different assessment data in a biopsychosocial perspective is
essential, allowing a consistent and complete case conceptualization. Wincze and
Carey (2001) stated that this integrated case formulation communicates to the client
that (a) his difficulties are comprehensible, taking into account his psychophysiological
characteristics, medical history, life experiences, and so on, (b) there is reason for
optimism and hope regarding change, and (c) there is a conceptual “map” that
supports the therapeutic plan.
Cognitive Behavioral Therapy for Male Sexual Disorders
Cognitive behavioral therapy (CBT) for sexual disorders is the application of cognitive
and behavioral principles to the field of sexual problems. Therefore, CBT for male
sexual disorders uses treatment strategies similar to those for other psychological
disorders. Before starting treatment it is very important to conduct a thorough
assessment of the sexual difficulties and related problems (as described above).
In particular, therapists should collect rigorous and complete information on the
following topics:
1. relevant information in order to assign a reliable multiaxial diagnosis based on

DSM criteria;
2. information about the possible predisposing factors (e.g., sexual and life expe-
riences, family and sexual education, sexual and interpersonal relationships) and
precipitating aspects (life events that occur at the time of the beginning of
difficulties) of sexual dysfunction;
3. information about the current difficulties and their maintenance factors (e.g.,
severity of the problem, precedents and consequents of the problem, and condi-
tions that intensify and relieve).
After this information is collected and case formulation is completed, the therapist
should give feedback to the patient, explain the CBT rationale, and discuss the
treatment plan.
Most cognitive behavioral treatment protocols for sexual dysfunction use a common
list of intervention techniques (Bach, Wincze, & Barlow, 2001; Hawton, 1989; Rosen,
Leiblum, & Spector, 1994; Wincze & Carey, 2001). The main components used are
(a) sensate focus, (b) stimulus control, (c) sexual skills training, and (d) cognitive
restructuring. We will present the main objectives and processes involved in these
techniques, with special emphasis on cognitive restructuring.
Sensate Focus
Sensate focus is a technique developed by Masters and Johnson (1970) that aims
to desensitize clients from their discomfort (anxiety, negative mood) levels when
approaching sexual situations. Similarly to systematic desensitization, this technique
uses a gradual exposure to sexual activity, starting with nondemanding and pleasurable
exercises and continuing to genital and intercourse oriented exercises. The main goal
is to reduce performance anxiety and help patients focus their attention on sexual
enjoyment and pleasure rather than on performance. The idea is to expose the couples
to gradually demanding sexual exercises (genital touch, intercourse), starting with
nondemanding and pleasurable situations (touching each other excluding genitals)
and moving on to the next step whenever they feel comfortable with the previous
exercise. The usual steps are as follows:
1. During the first step the therapist instructs the couple to avoid intercourse or
any other form of direct genital contact. The couple is encouraged to take part
in exercises designed to promote feelings of comfort and pleasure in the absence
of any type of performance demand. Usually, these exercises include touching
each other’s bodies in a sensitive and pleasurable way excluding the genital area
(the couples should choose the type of nongenital touching according to their
mutual preferences). It is also very important to create an intimate and romantic
atmosphere where privacy is guaranteed. The ultimate goal is to focus on positive
and pleasurable feelings associated with the exercise.
2. The second step is an extension of the first with the addition of direct genital
contact. It is important to include genital touch in the previous intimate and
pleasurable atmosphere, rather than orient the couple to focus on genital touch.
3. The third step usually includes intercourse; the goal is similar to the previous
exercises, to create a positive and intimate atmosphere, focusing on the pleasure
of nongenital and genital touch. Intercourse should be tried only if both partners
are prepared and comfortable. The couple is encouraged to focus on the pleasure
sensations of intercourse and to try different positions as long as they feel
comfortable. During this step partners are encouraged to control orgasm, in order
to avoid focusing on achieving orgasm, but rather on the positive sensations of
intercourse.
4. The final step consists of the integration of the previous steps without the ban on
orgasm. It is again essential that the couple follow the complete process, starting
with nongenital and genital foreplay, continue with intercourse when they feel
comfortable, and end in orgasm if desired. The main goal is always enjoyment
and pleasure using the most diverse touching and positions they feel comfortable
with, and reducing the anxiety related to sexual performance.
Stimulus Control
Stimulus control is a therapeutic procedure, oriented to associate sexual events with
pleasurable and comfortable situations. Since many patients present a history of sexual
activity in nonintimate and sometimes uncomfortable settings, it is important to
change the usual circumstances in which sexual activity usually occurs, and create
more pleasant and erotic environments. This technique could be used in the sensate
focus procedure during the preparation of the first step. An appropriate stimulus
is essential to create a comfortable and erotic atmosphere to start sensate focus
exercises.
Sexual Skills Training

Most patients present a rigid and limited sexual script (the usual pattern of sexual activ-
ity in which couples engage). Since most patients are oriented to performance and goal
achievement, their sexual activity is mostly directed to intercourse and orgasm. This
approach in return invites patients to focus on performance, and sometimes prevents
them from focusing on pleasurable sensations. One strategy of modifying these sexual
scripts to involve more flexible and less restrictive sexual behaviors is to discuss with
them the ideal scripts, sexual stimulus, and behaviors that they would like to perform
but for any reason never tried (shame, guilt, lack of confidence, lack of communica-
tion, etc.). It is important that the ideal scripts chosen meet both partners’ desires,
in order to prevent more negative feelings and discomfort during sexual activity. The
practice of these new sexual behaviors would typically increase their enjoyment and
arousal during sexual activity, and prevent them from focusing exclusively on perfor-
mance demands. These new sexual practices may also be incorporated into sensate
focus exercises, when deciding which sexual stimulus to include in the different phases.
Cognitive restructuring includes a variety of processes and techniques. In order to
simplify the subject, we will divide the process into two major components: (a)
identification of the cognitive structures, and (b) cognitive restructuring techniques.
Identification of the cognitive system.

Automatic thoughts. One of the first steps of cognitive restructuring consists
in the identification of automatic thoughts, which are conceptualized as automatic
and involuntary thoughts or images that result as a product of cognitive processing
and constitute the most accessible component of the cognitive structure (despite its
preconscious level; Alford & Beck, 1997). Moreover, automatic thoughts are the most
direct determinant of behavioral and emotional responses. Accordingly, interventions
seeking to modify dysfunctional behavior or emotions should give priority attention
to the identification and evaluation of underlying automatic thoughts. The process of
identification of automatic thoughts must begin with an explanation of the process
and use the patient’s own examples:
THERAPIST: Focus on a sexual situation in which you have failed recently (e.g., erection
was not as rigid as you would like). When you were in the midst of sexual activity, what
ideas have passed through your head? What thoughts or images were occurring at that
moment?
PATIENT: I am not sure. I think I was worried about not being able to achieve. This is
not working out, my penis is not responding …
Subsequently, the therapist should demonstrate the relationship between the auto-
matic thoughts and the emotional and behavioral responses in the same context:
THERAPIST: While these ideas were going through your head, how were you feeling
(sad, anxious, pleasure … )?
PATIENT: I was feeling bad, maybe a little worried and sad …

THERAPIST: While these ideas were going through your mind (“I’m not going to
achieve …”) and you were feeling worried and sad, what actually was going on?
PATIENT: Nothing … that is, the penis was not reacting and I was becoming
increasingly desperate.
THERAPIST: What did you do to change this situation?
PATIENT: I kept trying but nothing, there was no reaction, and the more I worried the
worse it was … until I gave up.
At this stage the therapist should explain to the patient the important link between
automatic thoughts, emotions, and sexual response. By counterpoint, the therapist
should also ask the patient to describe thoughts and emotions experienced during
successful sexual situations:
THERAPIST: Try to remember the last sexual intercourse that went well. What ideas or
thoughts were going through your head?
PATIENT: I don’t know exactly… things were going well, I was enjoying it.
THERAPIST: What kind of ideas were going through your mind?
PATIENT: Well, today this is going well, she is enjoying it, I can do it, this is great…
THERAPIST: While these ideas were occurring, how were you feeling?
PATIENT: I was feeling great, enjoying it, and very confident.
THERAPIST: What was going on, what were your behaviors?
PATIENT: Things were going well, the penis was reacting, I was getting a full erection
and was able to penetrate.
The reference to two distinct situations, a successful and a negative one, helps
the patient understand the impact of thoughts on emotions and sexual response.
Of course, this relationship is not necessarily causal, but circular (Beck, 1996). The
main message should be that changes in the content of automatic thoughts may
help change emotions and sexual responses. Therefore, a first step is to train patients
in identifying automatic thoughts occurring during sexual activity, as well as the
associated emotions and sexual response.
In addition to the automatic thoughts query, the therapist should instruct the
patient to monitor the main thoughts and emotions occurring during sexual situations
and the related sexual responses and behaviors. Patients should use a self-record diary
describing the situation, the thoughts that have occurred, and their degree of belief
in them (on a scale from 0 to 100), the emotions experienced as well as their intensity
(from 0 to 100), and the associated behaviors (see Table 28.2).
In addition to the record of thoughts, the patients may also respond to the Sexual
Modes Questionnaire (SMQ; Nobre & Pinto-Gouveia, 2003). This questionnaire
lists a set of typical negative and positive automatic thoughts that may occur during
sexual activity, and patients are asked to rate the frequency with which they occur, as
well as the associated emotions and subjective sexual arousal.
Cognitive schemas. According to Beck (1996), schemas are cognitive structures

responsible for the meaning individuals assign to events, and guide information
processing, determining emotional and behavioral responses. Thus, evaluation of
Table 28.2 Self-Record of Automatic Thoughts, Emotions, and Behaviors during Sexual
Activity
Date Situation Automatic thoughts Emotions Behaviors

(degree of belief 0–100) (intensity 0–100)
Sexual penetration “If I fail, I’m lost” (70) Worry (80) Withdrawal of
difficult to sexual activity
achieve
“This is not going Sadness (70)
anywhere” (80)
“I am not able to satisfy Disappointment
my partner” (80) (90)
cognitive schemas activated in sexual context is crucial, since they supposedly guide
the meaning assigned to sexual events and underlie automatic thoughts and emotions
during sexual activity. Since schemas work at a preconscious and automatic level
(Alford & Beck, 1997), they are very difficult to assess. However, a few strategies may
be used to facilitate the elicitation of cognitive schemas in sexual context:
• First, recurring themes of the patient’s automatic thoughts during sexual activity
should be analyzed.
• This analysis helps understanding the patient’s central concerns, thereby facilitating
the identification of cognitive schemas.
• Beliefs and attitudes toward sexual themes can be directly questioned.
• The downward arrow technique can be used. This is a technique that helps
evaluate cognitive schemas, through questioning the meaning and consequences
of each of the most typical negative automatic thoughts presented by the patient,
as shown in the following example.
PATIENT’S AUTOMATIC THOUGHT: “I cannot get an erection.”

THERAPIST: What does this thought mean for you?
PATIENT: It means that I cannot have sex as it should be.
THERAPIST: And what does it mean for you, not being able to have sex as you should?
What consequences may come from that?
PATIENT: It is a complete failure to me … It makes me think that I am not doing my job
I am not a real man … I’m weak.
• Questionnaires can be used, such as the Dysfunctional Sexual Beliefs questionnaire

(SDBQ; Nobre, Pinto-Gouveia, & Gomes, 2003), which evaluates the sexual
beliefs and myths usually presented by men with sexual dysfunction, and the
Questionnaire of Cognitive Schema Activation in Sexual Context (QCSASC;
Nobre & Pinto-Gouveia, 2009a), which evaluates negative self-schemas activated
after exposure to negative sexual events.
Cognitive Restructuring Techniques

After the identification and assessment of the cognitive structure, it is possible to
initiate the process of cognitive restructuring. We will briefly present the main
techniques that can be used to challenge dysfunctional schemas and sexual beliefs.
Information and sex education. One of the first steps in confronting patients with their
distorted and maladaptive beliefs is to give them accurate information about the basic
psychophysiological processes of sexual response. Several studies have highlighted the
extent of myths and misleading ideas that patients present about basic aspects of
sexual response (Baker & de Silva, 1988; Nobre & Pinto-Gouveia, 2006a). There
is a list of self-help and educational books that can be used (e.g., Heiman & Lo
Piccolo, 1988; McCarthy, 1998; Wincze & Barlow, 1997; Zilbergeld, 1999). Some
false beliefs could be changed easily after the provision of evidence by the therapist
or the reading of educational books, but others are strongly related to personal
structural beliefs and need a more systematic cognitive intervention in order to be
challenged.
Evaluating the advantages and disadvantages of sexual beliefs. One of the first tech-
niques that could be used in the process of cognitive restructuring is to encourage
the patient to analyze the benefits and disadvantages of the main sexual beliefs that
they present with. In the following dialogue, the patient holds the sexual belief that
“A man who fails to maintain an erection may be abandoned by his sexual partner.”
THERAPIST: What kind of advantages do you see in having this belief? Does it help you
in any way?
PATIENT: Well, maybe it does not have any direct advantage, but obliges me to work
harder to prevent failure.
THERAPIST: And does that prevent you from failing?
PATIENT: Unfortunately not.
THERAPIST: Can you see any disadvantage?
PATIENT: I don’t know … maybe it makes me feel even more tense and nervous.
Analysis of evidence. Once the patient is educated on the basics of sexual response
and has learned to question the usefulness of his own sexual beliefs, it is easier to
encourage him to confront the evidence for and against the beliefs. The analysis
of the evidence can rely on a logical debate (Ellis, 1962), where the patient is
encouraged to list a number of arguments for and against each of his sexual beliefs
based on evidence and/or logical thinking. In addition, training in the identification
of cognitive distortions or errors in the processing of information (Beck, 1967)
related to sexual events is another useful technique in questioning the evidence for
the sexual beliefs. Here are some common cognitive errors presented by men with
sexual dysfunction (Rosen et al., 1994):
• all-or-nothing thinking (“I’m a complete failure because my erection was not

100% rigid”);
• overgeneralization (“I had trouble getting an erection last night. I will never be
able to get an erection during intercourse”);
• disqualifying the positive (“My partner says that I satisfy her sexually. She only
says this because she feels sorry for me”);
• mind reading (“My partner must think that I’m a failure or a poor sexual partner”);
• fortune-telling (“I will lose my erection during intercourse tonight”);
• emotional reasoning (“I feel like I’m incompetent; therefore, I really must be
incompetent”);
• categorical imperatives (“I should be able to get an erection whenever my partner
wants to have sex”);
• catastrophizing (“If I lose my erection tonight, my partner will leave me”).
Reality testing. Reality testing (also known as behavioral experiments) is the use of
real-life situations to test hypotheses resulting from patients’ dysfunctional beliefs.
One very useful way of conducting behavioral experiments to test beliefs is the use of
sensate focus exercises. Sensate focus promotes the involvement of partners in a variety
of sexual activities without intercourse, thus providing opportunities to disconfirm
the idea that sexual pleasure and women’s satisfaction and orgasm require an erect
penis and vaginal penetration.
Formulating alternative beliefs. Once the patients have learned to identify their own
cognitive distortions, and the lack of evidence for their sexual beliefs, it is important
that they develop alternative and more accurate beliefs that make sense for them.
One technique that may help patients identify alternative beliefs is the use of Socratic
questioning. This technique is based on the teaching method used by the Greek
philosopher, and helps to guide the patient’s process of self-discovery, reflecting on
his own beliefs and facilitating the development of new alternative interpretations
for his life events (i.e., new beliefs). In the following dialogue, the patient holds the
sexual belief that “A man who fails to get an erection is not a real man.”
THERAPIST: On a scale from 0 to 100, to what degree do you believe in this statement?
PATIENT: Maybe 90.
THERAPIST: So you strongly believe that whenever someone fails to get an erection it
means he is less of a man.
PATIENT: Well, perhaps not always, sometimes there are other reasons.
THERAPIST: What reasons?
PATIENT: Don’t know … he might be tired or preoccupied with something and things
don’t work very well.
THERAPIST: You mean that this tiredness or concern can explain the failure, without
meaning a loss of masculinity?
PATIENT: Yes, sometimes.
THERAPIST: How many times (on a scale from 0 to 100)?
PATIENT: Maybe 30.
THERAPIST: Is there any other possible explanation for a failure?
PATIENT: Well … maybe sometimes women also do not help much.
THERAPIST: And this explains how much (on a scale from 0 to 100)?
PATIENT: Maybe 10.
THERAPIST: Is there any other possible explanation?

PATIENT: I do not know, but in my case I also feel very anxious about what is about to
happen. I just keep thinking that my penis may not respond and things get worse.
THERAPIST: And to what extent does this hypothesis explain the failure?
PATIENT: In my case maybe 50 or 60.
Practicing alternative beliefs. Once the patient has identified alternative beliefs, he
should be given the opportunity to practice and exercise his “new role.” In this sense,
the technique of point-counterpoint, also designated rational-emotive role play, is very
useful. The technique consists of the dramatization of a dialogue between the patient
and the therapist where they exchange roles and represent the dysfunctional and
the alternative beliefs position. The patient may begin by representing his usual role
(dysfunctional beliefs) and then change with the therapist, putting himself in the new
position (defending the alternative beliefs). This technique is of central importance
since it allows the patient to decenter from his usual point of view and to play a new
role whose job is to convince the former of the inaccuracy and dysfunctional nature
of his sexual beliefs.
Additionally, the patient is encouraged to practice alternative beliefs and thoughts
in everyday life whenever any negative automatic thought arises. He must report the
original level of belief in the negative thought and the level of belief in the alternative
thought. He must also report the new level of belief in the previous negative thought
as a result of the alternative thought (see Table 28.3).
New Treatment Approaches/Mindfulness-Based Cognitive

Behavioral Therapy
Besides the more classic cognitive behavioral interventions, mindfulness-based

approaches have been recently used with promising results in the treatment of sexual
dysfunctions. Mindfulness-based treatments have shown psychological effectiveness
across a wide range of clinical problems, ranging from chronic pain to psychological
problems such as generalized anxiety disorder, eating disorders, ruminative thoughts,
negative affect, and recurrent depression (e.g., Baer, 2003; Grossman, Niemann,
Schmidt, & Walach, 2004; Shigaki, Glass, & Schopp, 2006).
Mindfulness is broadly defined as the promotion of nonjudgmental attention
and awareness of the unfolding of experience moment by moment (Kabat-Zinn,
2003). Shapiro, Carlson, Astin, and Freedman (2006) suggest that the main com-
ponents of mindfulness are intention (i.e., why one is practicing), attention (i.e.,
observing one’s moment-to-moment experiences), and attitude (i.e., absence of
judgment).
Recent studies have shown that the practice of meditation, besides increasing the
ability to focus attention, also promotes neurological changes. Brain imaging research
suggests that mindfulness practice is associated with lower neural activation in brain
regions involved with discursive thoughts and higher activation in circuits related to
attention (Brefczynski-Lewis, Lutz, Schaefer, Levinson, & Davidson, 2007; Cahn &
Polich, 2006).
Table 28.3 Self-Record of Automatic Thoughts and Emotions during Sexual Activity and Alternative Cognitions
Date Situation Automatic thoughts Emotions Alternative cognitions Result

(degree of belief (intensity (degree of belief) (degree of belief in the
0–100) 0–100) original automatic thoughts)
Sexual penetration difficult “If I fail, I’m lost” Worry (80) “Sometimes real men also “If I fail, I’m lost”
to achieve (70) fail” (50) (40)
“This is not going Sadness (70) “There is nothing that says “This is not going
anywhere” (80) that I am not going to anywhere” (50)
achieve” (50)
“I am not able to Disappointment (90) “It will not be the end of “I am not able to
satisfy my partner” the world ” (70) satisfy my partner”
(80) (40)
Taking into consideration that attentional processes during sexual activity are
central to sexual response and may facilitate the experience of subjective sexual arousal
(Barlow, 1986; De Jong, 2009), there is a clear theoretical background to support
the potential benefits of mindfulness-based approaches to sexual dysfunction.
Recent studies have suggested a positive effect of mindfulness on women’s sexual
health (Brotto, Basson, & Luria, 2008; Brotto & Heiman, 2007). Although these are
only preliminary findings and there is still a lack of studies on men with sexual dys-
function, the integration of mindfulness into cognitive behavioral treatment programs
for sexual dysfunction is promising.
The State of the Art of Empirically Supported Treatments for

Sexual Dysfunction
Despite the growing body of empirical data on and conceptual models of psychological
factors of sexual problems and specifically on the role of cognitive and emotional
variables, the application of this knowledge in terms of treatment approaches is still very
narrow. Regardless of the existence of some therapeutic proposals based on cognitive
behavioral principles (Bach, Wincze, & Barlow, 2001; Hawton, 1989; Rosen et al.,
1994; Wincze & Carey, 2001), the majority of sex therapists primarily use sensate focus
techniques, systematic desensitization, or specific behavioral procedures. Moreover,
training programs, although they may incorporate some knowledge of cognitive
determinants and interventions, are mostly based on sensate focus techniques.
Finally, empirically validated psychological treatments for sexual dysfunction are
scarce and mostly based on Masters and Johnson’s sensate focus or systematic desen-
sitization procedures (Heiman, 2002; Heiman & Meston, 1998). No randomized
controlled trial studies have been published so far testing the efficacy of cognitive
behavioral interventions for male sexual problems. Results from two pilot studies
(Bach, Barlow, & Wincze, 2004; Banner & Anderson, 2007) have indicated that
a combination of oral treatment (sildenafil) and CBT produced better treatment
outcomes (sexual functioning satisfaction) in men with erectile dysfunction compared
to pharmacological treatment alone.
Taking these findings into consideration, and bearing in mind that CBT has
proved to be the most efficacious treatment for a variety of psychological problems
(Chambless & Ollendick, 2001) and to present long-term effects superior to pharma-
cological treatments (Craske, Brown, & Barlow, 1991; DeRubeis & Crits-Christoph,
1998; Hollon et al., 2005; Shapiro et al., 2007), we think that the systematic test
of the treatment efficacy of CBT for sexual dysfunction, as well as the study of the
underlying mechanisms of change, may play an important role in developing better
treatment options for a major clinical complaint.
References
Alford, B. A., & Beck, A. T. (1997). The integrative power of cognitive therapy. New York, NY:
Guilford Press.
Andersen, B. L., Cyranowski, J. M., & Espindle, D. (1999). Men’s sexual self-schema. Journal
of Personality and Social Psychology, 76, 645–661.
Bach, A. K., Barlow, D. H., & Wincze, J. P. (2004). The enhancing effects of manualized
treatment for erectile dysfunction among men using Sildenafil: A preliminary investigation.
Bach, A. K., Brown, A. T., & Barlow, D. H. (1999). The effects of false negative feedback on
efficacy expectancies and sexual arousal in sexually functional males. Behavior Therapy, 30,
79–95.
Bach, A. K., Wincze, J. P., & Barlow, D. H. (2001). Sexual dysfunction. In D. H. Barlow
(Ed.), Clinical handbook of psychological disorders: A step by step treatment manual (3rd
Baer, R. (2003). Mindfulness training as a clinical intervention: A conceptual and empirical
review. Clinical Psychology: Science and Practice, 10, 125–143.
Baker, C. D., & de Silva, P. (1988). The relationship between male sexual dysfunction and
belief in Zilbergeld’s myths: An empirical investigation. Sexual and Marital Therapy, 3,
229–238.
Bancroft, J., Graham, C., Janssen, E., & Sanders, S. (2009). The dual control model: Current
status and future directions. Journal of Sex Research, 46, 121–142.
Bancroft, J., & Janssen, E. (2000). The dual control model of male sexual response: A theoretical
approach to centrally mediated erectile dysfunction. Neuroscience and Biobehavioral
Reviews, 24, 571–579.
Banner, L., & Anderson, R. (2007). Integrated sildenafil and cognitive-behavior sex therapy for
psychogenic erectile dysfunction: A pilot study. Journal of Sexual Medicine, 4, 1117–1125.
Barlow, D. H. (1986). Causes of sexual dysfunction: The role of anxiety and cognitive
interference. Journal of Consulting and Clinical Psychology, 54, 140–148.
Barlow, D. H. (2002). Anxiety and its disorders: The nature and treatment of anxiety and panic.
Barlow, D. H., Sakheim, D. K., & Beck, J. G. (1983). Anxiety increases sexual arousal. Journal
of Abnormal Psychology, 92, 49–54.
Beck, A. T. (1967). Depression: Causes and treatment. Philadelphia, PA: University of Pennsyl-
vania Press.
Beck, A. T. (1996). Beyond belief: A theory of modes, personality and psychopathology. In
P. M. Salkovskis (Ed.), Frontiers of cognitive therapy (pp. 1–25). New York, NY: Guilford
Press.
Brefczynski-Lewis, J., Lutz, A., Schaefer, H., Levinson, D., & Davidson, R. (2007). Neural
correlates of attentional expertise in long-term meditation practitioners. Proceedings of the
National Academy of Sciences of the United States of America, 104, 11483–11488.
Brotto, L., Basson, R., & Luria, M. (2008). A mindfulness-based group psychoeducational
intervention targeting sexual arousal disorder in women. Journal of Sexual Medicine, 5,
1646–1659.
Brotto, L., & Heiman, J. (2007). Mindfulness in sex therapy: Applications for women with
sexual difficulties following gynaecologic cancer. Sexual & Relationship Therapy, 22,
3–11.
Cahn, B., & Polich, J. (2006). Meditation states and traits: EEG, ERP, and neuroimaging
studies. Psychological Bulletin, 132, 180–211.
Carey, M. P., Wincze, J. P., & Meisler, A. W. (1993). Sexual dysfunction: Male erectile
disorder. In D. H. Barlow (Ed.), Clinical handbook of psychological disorders: A step by step
treatment manual (2nd ed., pp. 442–480). New York, NY: Guilford Press.
Carvalho, J., & Nobre, P. J. (2010). Sexual desire in women: An integrative approach regarding
psychological, medical, and relationship dimensions. Journal of Sexual Medicine, 7 ,
1807–1815.
Carvalho, J., & Nobre, P. J. (2011). Biopsychosocial determinants of men’s sexual desire:
Testing an integrative model. Journal of Sexual Medicine, 8, 754–763.
Carvalho, J., Vieira, A. L., & Nobre P. (2011). Latent structures of male sexual functioning.
Journal of Sexual Medicine, 8, 2501–2511.
Chambless, D. L., & Ollendick, T. H. (2001). Empirically supported psychological interven-
tions: Controversies and evidence. Annual Review of Psychology, 52, 685–716.
Craske, M. G., Brown, T. A., & Barlow, D. H. (1991). Behavioral treatment of panic: A
two-year follow-up. Behavior Therapy, 22, 289–304.
De Jong, D. (2009). The role of attention in sexual arousal: Implications for treatment of
sexual dysfunction. Journal of Sex Research, 46, 237–248.
DeRubeis, R. J., & Crits-Christoph, P. (1998). Empirically supported individual and group
psychological treatments for adult mental disorders. Journal of Consulting and Clinical
Fugl-Meyer, A. R., & Fugl-Meyer, K. Sjögren (1999). Sexual disabilities, problems and
satisfaction in 18–74 year old Swedes. Scandinavian Journal of Sexology, 2, 79–105.
35–43.
Hawton, K. (1989). Sexual dysfunctions. In K. Hawton, P. M. Salkovskis, J. Kirk, &
D. M. Clark, Cognitive behaviour therapy for psychiatric problems: A practical guide
(pp. 374–405). Oxford, England: Oxford University Press.
Heiman, J. (2002). Psychologic treatments for female sexual dysfunction: Are they effective
and do we need them? Archives of Sexual Behavior, 31, 445–450.
Heiman, J. R., & LoPiccolo, J. (1988). Becoming orgasmic: A sexual and personal growth
program for women (rev. ed.). New York, NY: Prentice-Hall.
Heiman, J. R., & Meston, C. M. (1998). Empirically validated treatments for sexual dysfunc-
tion. In K. S. Dobson & K. D. Craig (Eds.), Empirically supported therapies: Best practice
in professional psychology (pp. 259–303). New York, NY: Sage.
Hollon, S. D., DeRubeis, R. J., Shelton, R. C., Amsterdam, J. D., Salomon, R. M., O’Reardon,
J. P., … Gallop, R. (2005). Prevention of relapse following cognitive therapy vs medica-
tions in moderate to severe depression. Archives of General Psychiatry, 62, 417–422.
Janssen, E., Vorst, H., Finn, P., & Bancroft, J. (2002). The Sexual Inhibition (SIS) and Sexual
Excitation (SES) Scales: I. Measuring sexual inhibition and excitation proneness in men.
Journal of Sex Research, 39, 114–126.
Kabat-Zinn, J. (2003). Mindfulness-based interventions in context: Past, present, and future.
Kaplan, H. S. (1979). Disorders of sexual desire. New York, NY: Brunner/Mazel.
Laumann, E. O., Nicolosi, A., Glasser, D. B., Paik, A., Gingell, C., Moreira, E., & Wang, T.
(2005). Sexual problems among women and men aged 40–80 years: Prevalence and
correlates identified in the Global Study of Sexual Attitudes and Behaviors. International
Journal of Impotence Research, 17 , 39–57.
Laumann, E., Paik, A., & Rosen, R. (1999). Sexual dysfunction in United States: Prevalence
and predictors. Journal of the American Medical Association, 281, 537–544.
Lewis, R. W., Fugl-Meyer, K. S., Bosch, R., Fugl-Meyer, A. R., Laumann, E. O., Lizza, E., &
Martin-Morales, A. (2004). Epidemiology/risk factors of sexual dysfunction. Journal of
Sexual Medicine, 1, 35–39.
Lue, T., Bassson, R., Rosen, R., Giuliano, F., Khoury, S., & Montorsi, F. (Eds.). (2004).
Sexual dysfunctions in men and women. In The 2nd International Consultation on Sexual
Dysfunction (pp. 39–72). Paris: Health Publications.
Masters, W. H., & Johnson, V. E. (1966). Human sexual response. Boston, MA: Little, Brown.
Masters, W. H., & Johnson, V. E. (1970). Human sexual inadequacy. Boston, MA: Little,
Brown.
McCarthy, B. W. (1998). Male sexual awareness: Increasing sexual satisfaction. New York, NY:
Carroll & Graf.
Mercer, C. H., Fenton, K. A., Johnson, A. M., Wellings, K., Macdowall, W., McManus, S.,
Nanchahal, K., & Erens, B. (2003). Sexual function problems and help seeking behaviour
in Britain: National probability sample survey. British Medical Journal, 327 , 426–427.
Mitchell, W. B., DiBartolo, P. M., Brown, T. A., & Barlow, D. H. (1998). Effects of positive
and negative mood on sexual arousal in sexually functional males. Archives of Sexual
Behavior, 27 , 197–207.
National Institutes of Health Impotence. (1993). Consensus development conference state-
ment. International Journal of Impotence Research, 5, 181–199.
Nobre, P. J. (2009). Determinants of sexual desire problems in women: Testing a cognitive-
emotional model. Journal of Sex & Marital Therapy, 35, 360–377.
Nobre, P. J. (2010). Psychological determinants of erectile dysfunction: Testing a cognitive-
emotional model. Journal of Sexual Medicine, 7 , 1429–1437.
Nobre, P. J., & Pinto-Gouveia, J. (2003). Sexual modes questionnaire: Measure to assess the
interaction between cognitions, emotions and sexual response. Journal of Sex Research,
40, 368–382.
Nobre, P. J., & Pinto-Gouveia, J. (2006a). Dysfunctional sexual beliefs as vulnerability factors
to sexual dysfunction. Journal of Sex Research, 43, 68–75.
Nobre, P. J., & Pinto-Gouveia, J. (2006b). Emotions during sexual activity: Differences
between sexually functional and dysfunctional men and women. Archives of Sexual
Behavior, 35, 8–15.
Nobre, P. J., & Pinto-Gouveia, J. (2008). Differences in automatic thoughts presented during
sexual activity between sexually functional and dysfunctional males and females. Journal
of Cognitive Therapy and Research, 32, 37–49.
Nobre, P. J., & Pinto-Gouveia, J. (2009a). Questionnaire of cognitive schema activation in
sexual context. A questionnaire to assess cognitive schemas activated in sexual failure
situations. Journal of Sex Research, 46, 425–437.
Nobre, P. J., & Pinto-Gouveia, J. (2009b). Cognitive schemas associated with negative sexual
events: A comparison of men and women with and without sexual dysfunction. Archives
of Sexual Behavior, 38, 842–851.
Nobre, P. J., Pinto-Gouveia, J., & Gomes, F. A. (2003). Sexual dysfunctional beliefs question-
naire: An instrument to assess sexual dysfunctional beliefs as vulnerability factors to sexual
problems. Sexual & Relationship Therapy, 18, 171–204.
Nobre, P. J., Wiegel, M., Bach, A., Weisberg, R., Brown, T., Wincze, J., & Barlow, D. H.
(2004). Determinants of sexual arousal and the accuracy of its self-estimation in sexually
functional males. Journal of Sex Research, 41, 363–371.
Oliveira, C., & Nobre, P. (2012). The role of trait-affect, depression, and anxiety in women
with sexual dysfunction: A pilot study. Journal of Sex and Marital Therapy, 39, 436–452.
doi:10.1080/0092623X.2012.665813
Quinta Gomes, A., & Nobre, P. J. (2011). Personality traits and psychopathology on male
sexual dysfunction: An empirical study. Journal of Sexual Medicine, 8, 461–469.
Richters, J., Grulich, A. E., de Visser, R. O., Smith, A. M. A., & Rissel, C. E. (2003). Sex
in Australia: Sexual difficulties in a representative sample of adults. Australian and New
Zealand Journal of Public Health, 27 , 164–170.
Rosen, R. C. (2000). Prevalence and risk factors of sexual dysfunction in men and women.
Current Psychiatry Reports, 2, 189–195.
Rosen, R. C., Leiblum, S. R., & Spector, I. (1994). Psychologically based treatment for male
erectile disorder: A cognitive-interpersonal model. Journal of Sex & Marital Therapy, 20,
67–85.
Rosen, R. C., Riley, A., Wagner, G., Osterloh, I. H., Kirkpatrick, J., & Mishra, A. (1997). The
International Index of Erectile Function (IIEF): A multidimensional scale for assessment
of erectile dysfunction. Urology, 49, 822–830.
Sbrocco, T., & Barlow, D. H. (1996). Conceptualizing the cognitive component of sexual
arousal: Implications for sexuality research and treatment. In P. M. Salkovskis (Ed.),
Frontiers of cognitive therapy (pp. 419–449). New York, NY: Guilford Press.
Segraves, R. T. (2010a). Considerations for diagnostic criteria for erectile dysfunction in
DSM-V. Journal of Sexual Medicine, 7 , 654–660.
Segraves, R. T. (2010b). Considerations for an evidence-based definition of premature ejacu-
lation in the DSM-V. Journal of Sexual Medicine, 7 , 672–679.
Segraves, R. T. (2010c). Considerations for a better definition of male orgasmic disorder in
DSM-V. Journal of Sexual Medicine, 7 , 690–695.
Shapiro, J. R., Berkman, N. D., Brownley, K. A., Sedway, J. A., Lohr, K. N., & Bulik, C. M.
(2007). Bulimia nervosa treatment: A systematic review of randomized controlled trials.
Shapiro, S., Carlson, L., Astin, J., & Freedman, B. (2006). Mechanisms of mindfulness. Journal
of Clinical Psychology, 62, 373–386.
Shigaki, C., Glass, B., & Schopp, L. (2006). Mindfulness-based stress reduction in medical
settings. Journal of Clinical Psychology in Medical Settings, 13, 209–216.
Simons, J. S., & Carey, M. P. (2001). Prevalence of sexual dysfunctions: Results from a decade
of research. Archives of Sexual Behavior, 30, 177–219.
Soares, C., & Nobre, P. J. (2013). Sexual problems and psychotherapy in Portugal. In K. Hall
and C. Graham (Eds.), The cultural context of sexual pleasure and problems: Psychotherapy
with diverse clients (pp. 279–306). New York, NY, and Hove, England: Routledge.
Spanier, G. B. (1976). Measuring dyadic adjustment: New scales for assessing the quality of
marriage and similar dyads. Journal of Marriage and the Family, 38, 15–23.
Vilarinho, S. & Nobre, P. J. (2008). Portuguese women’s sexuality and biopsychosocial
determinants. Sexologies, 17 , S 149.
Weisberg, R., Brown, T., Wincze, J. P., & Barlow, D. H. (2001). Causal attributions and male
sexual arousal: The impact of attributions for a bogus erectile difficulty on sexual arousal,
cognitions and affect. Journal of Abnormal Psychology, 110, 324–334.
Wiegel, M., Scepkowski, L., & Barlow, D. (2007). Cognitive-affective processes in sex-
ual arousal and sexual dysfunction. In E. Janssen (Ed.), The psychophysiology of sex
(pp. 143–165). Bloomington, IN: Indiana University Press.
Wincze, J. P., & Barlow, D. H. (1997). Enhancing sexuality: A problem solving approach
(therapist guide). Albany, NY: Graywind.
Wincze, J. P., & Carey, M. P. (2001). Sexual dysfunction: A guide for assessment and treatment
World Health Organization. (1992). The ICD–10 Classification of Mental and Behavioural
Disorders: Clinical descriptions and diagnostic guidelines. Geneva, Switzerland: Author.
Zilbergeld, B. (1999). The new male sexuality (rev. ed.). New York, NY: Bantam.
29
The Paraphilias
W. L. Marshall and L. E. Marshall
Rockwood Psychological Services, Kingston, Canada
The Diagnostic and Statistical Manual of Mental Disorders (DSM), in all its iterations,
has a category of disorders that are identified as paraphilias. The behavior of some
of these paraphilics (i.e., those who commit crimes related to their paraphilias) cause
distress and harm to others, while the remainder cause distress, if at all, only to
themselves. The former are likely to involve the paraphilic with the criminal justice
system where he will be described as a sexual offender. Since the majority of paraphilics
appear to be men, and research has for the most part focused only on men, we will use
the masculine form throughout this chapter. There are other types of sexual offenders
who do not meet criteria for a DSM diagnosis (e.g., nonpedophilic child molesters,
and rapists). We will also address their issues.
This chapter will begin with a brief description of these various disorders with
remarks about some of the problematic issues. Next we will comment on the
reliability and nosological status of the paraphilias. We will then move to the primary
focus of the chapter: namely, treatment and the evaluation of its effectiveness.
The Nature of the Paraphilias
The current edition of the DSM (4th ed., text rev.; DSM-IV-TR; American Psychiatric
Association [APA], 2000) identifies the paraphilias as involving “recurrent, intense
sexually arousing fantasies, sexual urges, or behaviors generally involving 1) nonhuman
objects, 2) the suffering or humiliation of oneself or one’s partner, or 3) children or
other nonconsenting persons that occur over a period of at least 6 months” (APA,
2000, p. 566). Of course, for each paraphilia, the DSM-IV-TR provides specific details
of the criteria.

DOI: 10.1002/9781118528563.wbcbt29
As noted, the paraphilias include some criminal, or potentially criminal, acts, and
noncriminal acts. In addition there are other criminal sexual behaviors linked to
fantasies and urges that do not appear in the DSM. The following section describes
these various problematic behaviors.
One important point to note, before we proceed, is that there is evidence that a
number of paraphilics have other paraphilias, in addition to their primary diagnosis. For
instance, Abel and Rouleau (1990) showed that among nonfamilial child molesters,
61.4% reported having three or more paraphilias, as did 46% of incest offenders.
However, Abel and Rouleau included what appear to be transitory (i.e., less than 6
months) interests in their count of paraphilias. When W. L. Marshall, Barbaree, and
Eccles (1991) conducted a similar study, but excluded these transitory inclinations,
they found that only 12% of child molesters reported more than one paraphilia and
only one offender had three additional paraphilias.
Offense-Related Disorders
Frotteurism
According to the DSM-IV-TR this behavior “involves touching and rubbing against
a nonconsenting person” (APA, 2000, p. 570). The frotteur will typically have an
erection and may have an orgasm during the act. Frotteurism represents a threat to
the personal integrity and well-being of (mostly) women on packed public transit
systems and other densely crowded places, but little is known about it as the offenders
are rarely reported or prosecuted. Despite the fact that Krueger and Kaplan (1997)
could find only 17 papers on frotteurism after a complete Medline search, it appears
to be a common offense. Fisher, Cullen, and Turner (2000), for example, found that
35% of a sample of 4,446 females reported being victims of frotteurs.
Voyeurism
The DSM-IV-TR describes this as involving acts of “observing unsuspecting individ-
uals, usually strangers, who are naked, in the process of disrobing, or engaging in
sexual activity” (APA, 2000, p. 575). In most cases, and certainly in the early stages
of the development of this interest, the voyeur wants the victim to be unaware of
his presence. The voyeur may masturbate while observing or he may use the images
in later masturbatory activity. Just as we saw with frotteurs, there are few studies of
voyeurs (Kaplan & Krueger, 1997), making it difficult to say anything with confidence
about their characteristics. Recently, McConaghy (2005) described a survey in which
50% of young males said they had engaged in voyeuristic acts without being detected.
Exhibitionism
Exhibitionists are said by DSM-IV-TR to be aroused by exposing their genitals to a
nonconsenting person, usually a stranger. This behavior is typically enacted at high
frequencies usually for relatively short periods but these short periods recur over many
The Paraphilias 675
years with an apparent decline after age 40 (W. D. Murphy, 1997). The data that are
available suggest that the incidence of these acts is high, particularly when anonymous
surveys of women are the basis for estimating frequency (Cox & MacMahon, 1978).
Gittleson, Eacott, and Mehta (1978), for example, reported that 44% of British nurses
said they had been exposed to exhibitionism outside the work situation. Most of the
literature on exhibitionism is from the 1960s and 1970s, so much of what we know
about these offenders may not reflect current issues.
An interesting facet of the recently expanding literature on hypersexuality (often
called “sexual addiction” or “sexual preoccupation”) concerns the observation that
35–40% of sexual offenders meet criteria for this associated problem (L. E. Marshall,
Marshall, Moulden, & Serran, 2008). More specifically it has been reported that a
significant proportion of exhibitionists display hypersexual behaviors (Långström &
Seto, 2006).
Pedophilia
This term describes a subset of child molesters. Only those molesters who are
persistently (i.e., over a period of more than 6 months) sexually aroused by children
meet criteria for a diagnosis of pedophilia. Strict application of the diagnosis suggests
that no more than 50% of men convicted of sexual offenses against children meet
criteria for this disorder (Seto, 2008). Unfortunately far too many reports in the
literature use the term “pedophilia” to describe all child molesters without concern
for the diagnostic criteria (W. L. Marshall, 2007).
There is now an extensive body of literature on men who have committed sexual
offenses against children and it is clear that the problem is both universal and
underreported (Seto, 2008). For example, in their study of males who have never
been identified as offenders, Brière and Runtz (1989) reported that 9% said they had
fantasized about having sex with a child and Smith (1994) found that 3% of college
males admitted having had sexual contact with females aged 12 or younger. There is a
particularly interesting ongoing research project (Beier et al., 2009) that has recruited
men in Germany who admit to, and are bothered by, a persistent sexual interest in
children but have never been identified by the justice system. In one of the reports
of this project, Schaefer et al. (2010) indicated that 39.4% of these men admitted
to having had undetected sexual contact with children. Apparently the strategies of
some child molesters effectively reduce their chances of being identified.
As Seto (2008) noted in his comprehensive appraisal of the literature, there are now
available several reasonably sound methods for assessing persistent sexual interests
in children, at least for adult males. After reviewing various methods, Seto (2008)
concluded that the evidence to date supports the use of phallometric measures as
currently the best way to assess the sexual interests of pedophiles. In fact, Freund
(1967; Freund & Watson, 1991) has for several years maintained that the only reliable
way to diagnose pedophilia is through the use of phallometry. Phallometry involves
measuring erectile responses while the man is viewing sexual scenes or listening to
audio recordings of sexual interactions. A man is said to be pedophilic if his sexual
arousal to children is equal to or greater than his arousal to adults (W. D. Murphy &
Barbaree, 1994). In fact, phallometry has been used to assess various paraphilics but
has not consistently produced valuable information for exhibitionists or for rapists
(W. L. Marshall & Fernandez, 2003).
More recently Seto and his colleagues (Seto, Harris, Rice, & Barbaree, 2004;
Seto & Lalumière, 2001) have developed an assessment procedure that relies on
offense history and crime scene data. This assessment produces results in line with
phallometric test data. Essentially what these two approaches (phallometry and Seto’s
measure) indicate is that unless the offender has more than two victims he is unlikely
to be identified by either of these methods as a pedophile. However, the problem of
accurately identifying pedophilia is more complex than simply examining the number
of victims, as reference to the DSM criteria makes clear (O’Donohue, Regev, &
Hagstrom, 2000).
Sadism and Masochism

Sadists engage in behaviors during sexual acts, or in fantasy, that involve the humil-
iation of, or the infliction of pain on, the other person. Some 10–20% of men
acknowledge being sexually aroused by sadistic stories (Kinsey, Pomeroy, & Martin,
1948). In fact, sadistic sexual fantasies occur to varying degrees among sexual murder-
ers, rapists who do not kill, and nonoffenders (Grubin, 1994). Some sadists seek out
cooperative partners who presumably are masochists, and, therefore, their actions do
not involve legally proscribed behavior. While some of these latter types of sadists may
be concerned about their interests and seek treatment, the ones who present the most
serious threats are those who inflict their interests on unwilling victims. Interestingly,
while the DSM-IV-TR (APA, 2000) also makes the distinction between consenting
and coerced victims in the preamble to identifying the criteria, the statement of the
primary criteria does not allow the diagnostician to apply differential labels to these
two quite different groups.
A continuing issue concerns whether or not masochism is a distinct disorder
or whether it occurs concurrent with sadism. Arndt, Foehl, and Good (1985)
found that persons who report being masochists are also likely to report engaging
in sadistic behaviors, and individuals who self-identify as sadomasochists alternate
between the two roles (Spengler, 1977). Yates, Hucker, and Kingston (2008) view
asphyxiophilia (self-induced suffocation) as “an expression of extreme masochism”
(p. 220) and asphyxiophilia is significantly common among sadistic murderers (Hucker
& Blanchard, 1992). Almost all survivors of self-hanging reported having repeated
masochistic fantasies during their asphyxiophilic act (Hucker, 2011).
Much of the recent research in this area focuses on what has been called “severe
sexual sadism”; that is, sexual sadism involving a coerced, unwilling victim. When
W. L. Marshall, Kennedy, Yates, and Serran (2002) asked renowned experts on sexual
sadism to indicate the relative importance for the diagnosis of 17 features derived
from a literature review, they found significant agreement across these experts in
their ratings of the importance of a set of these features. From this information
W. L. Marshall and Hucker (2006) devised a Sexual Sadism Scale in which items were
weighted according to the ratings provided by the experts. Subsequently, Nitschke,
Osterheider, and Mokros (2009) revised and shortened this scale and provided data
on its reliability and single-factor structure (Mokros, Osterheider, Schilling, Eher,
The Paraphilias 677
& Nitschke, 2011). Nitschke et al.’s scale allows for either a categorical diagnosis
or a dimensional determination of the degree of sexual sadism. Nitschke, Mokros,
Osterheider, and Marshall (2012) expressed the view that a dimensional index of
sadism would represent a better solution than a categorical diagnosis; perhaps the
same is true for all the paraphilias.
Paraphilia Not Otherwise Specified

Milner, Dopke, and Crouch (2008) described the variety of oddities of sexual
expression that are thought to occur with such low frequency that they are all placed
in the not otherwise specified (NOS) category. Included in this NOS group, however,
are some offense-related behaviors that appear not to be uncommon. Telephone
scatologia, for example, is reported by women who receive these unwanted calls as a
common event in their lives (Matek, 1988). Zoophilia (bestiality) has a long history
as evidenced in cave paintings from 20,000 years ago (Peretti & Rowan, 1983), and
Kinsey et al. (1948) found that among rural populations 40–50% reported engaging
in sex with animals. However, among the almost limitless number of other possible
NOS paraphilias, most seem to be rare. Descriptions of these varieties are provided
by Milner et al. (2008) but data on their frequency and the characteristics of these
paraphilics are all but absent.
Because rapists are not included in the DSM, but are routinely referred for
consideration for civil commitment, clinicians and evaluators working within sexually
violent predator (SVP) programs have adopted the tactic of using the NOS diagnosis
when assessing rapists (Doren, 2002). This appears to be unwise as there are no criteria
specified in the DSM for this diagnosis, thereby almost guaranteeing unreliability, and
yet such a diagnosis may lead to an offender being indefinitely incarcerated.
Nonoffending Disorders
Fetishism
The DSM-IV-TR (APA, 2000) defines fetishism as “involving the use of nonliving
objects (e.g., female undergarments)” (p. 570) for the purpose of generating sexual
arousal. For the behavior to meet diagnostic criteria it has to produce distress and
yet many men who engage in fetishistic behaviors are not upset by the activities.
For example, although the prevalence appears to be reasonably common (Gosselin &
Wilson, 1980) very few appear at clinics for treatment (Chalkley & Powell, 1983).
In fact, it seems that many fetishists who seek treatment do so because their partners
express distress (Mason, 1997).
There are numerous web sites that specifically cater to fetishistic interests. These
sites, and evidence reviewed by Junginger (1997), indicate a broad range of objects
and activities associated with fetishisms. The most common objects are articles of
underwear, shoes, and leather or plastic articles (Mason, 1997). One diagnostic issue
that remains unresolved concerns whether “partialism” (defined as a fetish for specific
body parts such as breasts or buttocks) should be considered a fetish or an aspect of
transvestic fetishism. Alternatively, it may be seen as a normal sexual interest since

partialisms are commonly reported by a substantial number of men who appear to
consider these interests to be quite normal (Wise, 1985). The diagnostic manual
excludes body parts from the definition of fetishism but does include partialism as
an example of paraphilia NOS. Exactly why this distinction is made is not clear since
the features of the two supposedly distinct disorders are remarkably similar (Mason,
1997).
Junginger (1997) discusses the diagnostic criterion of distress in some detail. He
claims that the “overwhelming majority of fetishists have adjusted to their ‘disorder’”
(p. 107) and that in the current social climate where there is, so he says, “increasing
acceptance of almost all forms of sexual expression” (p. 107) it seems inappropriate
to consider fetishism as a disorder. This issue is, however, unlikely to be resolved in
the near future.
Transvestic Fetishism
Transvestic fetishism and fetishism appear to have a significant feature in common, as
is implied by the inclusion of the term fetishism in the DSM label. Cross-dressing is a
defining part of DSM criteria for transvestic fetishism where the wearing of clothing
of the opposite sex is said to be sexually arousing. The same articles that a fetishist
fondles (e.g., women’s underwear or other articles of women’s clothing) to generate
arousal are the very articles cross-dressers wear to generate arousal. Clearly the two
disorders have much in common.
It is necessary to distinguish among cross-dressers those who meet criteria for
transvestic fetishism from those who do not. Some people cross-dress because they
believe they are biologically members of the “opposite” sex (transsexuals); some men
cross-dress to attract other males (so-called “drag queens”); some men cross-dress
in their role as entertainers; and some do so in order to generate sexual excitement
(i.e., the true transvestic fetishists). While some males who cross-dress claim it is not
sexually exciting, when these men are assessed by phallometric methods, they display
sexual arousal to the act (Blanchard, Racansky, & Steiner, 1986). As Croughan,
Saghir, Cohen, and Tobins (1981) note, while cross-dressing may not be a part of
sex with their partner, transvestic fantasies are typically required for orgasm to occur
during sex.
As was the case with fetishisms, researchers have questioned the validity of the
criterion of distress among transvestic fetishists (King, 1993), claiming that it is
usually only when someone else complains (e.g., the man’s wife) that the person
seeks treatment. Studies have reported that transvestic fetishists are satisfied with their
interests (Prince & Bentler, 1972) and that they report feeling comfortable and relaxed
when cross-dressed (Gosselin & Eysenck, 1980). However, Croughan et al. (1981)
found that 95% of transvestites reported at least one adverse consequence arising
from cross-dressing and that these consequences were related to disruptions in social
relations, impairments in education and employment, and negative self-denigrating
thoughts. Perhaps these somewhat conflicting observations can be understood if we
accept the claim by Weinberg, Williams, and Calhan (1995) that fetishisms (and by
implication transvestic fetishisms) lie along a continuum from a mild interest to a
The Paraphilias 679
strong preference. Consistent with this, apparently some men who cross-dress do so
only occasionally and although on these occasions it is sexually exciting, they do not
seem driven to cross-dress more frequently (Docter & Prince, 1997).
Diagnostic Reliability
For any diagnosis to serve a useful purpose it must be shown to be reliable (Nelson-
Gray, 1991). Standards of reliability suggest that for important decisions to be made
the kappa coefficient should be k = 0.8, while for very important decisions (i.e.,
SVP commitments) it should be k = 0.9 (K. R. Murphy & Davidshofer, 1998).
Since a diagnosis of a paraphilia (particularly pedophilia and sexual sadism) has serious
implications for both the client and the safety of the public, such diagnoses clearly meet
criteria for at least an important decision. Unfortunately none of the paraphilias that
has been examined meets such a standard even under rigorous conditions that ought
to maximize reliability and that ought to overestimate the reliability of diagnoses as
they are conducted under normal clinical conditions.
For example, O’Donohue et al. (2000) examined the criteria for pedophilia
and observed that, in almost all respects, the specification of each criterion was
sufficiently open to differing interpretations that reliability across diagnosticians was
almost guaranteed to be low. They also pointed out that the reliability of paraphilic
diagnoses reported in the field trials accompanying the DSM-III (American Psychiatric
Association, 1980) was unsatisfactory. O’Donohue at al. said they were unable to find
evidence of further DSM field trials of the paraphilias.
In a landmark study, Levenson (2004) examined this issue within the context of
SVP commitments for all of the diagnostic categories employed. She found that none
of the diagnoses met acceptable standards, with even the general category of “any
paraphilia” being far lower than desired (k = 0.47). The resulting coefficients for
the specific disorders were unsatisfactorily low (pedophilia, k = 0.65; exhibitionism,
k = 0.47; sexual sadism, k = 0.30; and paraphilia NOS, k = 0.36).
On a related issue, Kingston, Firestone, Moulden, and Bradford (2007) discerned
problems with a variety of methods for diagnosing pedophilia, including diagnoses
by experienced forensic psychiatrists, phallometric assessment data, and Seto and
Lalumière’s (2001) measure of sexual interests. First they found little correspondence
between any of these indices of pedophilia. However, the most important observation
was that, no matter what the basis, a diagnosis of pedophilia was unrelated to any of the
features indicative of future risk. A later study by this same group (Moulden, Firestone,
Kingston, & Bradford, 2009), using similar methods of diagnosing pedophilia, found
that none of the diagnoses derived from any of the procedures was related to actual
reoffending of any kind (i.e., sexual, violent, or nonsexual/nonviolent offending).
In their review of the available literature on sexual sadism, W. L. Marshall and
Kennedy (2003) noted that every reported study used either one or two unique
criteria or had a unique combination of criteria; no two studies employed matching
criteria. This, of course, made it impossible to come to confident conclusions about the
meaning of the overall findings. Subsequent studies found that the clinical application
of the diagnosis of sadism in a prison setting was not done reliably (W. L. Marshall,
Kennedy, & Yates, 2002) nor did 15 international experts agree on a diagnosis
(W. L. Marshall, Kennedy, Yates, & Serran, 2002), although, as noted earlier, they
did agree on the importance of the specific criteria.
Assessment Issues
Assessments conducted prior to treatment are meant to serve several purposes includ-
ing establishing the beginning of a developing case formulation and providing a
baseline against which to assess gains at the end of treatment. To serve these purposes,
some treatment programs have sexual offenders complete a comprehensive battery of
tests, most of which are self-report measures (see Craig & Beech, 2009, for details).
Such measures present problems with offenders who have serious trust issues and
who, accordingly, are motivated to present themselves as competent and prosocial.
Our experience is that case formulation can best be generated in the following way.
First there is a thorough understanding, at least for sexual offenders, of the problems
that put them at risk to reoffend (Hanson, 2006). When these features are potentially
modifiable, they are described as “criminogenic factors” and there is solid evidence
that addressing these issues in programs for sexual offenders (Hanson, Bourgon,
Helmus, & Hodgson, 2009) is essential to reduce reoffending. There is every reason
to suppose, from the available evidence, that these criminogenic factors identified in
sexual offenders are the same problems that beset all types of paraphilics (see Laws
& O’Donohue, 1997, 2008). Thus, a nomothetically-based case formulation would
assume that each client has some degree of problems in each of the criminogenic
areas of functioning. The second step in generating a case formulation is to enter the
client into a treatment program where the first stage provides specific information
about various deficits and strengths. Thus, the first stage of treatment needs to have
the client provide an autobiographical account of his life’s successes and problems
as well as an account of the events leading up to his offense or that resulted from
the shame associated with his paraphilic interests. As a result of this information the
nomothetic formulation can be adjusted to produce an idiographic formulation for
each individual (W. L. Marshall, Marshall, Serran, & O’Brien, 2011).
With regard to assessing the effects of treatment on each individual client,
W. L. Marshall et al. (2011) have developed an empirically validated Therapist
Rating Scale (TRS-2) which is applied at the point of discharge. This 10-item scale
requires the therapist to rate each client in terms of how well he understands each of
the treatment issues and how well he has internalized or demonstrated what he has
learned. There are data available (W. L. Marshall et al., 2011) indicating that these
posttreatment ratings predict the success or failure of treated sexual offenders whereas
various other assessments (e.g., actuarial risk evaluations or measures of psychopathy)
do not.
Assessments are also conducted prior to treatment to determine each client’s risk
to reoffend based on actuarially-determined static factors (see Doren, 2006, for a
summary of such measures). These assessments are done to assist in determining both
the need for treatment and how extensive and intensive treatment should be. Andrews
and Bonta (2006) have demonstrated across all offender types that treatment has its
The Paraphilias 681
greatest impact with higher-risk offenders and Hanson et al. (2009) have shown the
same to be true for sexual offenders. Of course, risk assessment results are also helpful
to institutional authorities (e.g., parole boards) who make release decisions.
Treatment
In the early days of the development of modern treatment programs for the para-
philias, as well as for sexual offenders more specifically, the focus of treatment was
circumscribed. For example, specific types of nonoffending paraphilics were treated
separately from others (e.g., Marks & Gelder, 1967) as were different types of sexual
offenders (e.g., Abel, Blanchard, & Becker, 1978). In addition, initially the targets
of treatment were almost exclusively deviant sexual preferences, an approach that was
based on McGuire, Carlisle, and Young’s (1965) conditioning model of the etiology
of paraphilic behavior. Over the past 40 years, however, the range of issues addressed
in treatment has expanded significantly and many programs now integrate all types of
sexual offenders in the same groups (Mann & Marshall, 2009).
Nonoffending Paraphilics
Except for interventions implemented in the 1960s and 1970s, there have been few
reports of treatment for these nonoffending paraphilics. This is also largely true for
some of the sexual offenses where the major thrust in the development of treatment
has been for child molesters and rapists. We will, however, provide a review of what
is available.
Junginger’s (1997) review of treatment for fetishists focused entirely on condi-
tioning procedures applied to sexual interests. Such approaches appear to have been
effective. For example, W. L. Marshall (1974) reported success using a condition-
ing procedure with a client who had a fetish for blue jeans; however, relationship
and social skills training were added to encourage this socially isolated young man
to become involved in friendships and to develop an intimate relationship. The
treatment-induced changes in this man’s sexual interests were retained at a 2-year
follow-up.
A rapist with a fetish for women’s pantyhose was referred to a treatment unit in
a Canadian federal penitentiary in mid-1975. This man’s offending routine involved
wearing women’s pantyhose under his trousers and then prowling city streets in search
of a woman wearing pantyhose whom he would then follow. If the woman finally
traveled to an isolated location he would attack and rape her. During the rapes he said
the sensations of his and the victim’s pantyhose rubbing against each other provided
the necessary stimulation for his orgasm; without these sensations he said he was
unable to ejaculate. He adopted similar tactile interactions with pantyhose during his
masturbatory activities. Accordingly a novel treatment approach was designed.
A collection of pantyhose was purchased and a new one was presented to the
client at each treatment session during which time he was alone in an isolated room.
The client was instructed to masturbate to orgasm using the pantyhose in his usual
manner and then to continue to caress the pantyhose during the postorgasm refractory
period while articulating aloud his typical fetishistic thoughts. Masters and Johnson
(1966) had shown that immediately after orgasm men enter a period where they
are unresponsive (i.e., refractory) to sexual stimuli that would otherwise be arousing
to them. Repeatedly associating the fetish object and behavior with this state of
sexual unresponsiveness would, it was assumed, induce the extinction of the erotic
valence attached to the pantyhose and its associated rituals. Phallometric testing
revealed a remarkable diminution of arousal to the pantyhose over treatment sessions
with the client reporting a complete loss of interest in the fetishistic activity (W. L.
Marshall & Lippens, 1977). These changes were maintained over the remainder of his
prison sentence (approximately 3 years) and there were no instances of reoffending
over several years postdischarge. This procedure was called “satiation,” and it has
been used effectively with several other nonfetish, paraphilic, and sexual offending
behaviors.
Given that fetishists commonly have features (e.g., poor social and relationship skills,
loneliness, deficiencies in empathy, low self-esteem) in common with sexual offenders
as well as a strong tendency to use sex as a coping strategy, it has been suggested
that the treatment approach applied to sexual offenders should prove effective with
fetishists (Darcangelo, Hollings, & Paladino, 2008). In fact, all paraphilics seem to
have problematic features common to sexual offenders, so it seems likely that similar
treatment is likely to be effective across all paraphilias.
As was the case with fetishisms, early treatment for transvetic fetishists was directed at
eliminating arousal to cross-dressing by a variety of aversive conditioning procedures.
Using either nausea-inducing drugs or electric shocks, these approaches appear to
have been effective, at least across time-limited follow-up appraisals (Adshead, 1997).
More recently it has been suggested that the components of comprehensive sexual
offender treatment should be applied to transvestic fetishists (Newring, Wheeler, &
Draper, 2008).
There is little in the way of reported psychological treatment outcome studies with
the various other nonoffending paraphilics. The best evidence on effective treatment
with a range of nonoffending paraphilics is derived from interventions employing
one or another of the selective serotonin reuptake inhibitors (Grubin, 2008). While
the data from these studies convincingly demonstrate enhanced control over the
expression of paraphilic interests, such treatment has not been shown to enhance
prosocial skills (particularly intimacy skills) or to improve self-worth and diminish
shame. As W. L. Marshall (1971) noted, normalizing sexual interests does not
necessarily lead to the generation of the skills necessary to secure the variety of needs
that are typically pursued in sexual relations, and yet the absence of stable relationships
has been shown to increase the likelihood of a relapse, at least among sexual offenders
(Hanson & Harris, 2000).
Sexual Offenders
As noted earlier, not all sexual offenders meet criteria for a paraphilia, although some
do. However, several studies suggest that paraphilic and nonparaphilic sexual offenders
respond equally well to the same comprehensive treatment programs (W. L. Marshall,
2008). As a consequence we will ignore the diagnostic distinction in this section.
The Paraphilias 683
Treatment for sexual offenders has a long history dating back to the late 1800s
and early 1900s (Laws & Marshall, 2003), although systematic approaches were not
initiated until the 1970s when treatment targets began to be expanded beyond simply
modifying sexual interests (W. L. Marshall & Laws, 2003).
Exhibitionists. Early in the modern approach to treating sexual offenders, some of

the most systematic treatment attempts were with exhibitionists (Cox & Daitzman,
1980). As was the case with fetishisms, most of these early programs involved various
procedures aimed primarily at changing sexual interests. Given this limited focus, it
is interesting that subsequent phallometric studies failed to identify deviant interests
among exhibitionists (W. L. Marshall, Payne, Barbaree, & Eccles, 1991). When we
questioned these offenders the majority indicated that, rather than imaging exposing,
their masturbatory fantasies involved one of their victims requesting intercourse with
them. Thus, their fantasies were in most respects normative, if somewhat unlikely to
be realized.
In their recent appraisals of the literature on the treatment of exhibitionists, Morin
and Levenson (2008) gave most attention to procedures aimed at altering deviant
interests, despite admitting to the ambiguous nature of the evidence for such interests
in these men. It must be conceded that the evidence does support the idea that
employing procedures derived from conditioning theory is effective in providing
exhibitionists with control over their urges to expose and thus reduces the incidence
of exposing behavior (Maletzky, 1991).
As an illustration of one of the most commonly used conditioning procedures with
exhibitionists, W. L. Marshall (2006) reported the treatment of a man with 20 years
of daily exposing. Although Marshall encouraged this man to become involved in a
comprehensive approach, he suggested that a necessary first step, given that the man
was free in the community, would be to introduce a strategy to immediately increase
his control over his urges to expose. The client agreed so an aversion technique was
implemented. In this procedure the client carried with him at all times a small vial
of salts of ammonia (i.e., smelling salts). He was told that whenever he experienced
an urge he was to uncap the vial, hold it just below his nose, and take a quick nasal
inhalation. It was explained that the effect of this is to remove all current thoughts and
urges, thereby providing an opportunity to initiate alternate nondeviant thoughts.
The client reported diligently practicing this. In a controlled, single case experimental
design, Marshall demonstrated control over these urges and exposing behavior as a
result of introducing this use of the smelling salts. The client was so impressed by
these effects, and so confident in his newfound success at controlling his here-to-
fore irresistible urge, that he pronounced himself cured and in no need of further
treatment. Against Marshall’s advice he terminated his involvement in treatment.
Nevertheless, a 20-year follow-up check on the national data base revealed no further
arrests or convictions which, given this man’s prior rate of offending, provides rather
convincing proof of his success.
Morin and Levenson (2008) mention more comprehensive approaches but they
are dealt with in far less detail than the conditioning procedures. W. L. Marshall,
Eccles, and Barbaree (1991) compared two treatments for exhibitionists: One was
a behavioral program that was mostly focused on modifying sexual interests and
urges, while the other focused far more on enhancing relationship skills, building the
capacity for empathy, and strengthening self-efficacy and coping skills. The effects of
these two programs were compared with the subsequent rates of reoffending among
untreated exhibitionists. Official police records revealed that 26% of the untreated
exhibitionists reoffended over an 8.8-year follow-up while 14% of the men given the
behavioral program relapsed, but only 8% of those given the more comprehensive
treatment failed to remain offense-free. Although generated by only one study, these
findings suggest that programs addressing a broad range of the common deficits
among exhibitionists are the treatments most likely to be maximally effective.
Frotteurs and voyeurs. The literature on the treatment of frotteurs and voyeurs is
limited. As Krueger and Kaplan (1997) noted, “aside from a few case reports, therapy
suggestions have been developed with a heterogeneous group of paraphilics in general
and not derived specifically for the treatment of frotteurs” (p. 139). The same can
be said for voyeurs where the extant literature amounts to no more than a handful
of single case reports (Hanson & Harris, 1997). In their chapter on the treatment
of voyeurs, Mann, Ainsworth, Al-Attar, and Davies (2008) outline suggestions for
a broad-based treatment program for voyeurs, largely based on programs for child
molesters and rapists. However, they were unable to point to any current program of
this kind much less outcome data supporting its utility.
Child molesters and rapists. By far the majority of reported studies of the treatment
of sexual offenders have included only child molesters and rapists. There is now an
extensive body of reports on the treatment of these offenders.
After the 1970s move to more comprehensive programs for these offenders, the
most significant change came when Janice Marques (1982) presented her adaptation
for sexual offenders of Alan Marlatt’s (1982) relapse prevention (RP) program for
addicts. Despite the fact that Marlatt had developed this approach as a way of
maintaining treatment gains among addicted clients, Marques’ approach quickly
evolved into a complete treatment program for sexual offenders (Pithers, Marques,
Gibat, & Marlatt, 1983). Within a few short years this approach became entrenched
across North America as the accepted standard for treating these men, despite an
absence of evidence supporting its efficacy. RP endured unchallenged until Ward and
his colleagues (Ward & Hudson, 1996; Ward, Hudson, & Siegert, 1995) began to
critically examine its theoretical bases while others demonstrated that RP, either on
its own or as an adjunct to otherwise comprehensive programs, showed no beneficial
effects (W. L. Marshall & Anderson, 2000). Eventually, Marques’ own long-term
randomized controlled trial of RP demonstrated no differences between treated and
untreated sexual offenders (Marques, Weideranders, Day, Nelson, & van Ommeren,
2005). Unfortunately the outcome of this well-designed study did not toll the death
knell for RP, with many current programs continuing to adhere to most, if not all,
of its elements, and its advocates continue to sing its praise (Carich, Dobkowski, &
Delehanty, 2009).
Despite these dismal results with the RP model, other comprehensive programs
appeared to produce effective results. Two large-scale meta-analyses demonstrated
that treatment could be effective with these problematic offenders. Hanson et al.
The Paraphilias 685
(2002) evaluated the overall effects of 43 treatment outcome studies involving

9,454 sexual offenders, half of whom received treatment while the other half were
matched untreated offenders. Hanson et al. reported that 16.8% of the untreated men
reoffended over a 5-year follow-up while only 12.3% of the treated group recidivated.
Lösel and Schmucker (2005) conducted a similar, but much larger meta-analysis
of sexual offender programs (k = 81; N = 22,181). They found reoffense rates in
the untreated group (i.e., 17.5%) to be remarkably similar to the rates reported by
Hanson et al. while among the treated offenders only 11.1% committed a subsequent
offense. In both these reports, cognitive behavioral programs appeared to be the most
effective.
In both these meta-analyses one surprising observation was that the propensity
of these treated sexual offenders to commit nonsexual offenses was also markedly
reduced. Hanson et al. (2002) reported that 51% of the untreated men were
subsequently convicted of a nonsexual crime whereas only 32% of the treated men
committed another nonsexual offense. Among Lösel and Schmucker’s treated clients,
22.4% committed a nonsexual crime after release while 32.5% of the untreated men
did.
Even among the higher-risk, and therefore quite dangerous, sexual offenders,
treatment has been shown to be effective. Compared with a reoffense rate of
51.7% in an untreated group of these highest risk offenders, Looman, Abracen,
and Nicholaichuk (2000) demonstrated that among the matched group of treated
offenders only 23.6% recidivated over a 10-year follow-up. In another study of slightly
lower, but nevertheless high-risk sexual offenders, Nicholaichuk, Gordon, Gu, and
Wong (2000) reported that 33.2% of untreated sexual offenders relapsed against only
14.5% of matched treated offenders.
All the programs entering the four evaluations described above, however, were
implemented prior to the availability of a number of important reports, not the
least of which were studies by Hanson and his colleagues (Hanson, 2006; Hanson
& Harris, 2000) in which they empirically demonstrated that certain potentially
modifiable features of sexual offenders (so-called criminogenic factors) predicted the
likelihood of a reoffense whereas other features (noncriminogenic factors) did not.
Many of the earlier programs did not target all the criminogenic factors and most
addressed numerous noncriminogenic features. As we will see, that made it unlikely
that these earlier programs would be maximally effective, if at all. In addition, most
of these earlier programs had a quite negative focus, much of which involved a
detailed analysis of past offenses and a rather harsh and critical style of challenging
or confronting the offenders. As we will see, there now exists evidence that such
approaches are not likely to generate benefits.
Strength-Based Treatment
Several important publications over the past 20 years have suggested the potential
value of the elements of an alternative, more positively focused, and strength-based
treatment approach. These elements derive from four sources: Andrews and Bonta’s
(2006) risk/needs/responsivity principles; Miller and Rollnick’s (2002) motivational
interviewing; Ward’s (2002) good lives model; and ideas derived from the recent
positive psychology movement (see Linley & Joseph, 2004, and Snyder & Lopez, 2005,
for numerous examples). We will discuss the relevance of each of these in turn before
describing our own program that integrates these four influences and its outcome
data.
Risk/Needs/Responsivity
Andrews, Bonta, and Hoge (1990) elucidated a set of principles derived from their
meta-analysis (Andrews, Zinger, et al., 1990) of outcome studies of treatment for
various types of offenders. They showed that three principles of effective offender
treatment could be derived from this meta-analysis which they described as risk,
needs, and responsivity. Independent meta-analyses confirmed Andrews’ findings
with general offenders (Aos, Miller, & Drake, 2006; Lösel, 1995; Redondo, Garrido,
& Sanchez-Meca, 1999) and Hanson et al. (2009) showed that these principles were
equally applicable to sexual offenders.
The risk principle suggested that the greatest benefits were likely to be apparent
when the highest-risk offenders were treated. However, in Andrews’ studies this
generated the lowest overall effect size (ES = 0.10) of the three principles and in
Hanson et al.’s (2009) replication with sexual offenders it essentially exerted little
effect at all. In practice this principle is interpreted as requiring that the greatest
treatment intensity and extensivity should be reserved for high-risk offenders, with
less energy being devoted to moderate or lower-risk offenders. Fortunately there
are now available empirically derived risk assessment instruments for sexual offenders
(Hanson & Thornton, 2000) which allow treatment planners to allocate them to
appropriate levels of intervention.
The needs principle demands that the issues targeted in treatment be limited to
those potentially changeable features that have been shown to predict reoffending;
the so-called “criminogenic factors.” Prior to the year 2000, there were no empirically
established criminogenic factors for sexual offenders as there were for other types
of offenders. Until the early part of the twenty-first century, treatment providers
addressed features that had either been shown to be unique to sexual offenders
compared to other males, or that the therapists believed were necessary treatment
targets. Some of the features that distinguished sexual offenders (e.g., an array of
distorted cognitions or an absence of victim empathy) were later determined not to
predict reoffending, and some that seemed obviously necessary to address (e.g., the
offender acknowledging responsibility for the offense details) similarly turned out not
to be criminogenic. Hanson and Harris (2000) report the results of a large-scale
study in which they identified a number of modifiable features that were related to
later sexual reoffending. This landmark study initiated various research projects that
have revealed various targets meeting the needs principle (Craig, Browne, & Beech,
2008; Mann, Hanson, & Thornton, 2010). Presumably as this work continues other
appropriate treatment targets will be identified.
It is, however, important to note that, as Andrews and Bonta (2006) point out,
it may also be valuable to target some, but few, noncriminogenic characteristics if
treatment is to be effective. For example, both low self-esteem (Baumeister, 1993)
The Paraphilias 687
and shame (Tangney & Dearing, 2002) have been shown to block attempts at
any type of change. Since sexual offenders characteristically display low self-esteem
(W. L. Marshall, Anderson, & Champagne, 1997) and marked shame (Sparks, Bailey,
Marshall, & Marshall, 2003), it would appear necessary to overcome these obstacles
in order to engage these men in treatment. Nevertheless, treatment providers should
not take this caveat by Andrews and Bonta as license to address whatever they like in
treatment. The effect size of addressing criminogenic features increases proportional
to the number of these features that are targeted, while the effect size is diminished
proportional to the number of noncriminogenic features that are addressed (Gendreau,
French, & Gionet, 2004). Overall, the needs principle generated an effect size of 0.19.
Of the three principles identified by Andrews and Bonta (2006), it is the proper
application of the responsivity principle that appears to account for the greatest benefits.
They report that it produced a significant effect size (ES = 0.23) which approached
the overall effect size (ES = 0.28) of all three principles combined. As noted earlier,
Hanson et al.’s study specifically with sexual offenders replicated these effects. Clearly
the responsivity principle, if properly adhered to, is critical to obtaining beneficial
treatment effects.
This principle has both a general and a specific component. The latter states that
treatment providers should be responsive to the unique features of each client and
adjust their approach accordingly. Therapists should adopt different strategies, for
example, with offenders from different cultural backgrounds, and with those of dif-
fering intellectual levels and different world views, as well as with those having unique
personalities. In addition therapists should adapt to clients’ day-to-day fluctuations in
mood and motivation. The demands of specific responsivity are essentially the same as
the proper application of the notion of flexibility that has been shown to be important
in the delivery of treatment for various other Axis I and Axis II disorders (Duncan,
Miller, & Sparks, 2004).
It is, however, the general component of responsivity that exerts the most influence
on treatment outcome. While it has been somewhat mistakenly inferred that adopting
a cognitive behavioral approach will satisfy general responsivity, this is not necessarily
true. While it is true that meta-analyses of treatment for both sexual (Hanson et al.,
2002) and nonsexual offenders (Andrews, Zinger et al., 1990) have consistently
shown cognitive behavioral therapy (CBT) to be the most effective approach, these
data have not demonstrated that all CBT programs are effective nor have they shown
that non-CBT programs are all ineffective. What appears to be essential for programs
to meet the general responsivity principle is that they follow what Andrews and Bonta
(2006) describe as the “core correctional practices” (CCPs). Briefly, these practices
require the selection and training of therapists to be based on those characteristics
(e.g., empathy, warmth, support, respect) and skills (e.g., being rewarding, modeling
prosocial attitudes and behaviors) that have been shown in the general clinical
literature to facilitate beneficial changes (Norcross, 2002).
These CCP features are consistent with a growing body of independent research
on the effective elements of treatment delivery with sexual offenders. For example,
Drapeau (2005) reported that sexual offenders judged therapists to be crucial to
the benefits they derived from treatment but only when the therapists were warm,
empathic, respectful, supportive, and nonjudgmental. Consistent with these observa-

tions by clients, it has been shown that it is only when therapists actually display a warm
and empathic style, accompanied by being rewarding and somewhat directive, that
they produce the desired changes in treatment with sexual offenders (W. L. Marshall,
Serran, Moulden, et al., 2002; W. L. Marshall, Serran, Fernandez, et al., 2003).
Indeed, these four features of therapists accounted for between 30% and 60% of the
variance in the benefits derived from treatment across a range of targets. Finally, Beech
and his colleagues (Beech & Fordham, 1997; Beech & Hamilton-Giachritsis, 2005)
showed that only when therapists created a group climate that was characterized by
cohesiveness and expressiveness was treatment for sexual offenders effective.
Thus, to summarize the findings on Andrews and Bonta’s principles, the responsivity
principle clearly demonstrates that it is the way in which treatment is delivered that
is critical, while the needs principle shows it is essential to address all the potentially
changeable features of offenders that are known to predict reoffending. In fact,
the combination of the effective application of these two principles explains almost
all the variance in the demonstrated reductions in reoffending (Andrews & Bonta,
2006; Hanson et al., 2009). In the general clinical literature the employment of
appropriate procedures to modify treatment targets accounts for some 15% of the
evident beneficial changes (Norcross, 2002). If this latter finding holds true for sexual
offender treatment, then the addition of these effects to those evident in the proper
application of the needs and responsivity principles leaves little or nothing left to
explain in terms of treatment benefits.
Motivational Interviewing
In their initial book describing their motivational interviewing (MI) approach with
people with addictive problems, Miller and Rollnick (1991) specified a number
of techniques. Subsequently, they observed that in many of the later applications,
therapists had employed these techniques without understanding the “spirit” of
MI. As a result, in the second edition of their book (Miller & Rollnick, 2002)
they emphasized the various aspects of this spirit which they identified as requiring
collaboration between the therapist and client, evocation of insight by the client,
and autonomy which requires the client to be responsible for change. They also
described four guiding principles involving (a) empathy for the client’s perspective, (b)
generating a discrepancy in the client between his present behavior and his expressed
goals in treatment, (c) rolling with the client’s resistance, and (d) supporting the
client’s emerging self-efficacy.
The target of MI involves building the client’s motivation to engage fully with
the processes of treatment. This is particularly relevant with sexual offenders who
are typically ambivalent about treatment which they often see in advance as likely to
involve no more than attacking them about their history of offending. Mann and
Webster (2002) showed that this view is common among those sexual offenders who
refuse an offer of treatment and we have observed that it is characteristic of these men
in the initial stages of treatment.
The Paraphilias 689
The Good Lives Model

Ward (2002) adapted various empirically demonstrated aspects of human striving from
the general literature (e.g., Austin & Vancouver, 1996; Emmons, 1996; Schmuck
& Sheldon, 2001) that emerged after the publication of Abraham Maslow’s (1968)
original notion that all people, whether they are aware of it or not, work toward the
self-actualization of their potentials. From this literature, Ward derived nine domains
of functioning within which people strive to succeed: (a) optimal mental, physical, and
sexual health, (b) knowledge of one or another field of endeavor, (c) mastery in work
and leisure activities, (d) autonomy, (e) inner peace, (f) creativity, (g) relatedness,
(h) spirituality, and (i) happiness. Like Maslow, Ward saw this striving toward self-
attainment as a lifelong process. This point is quite important as it is undesirable for
clients to think that once they have completed a treatment program further efforts on
their part are unnecessary. The good lives model (GLM) insists that treatment simply
initiates a process that clients must continue to develop throughout their lives if they
are to attain a good life.
Ward and Gannon (2006) have demonstrated the potential application of the
GLM to the treatment of sexual offenders. Ward, Collie, and Bourke (2009) have
shown that the GLM does not stand in contradiction to the risk/needs/responsivity
principles. Indeed, they have suggested that building the strengths necessary to meet
the goals of the GLM will necessarily reciprocally eliminate the deficits identified as
criminogenic factors for sexual offenders.
Principles of Positive Psychology

Seligman (1999) suggested that clinical efforts to assist people with psychological
disorders had, since the Second World War, focused almost exclusively on clients’
deficits. He pointed to a need to refocus these efforts by additionally eliciting clients’
strengths and utilizing these strengths as a basis for developing resilience which would
serve as a protective factor for their future. As Peterson (2006) pointed out, this
shift away from a deficit-oriented approach does not ignore the problems clients
present with. The appropriate application of a positive psychology would attend to
problems by helping clients identifying current strengths and by developing additional
strengths necessary to overcome current deficits. Consistent with this view, Ryff and
Singer (1996) noted that the absence of well-being creates vulnerability and it is this
vulnerability that leads to problems. Thus, building resilience by focusing on clients’
strengths should generate better outcomes than simply eliminating deficits. After
examining this literature, W. L. Marshall et al. (2011) concluded, “it is not so much
vulnerabilities that need to be attended to in interventions (with sexual offenders) but
rather factors that provide resilience” (p. 19).
In this sense the GLM can be seen as one specific form of the positive psychology
movement. There are, however, other approaches that can be utilized valuably, such
as Snyder’s (2000) hope theory. The installation of hope in clients is, as Snyder has
shown, significantly related to treatment benefits. Hope as expressed by the therapist
is also critical and can be assumed to facilitate the client’s development of self-efficacy
(Bandura, 1977). Moulden and Marshall (2005) outlined the role hope can play in
the treatment of sexual offenders, and L. E. Marshall, Marshall, Fernandez, Malcolm,

and Moulden (2008) later demonstrated that hope generated during treatment was
related to more effective involvement in treatment and to subsequent reductions in
reoffending.
A Positive, Strength-Based Program
W. L. Marshall et al. (2011) developed a sexual offender treatment program embody-

ing the above four sources. Table 29.1 provides an outline of this program. As can
be seen from this table the program unfolds in three phases. The first phase is entirely
aimed at engaging the clients. Clients are initially told that treatment will not be
exclusively focused on past offending but rather will be aimed at developing the
clients’ strengths across the domains identified in the GLM so that they can have a
more satisfying and happier life. In this initial phase procedures are implemented to
Table 29.1 Phases of Treatment
Phase 1: Aim is treatment Phase 2: Aim is to enhance Phase 3: Integrate learning

engagement strengths that are into future
deficient in self-management
criminogenic
targets
(a) Identify the goal of (a) Challenge antisocial and (a) Develop good lives model
treatment offense-supportive plans
attitudes/beliefs and
reinforce and model
prosocial attitudes/beliefs
(b) Address issues of (b) Enhance self-regulatory (b) Generate limited relapse
confidentiality strengths including prevention plans
behavioral and emotional
self-regulation
(c) Request an (c) Build relationship (c) Elicit list of supports
autobiography (intimacy and attachment)
skills
(d) Elicit immediate (d) Develop sexual health (d) Define release/discharge
precipitants to offense - expand sexual plans
knowledge
(e) Initiate procedures to - enhance skills to attain
enhance self-esteem/ sexual satisfaction
reduce shame - reduce sexual
(f) Begin building coping preoccupation
and mood management - modify sexual interests
skills
(g) Expand empathic skills
Note. Adapted from W. L. Marshall, Marshall, Serran, and O’Brien (2011).

The Paraphilias 691
enhance clients’ self-esteem and reduce their feelings of shame. Clients are also trained
in effective empathy, coping strategies, and mood management, and the therapist
elicits a history of their successes and the problems they have encountered in the
past.
In the second phase offenders are assisted in developing the behavioral skills, as
well as the cognitions and attitudes, necessary to overcome the deficits they display
on all the criminogenic factors. Since antisocial attitudes and beliefs, as well as
offense-supportive ideas, only occur within the context of the discussion of various
topics (e.g., when addressing offense-related issues, when targeting relationship issues,
when discussing incidents of antisocial behaviors), these problematic cognitions are
challenged throughout treatment whenever they occur. Alternative prosocial views
are elicited from other participants and suggestions are made by the therapist who
models prosocial attitudes and behaviors. When antisocial or otherwise unhelpful
remarks are made by clients seeking attention, then as far as possible these are simply
ignored; lack of attention typically reduces the frequency of such remarks.
The evidence from the general literature suggests that behavioral self-regulation is
largely a product of emotional self-regulation (Carver, 2004). Clients are therefore
encouraged to be as naturally emotionally expressive as possible. This facilitates
discussions leading to an enhancement of the clients’ abilities to recognize their
own emotions and those of others, which is the first step in developing regulated
expressions. Emotional disruptions resulting from a distressing experience typically
cause people to make poor choices and this is frequently apparent in sexual offenders.
Training in coping skills, particularly problem solving, is effective in helping clients
both to modulate their moods and to make decisions that are in their best interests
and that best serve the interests of others.
Relationship difficulties appear frequently to disrupt behavioral and sexual reg-
ulation in sexual offenders and so comprehensive training is offered that aims at
identifying and enhancing the skills and attitudes necessary to achieve effective inti-
macy. It is within the context of an effective intimate relationship that a significant
range of human needs are met. It seems that sexual offenders seek these same needs
but pursue them in inappropriate ways.
A brief version of sex education is provided that outlines the ways well-functioning
people achieve sexual satisfaction. In this context an attempt is made to reduce
prudishness which is common in sexual offenders (L. E. Marshall, O’Brien, Woods, &
Nunes, 2011) and which seems to block their attempt at satisfactory sexual intimacy.
Sexual preoccupation is one of the strongest predictors of reoffending among sexual
offenders (L. E. Marshall & O’Brien, 2009) and is, therefore, a significant target in
treatment. Finally in Phase 2, procedures are implemented to change inappropriate
sexual interests when these are apparent (W. L. Marshall, O’Brien, & Marshall, 2009).
In the final phase, clients are helped to integrate what they have learned into
effective release plans. These release plans include continuing to work on the issues
involved in each of the GLM domains, as well as identifying people who can serve as
supports to encourage further development. Clients are also encouraged to generate a
limited set of individualized potential risks that they should attempt to avoid. Finally
they are required to identify strategies to obtain jobs and accommodations, and to
develop enjoyable leisure activities.
Recently two research assistants, who were naive regarding the sexual offender
literature and who had no expectations about rates of reoffending, conducted inde-
pendent appraisals of this program. The first research assistant conducted an appraisal
at a point where the average time at risk of 535 treated offenders was 5.4 years, while
the second did so after 8.4 years at risk. The data generated by the second research
assistant also provided a check on the reliability of the initial data extraction from
official records; there was an exact match. The official records included the Royal
Canadian Mounted Police national data base of all charges and convictions, as well
as the Correctional Service of Canada’s Offender Management System which records
all parole suspensions and revocations. The combined information from these two
sources represented the data on reoffending.
There are actually at least three indices of the potential value of a treatment
program: the percentage of the available offenders who accept the offer of treatment;
the percentage of those who enter and also complete treatment; and the rate of
relapses among those who complete treatment.
High rates of refusal to enter treatment are common among sexual offenders (Lee,
Proeve, Lancaster, & Jackson, 1996; Mann & Webster, 2002) with these rates ranging
from 25% to 86%. Several studies (Browne, Foreman, & Middleton, 1998; Lee et al.,
1996; McGrath, Cumming, Livingston, & Hoke, 2003) have reported high dropout
rates among sexual offenders who entered treatment. This is problematic as dropouts
have higher reoffense rates than those who refuse to enter treatment.
The offer of treatment is made by W. L. Marshall et al. (2011) to all sexual offenders
within the prison system where all but 3.8% accept and enter the program. Of those
who enter treatment, 95.8% complete the program. Thus, this program is successful
on the first two indices of the value of treatment, which seems likely to be due to the
motivational aspects of the approach and the focus on building a better life.
Most importantly, however, long-term outcome evaluations reveal significant reduc-
tions in recidivism. Table 29.2 outlines the outcome data associated with this program.
Unfortunately since almost all offenders are recruited into and remain in treatment,
Table 29.2 Outcome Data
1. Prison-based program (N = 535) Treated (FU = 8.4 years) Expected*

Sexual reoffense 5.6% 23.8%
Violent reoffense 8.4% 34.8%
Nonsexual/nonviolent reoffense 13.6% 40.0%
2. Community-based program Treated (FU = 10 years) Untreated (FU = 10 years)
Reoffense rates for:
Nonfamilial child molesters 5.2% 17.2%
Incest offenders 3.2% 8.7%
Exhibitionists: Group 1 7.6% 18.4%
Group 2 12.6% -----
Notes. * Expected rates are based on pretreatment evaluations using the following actuarial risk assessment
instruments: sexual offenses, STATIC-99 (Hanson & Thornton, 1999); violent offenses, VRAG (Harris,
Rice, & Quinsey, 1993); nonsexual/nonviolent, LSI-R (Andrews & Bonta, 1995). FU = follow-up.
Adapted from W. L. Marshall, Marshall, Serran, and O’Brien (2011).
The Paraphilias 693
there are no available untreated comparison groups. As a result the outcome for the
treated offenders is compared with what would be expected on the basis of the average
of the clients’ overall pretreatment risk assessments. As can be seen in Table 29.2 at
the 8.4-year follow-up assessment, the program has been very effective.
A similar evaluation was conducted on a community-based program that operated
on similar, although less comprehensive, principles to those outlined above (W. L.
Marshall & Barbaree, 1988). In this case, matched untreated samples were available
for each of three types of sexual offender. As can be seen from Table 29.2, treatment
significantly reduced reoffense rates.
Conclusions
In terms of the treatment of sexual offenders there appears to be a movement away

from the traditionally, negatively focused programs such as relapse prevention toward
a more strength-based orientation. However, these developments have not yet been
initiated widely nor have they been extended to the nonoffending paraphilias. For
the nonoffending paraphilics treatment efforts have for the most part been limited to
conditioning-based interventions with little or no recent developments. As has been
shown, at least one recent strength-based program for sexual offenders appears to
have been very effective and we can see no reason why this same approach, involving
similar targets, should not be applied to all the paraphilias.
References
Abel, G. G., Blanchard, E. B., & Becker, J. V. (1978). An integrated treatment program for
rapists. In R. Rada (Ed.), Clinical aspects of the rapist (pp. 161–214). New York, NY:
Grune & Stratton.
Abel, G. G., & Rouleau, J. L. (1990). The nature and extent of sexual assault. In W. L.
Marshall, D. R. Laws, & H. E. Barbaree (Eds.), Handbook of sexual assault: Issues, theories
and treatment of the offender (pp. 9–21). New York, NY: Plenum Press.
Adshead, G. (1997). Transvestic fetishism: Assessment and treatment. In D. R. Laws &
W. T. O’Donohue (Eds.), Sexual deviance: Theory, assessment and treatment
(4th ed., text revision). Washington, DC: Author.
Andrews, D. A., & Bonta, J. (1995). LSI-R: The Level of Supervision Inventory. Toronto,
Canada: Multi-Health Systems.
Andrews, D. A., & Bonta, J. (2006). The psychology of criminal conduct (4th ed.). New
Providence, NJ: LexisNexis.
Andrews, D. A., Bonta, J., & Hoge, R. D. (1990). Classification for effective rehabilitation:
Rediscovering psychology. Criminal Justice and Behavior, 17 , 19–52.
Andrews, D. A., Zinger, I., Hoge, R. D., Bonta, J., Gendreau, P., & Cullen, F. T. (1990).
Does correctional treatment work? A clinically relevant and psychologically informed
meta-analysis. Criminology, 28, 369–404.
Aos, S., Miller, M., & Drake, E. (2006). Evidence-based adult corrections programs: What works
and what does not. Olympia, WA: Washington State Institute for Public Policy.
Arndt, W. B., Foehl, J. C., & Good, F. E. (1985). Specific sexual fantasy themes: A multidi-
mensional study. Journal of Personality and Social Psychology, 48, 472–480.
Austin, J. T., & Vancouver, J. B. (1996). Goal constructs in psychology: Structure, process,
and content. Psychological Bulletin, 120, 338–375.
Bandura, A. (1977). Self-efficacy: Toward a unifying theory of behavior change. Psychological
Review, 84, 191–215.
Baumeister, R. F. (Ed.). (1993). Self-esteem: The puzzle of low self-regard. New York, NY:
Plenum Press.
Beech, A. R., & Fordham, A. S. (1997). Therapeutic climate of sexual offender treatment
programs. Sexual Abuse: A Journal of Research and Treatment, 9, 219–237.
Beech, A. R., & Hamilton-Giachritsis, C. E. (2005). Relationship between therapeutic climate
and treatment outcome in group-based sexual offender treatment programs. Sexual Abuse:
A Journal of Research and Treatment, 17 , 127–140.
Beier, K. M., Neutze, J., Mundt, J. A., Ahlers, C. J., Goecker, D., Konrad, A., & Schaefer,
G. A. (2009). Encouraging self-identified pedophiles and hebephiles to seek professional
help: First results of the Prevention Project Dunkelfeld (PPD). Child Abuse & Neglect,
33, 545–549.
Blanchard, R., Racansky, I. G., & Steiner, B. W. (1986). Phallometric detection of fetishistic
arousal in heterosexual male cross-dressers. Journal of Sex Research, 22, 452–462.
Brière, J., & Runtz, M. (1989). University males’ sexual interest in children: Predicting
potential indices of “pedophilia” in a non-forensic sample. Child Abuse and Neglect, 13,
65–75.
Browne, K. D., Foreman, L., & Middleton, D. (1998). Predicting treatment dropout in sex
offenders. Child Abuse Review, 7 , 402–419.
Carich, M. S., Dobkowski, G., & Delehanty, N. (2009). No, the spirit of RP is important: A
response to Yates & Ward (2009) on abandoning RP. ATSA Forum, 21, 1–8.
Carver, C. S. (2004). Self-regulation of action and effect. In R. F. Baumeister & K. D. Vohs
(Eds.), Handbook of self-regulation: Research, theory, and applications (pp. 13–39). New
Chalkley, A. J., & Powell, G. E. (1983). The clinical description of forty-eight cases of sexual
fetishism. British Journal of Psychiatry, 142, 292–295.
Cox, D. J., & Daitzman, R. J. (Eds.). (1980). Exhibitionism: Description, assessment, and
treatment. New York, NY: Garland STPM Press.
Cox, D. J., & MacMahon, B. (1978). Incidence of male exhibitionism in the United States as
reported by victimized female college students. National Journal of Law and Psychiatry,
1, 453–457.
Craig, L. A., & Beech, A. R. (2009). Psychometric assessment of sexual deviance. In A. R.
Beech, L. A. Craig, & K. D. Browne (Eds.), Assessment and treatment of sex offenders: A
handbook (pp. 89–107). Chichester, England: John Wiley & Sons, Ltd.
Craig, L. A., Browne, K. D., & Beech, A. R. (2008). Assessing risk in sex offenders: A
practitioner’s guide. Chichester, England: John Wiley & Sons, Ltd.
Croughan, J. L., Saghir, M., Cohen, R., & Tobins, E. (1981). A comparison of treated and
untreated male cross-dressers. Archives of Sexual Behavior, 10, 515–528.
Darcangelo, S., Hollings, A., & Paladino, G. (2008). Fetishism: Assessment and treatment.
In D. R. Laws & W. T. O’Donohue (Eds.), Sexual deviance: Theory, assessment, and
treatment (pp. 119–130). New York, NY: Guilford Press.
Docter, R. F., & Prince, V. (1997). Transvestism: A survey of 1032 cross-dressers. Archives of
Sexual Behavior, 26, 589–605.
The Paraphilias 695
Doren, D. M. (2002). Evaluating sex offenders: A manual for civil commitments and beyond.
Thousand Oaks, CA: Sage.
Doren, D. M. (2006). Recidivism risk assessments: Making sense of controversies. In W. L.
Marshall, Y. M. Fernandez, L. E. Marshall, & G. A. Serran (Eds.), Sexual offender
treatment: Controversial issues (pp. 3–15). Chichester, England: John Wiley & Sons, Ltd.
Drapeau, M. (2005). Research on the processes involved in treating sexual offenders. Sexual
Abuse: A Journal of Research and Treatment, 17 , 117–125.
Duncan, B. L., Miller, S. D., & Sparks, J. A. (2004). The heroic client: A revolutionary way to
improve effectiveness. San Francisco, CA: Jossey-Bass.
Emmons, R. A. (1996). Striving and feeling: Personal goals and subjective well-being. In P. M.
Gollwitzer & J. A. Bargh (Eds.), The psychology of action: Linking cognition and motivation
to behavior (pp. 313–337). New York, NY: Guilford Press.
Fisher, B. S., Cullen, F. T., & Turner, M. G. (2000). The sexual victimization of college women.
Washington, DC: U.S. Department of Justice, National Institute of Justice.
Freund, K. (1967). Erotic preference in pedophilia. Behaviour Research and Therapy, 5,
339–348.
Freund, K., & Watson, R. J. (1991). Assessment of the sensitivity and specificity of a phallo-
metric test: An update of phallometric diagnosis of pedophilia. Psychological Assessment: A
Gendreau, P., French, S., & Gionet, A. (2004). What works (what doesn’t work): The principles
of effective correctional treatment. Journal of Community Corrections, 13, 4–6.
Gittleson, M. L., Eacott, S. E., & Mehta, B. J. (1978). Victims of indecent exposure. British
Gosselin, C., & Eysenck, S. (1980). The transvestite double image: A preliminary report.
Personality and Individual Differences, 1, 172–173.
Gosselin, C., & Wilson, G. (1980). Sexual variations. London, England: Faber & Faber.
Grubin, D. (1994). Editorial: Sexual sadism. Criminal Behavior and Mental Health, 4, 3–9.
Grubin, D. (2008). Medical models and interventions in sexual deviance. In D. R. Laws &
W. T. O’Donohue (Eds.), Sexual deviance: Theory, assessment and treatment (2nd ed.,
Hanson, R. K. (2006). Stability and change: Dynamic risk factors for sexual offenders. In
W. L. Marshall, Y. M. Fernandez, L. E. Marshall, & G. A. Serran (Eds.), Sexual offender
treatment: Controversial issues (pp. 17–31). Chichester, England: John Wiley & Sons,
Ltd.
Hanson, R. K., Bourgon, G., Helmus, L., & Hodgson, S. (2009). The principles of effective
correctional treatment also apply to sexual offenders: A meta-analysis. Criminal Justice
and Behavior, 36, 865–891.
Hanson, R. K., Gordon, A., Harris, A. J. R., Marques, J. K., Murphy, W. D., Quinsey, V. L.,
& Seto, M. C. (2002). First report of the Collaborative Outcome Data Project on the
Effectiveness of Psychological Treatment of Sex Offenders. Sexual Abuse: A Journal of
Research and Treatment, 14, 169–194.
Hanson, R. K., & Harris, A. J. R. (1997). Voyeurism: Assessment and treatment. In D. R.
Laws & W. T. O’Donohue (Eds.), Sexual deviance: Theory, assessment and treatment (pp.
Hanson, R. K., & Harris, A. J. R. (2000). Where should we intervene? Dynamic predictors of
sex offender recidivism. Criminal Justice and Behavior, 27 , 6–35.
Hanson, R. K., & Thornton, D. (1999). Static 99: Improving actuarial risk assessments for sex
offenders. User Report 99-02. Ottawa: Department of the Solicitor General of Canada.
Hanson, R. K., & Thornton, D. (2000). Improving risk assessments for sex offenders: A
comparison of three actuarial scales. Law and Human Behavior, 24, 119–136.
Harris, G. T., Rice, M. E., & Quinsey, V. L. (1993). Violent recidivism of mentally disordered
offenders: The development of a statistical prediction instrument. Criminal Justice and
Behavior, 20, 315–335.
Hucker, S. J. (2011). An internet study of hypoxyphilia. Archives of Sexual Behavior, 40,
1323–1326.
Hucker, S. J., & Blanchard, R. (1992). Death scene characteristics in 118 fatal cases of
autoerotic asphyxia compared with suicidal asphyxia. Behavioral Sciences and the Law, 10,
509–523.
Junginger, J. (1997). Fetishism: Assessment and treatment. In D. R. Laws & W. T. O’Donohue
(Eds.), Sexual deviance: Theory, assessment and treatment (pp. 92–110). New York, NY:
Guilford Press.
Kaplan, M. S., & Krueger, R. B. (1997). Voyeurism: Psychopathy and theory. In D. R. Laws
& W. T. O’Donohue (Eds.), Sexual deviance: Theory, assessment and treatment (pp.
King, D. (1993). The transvestite and the transsexual: Public categories and private identities.
Aldershot, England: Avebury.
Kingston, D. A., Firestone, P., Moulden, H. A., & Bradford, J. M. (2007). The utility of
the diagnosis of pedophilia: A comparison of various classification procedures. Archives of
Sexual Behavior, 36, 423–436.
Kinsey, A. C., Pomeroy, W. G., & Martin, C. E. (1948). Sexual behavior in the human male.
Philadelphia, PA: Saunders.
Krueger, R. B., & Kaplan, M. S. (1997). Frotteurism: Assessment and treatment. In D. R.
Laws & W. T. O’Donohue (Eds.), Sexual deviance: Theory, assessment and treatment (pp.
Långström, N., & Seto, M. C. (2006). Exhibitionistic and voyeuristic behavior in a Swedish
national population survey. Archives of Sexual Behavior, 35, 427–435.
Laws, D. R., & Marshall, W. L. (2003). A brief history of behavioral and cognitive behavioral
approaches to sexual offenders: Part 1. Early developments. Sexual Abuse: A Journal of
Research and Treatment, 15, 75–92.
Laws, D. R., & O’Donohue, W. (Eds.). (1997). Sexual deviance: Theory, assessment, and
treatment. New York, NY: Guilford Press.
Laws, D. R., & O’Donohue, W. (Eds.). (2008). Sexual deviance: Theory, assessment, and
treatment (2nd ed.). New York, NY: Guilford Press.
Lee, J. K. P., Proeve, M. J., Lancaster, M., & Jackson, H. J. (1996). An evaluation and 1-year
follow-up study of a community-based treatment program for sex offenders. Australian
Levenson, J. S. (2004). Reliability of sexually violent predator civil commitment criteria in
Florida. Law and Human Behavior, 28, 357–368.
Linley, P. A., & Joseph, S. (2004). Applied positive psychology: A new perspective for
professional practice. In P. W. Linley & S. Joseph (Eds.), Positive psychology in practice
Looman, J., Abracen, J., & Nicholaichuk, T. P. (2000). Recidivism among treated sexual
offenders and matched controls: Data from the Regional Treatment Centre (Ontario).
Journal of Interpersonal Violence, 15, 279–290.
Lösel, F. (1995). The efficacy of correctional treatment: A review and synthesis of meta-
evaluations. In J. McGuire (Ed.), What works: Reducing reoffending (pp. 79–111).
Lösel, F., & Schmucker, M. (2005). The effectiveness of treatment for sexual offenders: A
comprehensive meta-analysis. Journal of Experimental Criminology, 1, 1–29.
Maletzky, B. M. (1991). Treating the sexual offenders. Newbury Park, CA: Sage.
The Paraphilias 697
Mann, R. E., Ainsworth, F., Al-Attar, Z., & Davies, M. (2008). Voyeurism: Assessment and
treatment. In D. R. Laws & W. T. O’Donohue (Eds.), Sexual deviance: Theory, assessment,
and treatment (pp. 320–335). New York, NY: Guilford Press.
Mann, R. E., Hanson, R. K., & Thornton, D. (2010). Assessing risk for sexual recidivism?
Some proposals on the nature of psychologically meaningful risk factors. Sexual Abuse: A
Journal of Research and Treatment, 22, 191–217.
Mann, R. E., & Marshall, W. L. (2009). Advances in the treatment of adult incarcerated sex
offenders. In A. R. Beech, L. A. Craig, & K. D. Browne (Eds.), Assessment and treatment
of sexual offenders: A handbook (pp. 329–347). Chichester, England: John Wiley & Sons,
Ltd.
Mann, R. E., & Webster, S. (2002, October). Understanding resistance and denial. Paper
presented at the 21st Annual Research and Treatment Conference of the Association for
the Treatment of Sexual Abusers, Montreal, Canada.
Marks, I. M., & Gelder, M. G. (1967). Transvestism and fetishism: Clinical and psychological
changes during faradic aversion. British Journal of Psychiatry, 113, 711–729.
Marlatt, G. A. (1982). Relapse prevention: A self-control program for the treatment of addictive
behaviors. In R. B. Stuart (Ed.), Adherence, compliance and generalization in behavioral
medicine (pp. 329–378). New York, NY: Brunner/Mazel.
Marques, J. K. (1982, March). Relapse prevention: A self-control model for the treatment of
sex offenders. Paper presented at the 7th Annual Forensic Mental Health Conference,
Asilomar, CA.
Marques, J. K., Weideranders, M., Day, D. M., Nelson, C., & van Ommeren, A. (2005). Effects
of a relapse prevention program on sexual recidivism: Final results from California’s Sex
Offender Treatment and Evaluation Project (SOTEP). Sexual Abuse: A Journal of Research
and Treatment, 17 , 79–107.
Marshall, L. E., Marshall, W. L., Fernandez, Y. M., Malcolm, P. B., & Moulden, H. M. (2008).
The Rockwood Preparatory Program for sexual offenders: Description and preliminary
appraisal. Sexual Abuse: A Journal of Research and Treatment, 20, 25–42.
Marshall, L. E., Marshall, W. L., Moulden, H. M., & Serran, G. A. (2008). The prevalence of
sexual addiction in incarcerated sexual offenders and matched community nonoffenders.
Sexual Addiction & Compulsivity: The Journal of Treatment and Prevention, 15, 271–283.
Marshall, L. E., & O’Brien, M. D. (2009). Assessment of sexual addiction. In A. R. Beech,
L. A. Craig, & K. D. Browne (Eds.), Assessment and treatment of sex offenders: A handbook
(pp. 163–177). Chichester, England: John Wiley & Sons, Ltd.
Marshall, L. E., O’Brien, M. D., Woods, M. E., & Nunes, K. (2011, November). Sexual
attitudes in sexual offenders and two comparison groups. Paper presented at the 30th
Annual Research and Treatment Conference of the Association for the Treatment of
Sexual Abusers, Toronto, Canada.
Marshall, W. L. (1971). A combined treatment method for certain sexual deviations. Behaviour
Marshall, W. L. (1974). Case report: A combined treatment approach to the reduction
of multiple fetish-related behaviors. Journal of Consulting and Clinical Psychology, 42,
613–616.
Marshall, W. L. (2006). Ammonia aversion with an exhibitionist: A case study. Clinical Case
Studies, 5, 15–24.
Marshall, W. L. (2007). Diagnostic issues, multiple paraphilias, and comorbid disorders in
sexual offenders: Their incidence and treatment. Aggression and Violent Behavior, 12,
16–35.
Marshall, W. L. (2008). Czy pedofilia jest uleczalna? Wyniki badan pólnocnoamerykańskich

[Are pedophiles treatable? Evidence from North American studies]. Seksuologia Polska, 6,
1–6.
Marshall, W. L., & Anderson, D. (2000). Do relapse prevention components enhance treat-
ment effectiveness? In D. R. Laws, S. M. Hudson, & T. Ward (Eds.), Remaking
relapse prevention with sex offenders: A sourcebook (pp. 39–55). Newbury Park, CA: Sage
Publications.
Marshall, W. L., Anderson, D., & Champagne, F. (1997). Self-esteem and its relationship to
sexual offending. Psychology, Crime & Law, 3, 161–186.
Marshall, W. L., & Barbaree, H. E. (1988). The long-term evaluation of a behavioral treatment
program for child molesters. Behaviour Research and Therapy, 26, 499–511.
Marshall, W. L., Barbaree, H. E., & Eccles, A. (1991). Early onset and deviant sexuality in
child molesters. Journal of Interpersonal Violence, 6, 323–336.
Marshall, W. L., Eccles, A., & Barbaree, H. E. (1991). Treatment of exhibitionists: A focus
on sexual deviance versus cognitive and relationship features. Behaviour Research and
Therapy, 29, 129–135.
Marshall, W. L., & Fernandez, Y. M. (2003). Phallometric testing with sexual offenders: Theory,
research, and practice. Brandon, VT: Safer Society Press.
Marshall, W. L., & Hucker, S. J. (2006). Issues in the diagnosis of sexual sadism. Sexual
Offender Treatment, 1. http://www.iatso.org/ejournal/
Marshall, W. L., & Kennedy, P. (2003). Sexual sadism in sexual offenders: An elusive diagnosis.
Aggression and Violent Behavior, 8, 1–22.
Marshall, W. L., Kennedy, P., & Yates, P. M. (2002). Issues concerning the reliability and
validity of the diagnosis of sexual sadism applied in prison settings. Sexual Abuse: A
Marshall, W. L., Kennedy, P., Yates, P. M., & Serran, G. A. (2002). Diagnosing sexual sadism
in sexual offenders: Reliability across diagnosticians. International Journal of Offender
Therapy and Comparative Criminology, 46, 668–676.
Marshall, W. L., & Laws, D. R. (2003). A brief history of behavioral and cognitive behavioral
approaches to sexual offender treatment: Part 2. The modern era. Sexual Abuse: A Journal
of Research and Treatment, 15, 93–120.
Marshall, W. L., & Lippens, K. (1977). The clinical value of boredom: A procedure for reducing
inappropriate sexual interests. Journal of Nervous and Mental Diseases, 165, 283–287.
Marshall, W. L., Marshall, L. E., Serran, G., & O’Brien, M. D. (2011). Rehabilitating
sexual offenders: A strength-based approach. Washington, DC: American Psychological
Association.
Marshall, W. L., O’Brien, M. D., & Marshall, L. E. (2009). Modifying sexual preferences.
In A. R. Beech, L. A. Craig, & K. D. Browne (Eds.), Assessment and treatment of sex
offenders: A handbook (pp. 311–327). Chichester, England: John Wiley & Sons, Ltd.
Marshall, W. L., Payne, K., Barbaree, H. E., & Eccles, A. (1991). Exhibitionists: Sexual
preferences for exposing. Behaviour Research and Therapy, 29, 37–40.
Marshall, W. L., Serran, G. A., Fernandez, Y. M., Mulloy, R., Mann, R. E., &
Thornton, D. (2003). Therapist characteristics in the treatment of sexual offenders:
Tentative data on their relationship with indices of behaviour change. Journal of Sexual
Aggression, 8, 25–30.
Marshall, W. L., Serran, G. A., Moulden, H., Mulloy, R., Fernandez, Y. M., Mann, R. E.,
& Thornton, D. (2002). Therapist features in sexual offender treatment: Their reliable
identification and influence on behaviour change. Clinical Psychology and Psychotherapy,
9, 395–405.
The Paraphilias 699
Maslow, A. H. (1968). Toward a psychology of being (2nd ed.). New York, NY: Van Nostrand
Reinhold.
Mason, F. L. (1997). Fetishism: Psychopathology and theory. In D. R. Laws & W. T.
O’Donohue (Eds.), Sexual deviance: Theory, assessment and treatment (pp. 75–91). New
Masters, W., & Johnson, B. (1966). Human sexual response. Boston, MA: Little, Brown.
Matek, O. (1988). Obscene phone callers. Journal of Social Work and Human Sexuality, 7 ,
113–130.
McConaghy, M. (2005). Sexual dysfunctions and disorders. In J. E. Maddux & B. A. Winstead
(Eds.), Psychopathology: Foundations for a contemporary understanding (pp. 255–280).
McGrath, R. J., Cumming, G., Livingston, J. A., & Hoke, S. E. (2003). Outcome of
a treatment program for adult sex offenders: From prison to community. Journal of
Interpersonal Violence, 18, 3–17.
McGuire, R. J., Carlisle, J. M., & Young, B. G. (1965). Sexual deviation as conditioned
behaviour: A hypothesis. Behaviour Research and Therapy, 3, 185–190.
Miller, W. R., & Rollnick, S. (Eds.). (1991). Motivational interviewing: Preparing people to
change their addictive behavior. New York, NY: Guilford Press.
Miller, W. R., & Rollnick, S. (Eds.). (2002). Motivational interviewing: Preparing people for
change (2nd ed.). New York, NY: Guilford Press.
Milner, J. S., Dopke, C. A., & Crouch, J. L. (2008). Paraphilia not otherwise specified:
Psychopathology and theory. In D. R. Laws & W. T. O’Donohue (Eds.), Sexual deviance:
Theory, assessment and treatment (2nd ed., pp. 384–418). New York, NY: Guilford Press.
Mokros, A., Osterheider, M., Schilling, F., Eher, R., & Nitschke, J. (2012). The Severe
Sexual Sadism Scale: Cross-validation and scale properties. Psychological Assessment, 24,
764–769.
Morin, J. W., & Levenson, J. S. (2008). Exhibitionism: Assessment and treatment. In D. R.
Laws & W. T. O’Donohue (Eds.), Sexual deviance: Theory, assessment and treatment (2nd
Moulden, H. M., Firestone, P., Kingston, D. A., & Bradford, J. M. W. (2009). Recidivism in
pedophiles: An investigation using different methods of defining pedophilia. Journal of
Forensic Psychiatry and Psychology, 20, 680–701.
Moulden, H. M., & Marshall, W. L. (2005). Hope in the treatment of sexual offenders: The
potential application of hope theory. Psychology, Crime and Law, 11, 329–342.
Murphy, K. R., & Davidshofer, C. O. (1998). Psychological testing: Principles and applications
(4th ed.). Upper Saddle River, NJ: Prentice Hall.
Murphy, W. D. (1997). Exhibitionism: Psychopathology and theory. In D. R. Laws & W. T.
O’Donohue (Eds.), Sexual deviance: Theory, assessment and treatment (pp. 22–39). New
Murphy, W. D., & Barbaree, H. E. (1994). Assessments of sex offenders by measures of erectile
response: Psychometric properties and decision making. Brandon, VT: Safer Society Press.
Nelson-Gray, R. D. (1991). DSM-IV: Empirical guidelines from psychometrics. Journal of
Newring, K. A. B., Wheeler, J., & Draper, C. (2008). Transvestism: Assessment and treatment.
In D. R. Laws & W. T. O’Donohue (Eds.), Sexual deviance: Theory, assessment, and
treatment (pp. 285–304). New York, NY: Guilford Press.
Nicholaichuk, T., Gordon, A., Gu, D., & Wong, S. (2000). Outcome of an institutional sexual
offender treatment program: A comparison between treated and matched untreated
offenders. Sexual Abuse: A Journal of Research and Treatment, 12, 139–153.
Nitschke, J., Mokros, A., Osterheider, M., & Marshall, W. L. (2012). Sexual sadism: Diag-
nostics and treatment 125 years after the first description by Richard von Krafft-Ebing.
Journal of Offender Therapy and Comparative Criminology. Advance online publication.
doi:10.1177/0306624x12465923
Nitschke, J., Osterheider, M., & Mokros, A. (2009). A cumulative scale of severe sexual sadism.
Sexual Abuse: A Journal of Research and Treatment, 21, 262–278.
Norcross, J. C. (2002). Empirically supported therapy relationships. In J. C. Norcross (Ed.),
Psychotherapy relationships that work: Therapist contributions and responsiveness to patient
needs (pp. 1–10). New York, NY: Oxford University Press.
O’Donohue, W. T., Regev, L. G., & Hagstrom, A. (2000). Problems with the DSM-IV
diagnosis of pedophilia. Sexual Abuse: A Journal of Research and Treatment, 12, 95–105.
Peretti, P. O., & Rowan, M. (1983). Zoophilia: Factors related to its sustained practice.
Panminerva Medica, 25, 127–131.
Peterson, C. (2006). A primer in positive psychology. New York, NY: Free Press.
Pithers, W. D., Marques, J. K., Gibat, C. C., & Marlatt, G. A. (1983). Relapse prevention with
sexual aggressors: A self-control model of treatment and maintenance of change. In J. G.
Greer & I. R. Stuart (Eds.), The sexual aggressor: Current perspectives on treatment (pp.
214–239). New York, NY: Van Nostrand Reinhold.
Prince, V., & Bentler, P. M. (1972). Survey of 504 cases of transvestism. Psychological Reports,
31, 903–917.
Redondo, S., Garrido, V., & Sanchez-Meca, J. (1999). The influence of treatment programs
on the recidivism of juvenile and adult offenders: A European meta-analytic review.
Psychology, Crime, and Law, 5, 251–278.
Ryff, C. D., & Singer, B. H. (1996). Psychological well-being: Meaning, measurement, and
implications for psychotherapy research. Psychotherapy and Psychosomatics, 65, 14–23.
Schaefer, G. A., Mundt, I. A., Feelgood, S., Hupp, E., Neutze, J., Ahlers, C. J., … Beier, K. M.
(2010). Potential and Dunkelfeld offenders: Two neglected target groups for prevention
of child sexual abuse. International Journal of Law and Psychiatry, 33, 154–163.
Schmuck, P., & Sheldon, K. M. (Eds.). (2001). Life goals and well-being. Toronto, Canada:
Hogrefe & Huber.
Seligman, M. E. P. (1999). The president’s address. American Psychologist, 54, 559–562.
Seto, M. C. (2008). Pedophilia and sexual offending against children: Theory, assessment, and
intervention. Washington, DC: American Psychological Association.
Seto, M. C., Harris, G. T., Rice, M. E., & Barbaree, H. E. (2004). The screening scale
for pedophilic interests predicts recidivism among adult sex offenders with child victims.
Archives of Sexual Behavior, 33, 455–466.
Seto, M. C., & Lalumière, M. L. (2001). A brief screening scale to identify pedophilic interests
among child molesters. Sexual Abuse: A Journal of Research and Treatment, 13, 15–25.
Smith, T. P. (1994). Effects of the child’s relative age, appearance and attractiveness on
vulnerability to pedosexual interactions (Doctoral dissertation, University of Texas at
Austin, 1993). Dissertation Abstracts International, 54, 6472B. (UMI No. 9413603).
Snyder, C. R. (2000). The past and possible futures of hope. Journal of Social and Clinical
Snyder, C. R., & Lopez, S. J. (Eds.). (2005). Handbook of positive psychology. New York, NY:
Sparks, J., Bailey, W., Marshall, W. L., & Marshall, L. E. (2003, October). Shame and guilt in
sex offenders. Paper presented at the 22nd Annual Research and Treatment Conference of
the Association for the Treatment of Sexual Abusers, St Louis, MO.
Spengler, A. (1977). Manifest sadomasochism of males: Results of an empirical study. Archives
of Sexual Behavior, 6, 441–456.
The Paraphilias 701
Tangney, J. P., & Dearing, R. L. (2002). Shame and guilt. New York, NY: Guilford Press.
Ward, T. (2002). Good lives and the rehabilitation of offenders: Promises and problems.
Aggression and Violent Behavior, 7 , 513–528.
Ward, T., Collie, R. M., & Bourke, P. (2009). Models of offender rehabilitation: The
good lives model and the risk-need-responsivity model. In A. R. Beech, L. A. Craig, &
K. D. Browne (Eds.), Assessment and treatment of sex offenders (pp. 293–310). Chichester,
Ward, T., & Gannon, T. A. (2006). Rehabilitation, etiology, and self-regulation: The Good
Lives Model of sexual offender treatment. Aggression and Violent Behavior, 11, 77–94.
Ward, T., & Hudson, S. M. (1996). Relapse prevention: A critical analysis. Sexual Abuse: A
Ward, T., Hudson, S. M., & Siegert, R. J. (1995). A critical comment on Pithers’ relapse
prevention model. Sexual Abuse: A Journal of Research and Treatment, 7 , 167–175.
Weinberg, M. S., Williams, C. J., & Calhan, C. (1995). “If the shoe fits …”: Exploring male
homosexual foot fetishism. Journal of Sex Research, 32, 17–27.
Wise, T. N. (1985). Fetishism: Etiology and treatment, a review from multiple perspectives.
Yates, P. M., Hucker, S. J., & Kingston, D. A. (2008). Sexual sadism: Psychopathology and
theory. In D. R. Laws & W. T. O’Donohue (Eds.), Sexual deviance: Theory, assessment
and treatment (2nd ed., pp. 213–230). New York, NY: Guilford Press.
30
Couple Therapy
Melanie S. Fischer and Donald H. Baucom
University of North Carolina at Chapel Hill, United States
Kurt Hahlweg
Technische Universität Braunschweig, Germany
Norman B. Epstein
University of Maryland, United States
Background of Cognitive Behavioral Couple Therapy
The recognition of high divorce rates, the prevalence of relationship distress, and
the negative consequences of these problems for individual and family functioning
have led many researchers and clinicians to dedicate their efforts to the development
of effective couple therapies in recent years (Epstein & Baucom, 2002; Schindler,
Hahlweg, & Revenstorf, 2006; Snyder, Castellani, & Whisman, 2006; Whisman
& Baucom, 2012). In this chapter, we describe cognitive behavioral couple therapy
(CBCT) in a recent, enhanced form (Epstein & Baucom, 2002). CBCT is a contextual
approach that allows clinicians to address behaviors, cognitions, and emotions as they
relate to relationship functioning. At the same time, CBCT practitioners tailor the
treatment based on the unique needs of the couple under consideration, addressing
individual, dyadic, and environmental factors.
CBCT first emerged in the early 1980s but draws heavily from the traditions
of behavioral couple therapy (BCT), individual cognitive therapy (CT), and basic
cognitive and social psychology research on information processing. In early BCT,
basic learning principles and social exchange theories were applied to achieve a
more favorable ratio of positive versus negative behaviors between the partners (e.g.,
Stuart, 1969). Skills trainings and systematic functional analyses of behavioral patterns
of reinforcement and punishment were incorporated into the work with distressed
couples as well (e.g., Jacobson & Margolin, 1979; Liberman, 1970; Schindler et al.,
2006). However, the strictly behavioral approach was not without limitations. Most
importantly, it became clear that idiosyncratic interpretations of relationship events,

DOI: 10.1002/9781118528563.wbcbt30
causal attributions for one’s partner’s behavior, and longstanding cognitive schemas
have marked influence on the subjective emotional experience of each member
of the couple (Baucom & Epstein, 1990). Consequently, CBCT evolved through
the gradual incorporation of principles and interventions from individual cognitive
therapies (e.g., Beck, Rush, Shaw, & Emery, 1979; Ellis, 1962) and information
processing research (e.g., Fiske & Taylor, 1991; Fletcher & Fitness, 1996) into work
with distressed couples. Broadly speaking, the goal of the cognitive component in
CBCT is to help couples become more active observers of their own automatic
thoughts, assumptions, and standards, and to evaluate and revise them as needed. A
major premise of CBCT is that behaviors, cognitions, and emotions are inherently
interrelated, and that changes in one domain will influence other domains as well.
Thus, shifts in cognitions toward more balanced/adaptive views are thought to result
in positive changes in emotions and behaviors of the partners (Baucom & Epstein,
1990).
The most recent modifications of CBCT (Epstein & Baucom, 2002) incorporate
additional phenomena and allow for a more balanced attention to different aspects of
relationship functioning. This includes a greater emphasis on emotional experiences
as an area to be targeted, rather than relying on changes in cognitions and behaviors
to affect emotions indirectly. In addition, enhanced CBCT explicitly considers how
the couple responds to environmental demands and uses available resources, further
expanding the model’s systemic characteristics. Furthermore, broad “macro” level
interaction patterns and core relationship themes (e.g., partners’ differences in needs
for intimacy) are now emphasized, along with the traditional work on “micro” behav-
iors. Finally, stable characteristics that each partner brings into the relationship (e.g.,
personality traits, psychopathology) and their influence on relationship functioning
(Christensen & Heavey, 1993; Karney & Bradbury, 1995; Whisman & Baucom,
2012) also receive greater consideration in enhanced CBCT (Epstein & Baucom,
2002).
Other couple theorists and researchers shared the concerns about the restrictions of
a purely behavioral approach to treating relationship distress and constructed models
that were still based on the principles of BCT, but addressed the restrictions. Their
efforts have resulted in a number of other effective treatment approaches with roots
in BCT (e.g., Jacobson & Christensen, 1998).
Relationship Functioning and Cognitive Behavioral Couple

Therapy
Enhanced CBCT employs a broader contextual perspective than traditional BCT

or CBCT in defining a healthy relationship. It takes into account the partners as
individuals, the couple, and the couple’s environment; across these units, behaviors,
cognitions, and emotions are interrelated and equally important in relationship
functioning (Epstein & Baucom, 2002). Within this framework, a healthy relationship
is thought to contribute to the growth and well-being of both partners, the couple
forms a well-functioning team, and the couple responds adaptively to the demands
and resources of their physical and social environment (Baucom, Epstein, & Sullivan,
Couple Therapy 705
2004). Consequently, CBCT practitioners carefully assess a variety of factors within

these domains and units as they relate to relationship distress, as described later in this
chapter.
Enhanced CBCT distinguishes between primary distress and secondary distress
experienced by a couple, which are constituted by both the behavioral processes and
the content of the partners’ interactions and underlying major themes (Epstein &
Baucom, 2002). Primary distress results when the individuals’ fundamental needs
(relationship-focused needs such as affiliation and intimacy, or individually focused
needs such as achievement) are not met adequately within their couple relationship.
Individual differences in various needs between the partners can be difficult for a
couple to negotiate, and this may result in relationship distress (Epstein & Baucom,
2002). Secondary distress results when the couple engages in maladaptive strategies
in response to such unmet needs (e.g., withdrawing from one’s partner or becoming
hostile in response to an unmet need for intimacy). Often, secondary distress can
further prevent fulfillment of fundamental needs, and the dysfunctional patterns of
coping with unmet needs become a source of distress on their own. Thus, enhanced
CBCT interventions target both primary and secondary distress (Epstein & Baucom,
2002).
Gender, sexual orientation, ethnicity, cultural background, and other stable char-
acteristics can influence individual, couple, and environmental factors and how they
relate to relationship functioning. Although there has been some research identifying
particular challenges and experiences of minority couples, there have been few empir-
ical studies on ways that couple therapy can take such experiences into account or
address them directly. For example, divorce rates tend to be higher among some eth-
nic minority groups in the United States (e.g., African American couples; LaTaillade,
2006). This has mainly been attributed to stressors that disproportionally affect cou-
ples of ethnic minority status, such as unemployment, poverty, exposure to violence,
and experiences of racism and discrimination (LaTaillade, 2006). Generally, exposure
to such pervasive stressors tends to be associated with poorer relationship quality
(Bradbury & Karney, 2004; LaTaillade, 2006). Research on the unique experiences
of homosexual couples and their impact on relationship quality is similarly scarce,
although there are a number of challenges that same-sex couples commonly face that
are important to consider, such as stressors due to discrimination (Green & Mitchell,
2008). Treatment adaptations for specific populations have been discussed more
systematically in recent years (e.g., Boyd-Franklin, Kelly, & Durham, 2008; Green
& Mitchell, 2008; Hardy & Laszloffy, 2002; LaTaillade, 2006). However, couple
therapists also need to be aware of within-group diversity for any couple entering
therapy, regardless of their ethnic or sexual minority status, in order to avoid making
inaccurate assumptions about a particular couple’s problems or strengths. Conse-
quently, it is essential to conduct an idiosyncratic assessment of couple functioning
(Epstein & Baucom, 2002; Green & Mitchell, 2008). Nevertheless, research and
clinical considerations regarding couple therapy with specific populations can guide
a careful assessment of special challenges that a couple might face. There is clearly
a need for further research investigating the effects of tailoring couple interventions
to the needs of particular minority groups. However, the contextual focus of our
enhanced CBCT allows the clinician to identify unique themes that may characterize
conflict in diverse couple relationships and to help couples to build on their particular
strengths and resources (Kelly, 2006; LaTaillade, 2006).
Clinical Practice of Enhanced Cognitive Behavioral Couple

Therapy
CBCT has been implemented with a wide range of sessions, from several to over
20 weekly sessions in treatment outcome studies, and an unknown average number
of sessions in clinic and private practice settings. Although the length of treatment
cannot always be predicted for every couple, reasonable goals should be set with the
couple to orient the treatment and to enable both therapist and couple to assess the
progress along the way (Epstein & Baucom, 2002; Schindler et al., 2006; Wood
& Jacobson, 1985). Both “micro” and “macro” level goals should be set at the
beginning of therapy (e.g., having a “date night” twice a month vs. increasing a
couple’s overall sense of closeness). Goals should be reassessed later in therapy, and
the length of treatment can be renegotiated if needed, or goals can be shifted if new
challenges arise (Wood & Jacobson, 1985).
Across the course of treatment as well as within one session, a CBCT practitioner
purposefully assumes multiple roles to establish a supportive environment, provide
didactic information, set the pace of sessions, facilitate the treatment process, and
achieve therapeutic goals. Often, stylistic strategies include being more directive at
the beginning of treatment, especially with high conflict couples that are at risk of
behaving in hurtful ways in the session. Typically, the therapist will then gradually
move toward a more collaborative style to allow the couple more control as they learn
new skills and address their issues (Epstein & Baucom, 2002). However, a flexible
application of different roles within a session is equally important, as it allows the
therapist to respond most effectively to the needs of a couple.
Assessment and Treatment Planning
A clear conceptualization of the couple and their relationship functioning is crucial

for the therapist’s ability to tailor an effective treatment plan for a given couple.
It assists the therapist in organizing the broader interventions, and to respond at a
given moment in a way that facilitates change consistent with the needs and goals of
the couple. Thus, even though it may seem time-intensive, a thorough assessment
is important for the effective implementation of CBCT and often a first step toward
positive change.
The primary goals of assessment in CBCT are (a) to identify the concerns and
potential areas of growth for which a couple would like to receive help, (b) to develop
an understanding of the characteristics of the individuals, the couple, and their
environment that contribute to their concerns (cognitive, behavioral, and emotional
contributors), and (c) to determine whether CBCT is appropriate for addressing these
concerns. At the end of the assessment phase, the therapist shares and discusses his
Couple Therapy 707
or her case conceptualization and treatment recommendations with the couple. If

CBCT is determined not to be appropriate, alternative options are discussed with
the couple (e.g., individual therapy). Unless an acute crisis requires deviation from
the standard procedure with a couple, the initial assessment phase can require 2 to 3
hours, preferably within a 1- or 2-week period. After the assessment phase, ongoing
evaluation is a routine part of therapy, consistent with the tradition of empiricism in
CBCT (Baucom & Epstein, 1990; Schindler et al., 2006). Table 30.1 provides an
overview of the steps in the assessment process.
During the assessment phase, the therapist attends to important factors across all
three units: the individual partners, the couple as a dyad, and characteristics of the
couple’s environment. Characteristics of the individuals are assessed as they relate to
the presenting concerns, such as personality styles, symptoms of psychopathology, the
prominence of individually oriented and communal needs, as well as each person’s
experiences in his or her personal relationship history that continue to affect the
individual within the current couple relationship. With regard to the couple as a
dyad, both macro-level patterns (e.g., based on differences in needs) and specific
interaction patterns (e.g., quickly escalating arguments based on partners’ negative
attributions about each other’s motives, which remain unchallenged due to poor
Table 30.1 Steps in the Assessment Process
1. Orientation to assessment and brief identification of presenting problems

2. Relationship history • Initial interactions and attractions
• Serious relationship prior to marriage/
committed relationship
• Relationship since marriage or similar
committed relationship
3. Assessment of current • Current, specific concerns and relationship
relationship functioning strengths
◦ Overall relationship satisfaction/adjustment
◦ Dyadic functioning in different domains
◦ Communication patterns
◦ Stressors/resources
◦ Primary versus secondary distress
• Observation of couple’s interaction
4. Individual histories and current • Demographic information, developmental
functioning of each partner history
• Family of origin—early relationship models
• Previous significant romantic relationships
• Physical and mental health
• Current relationship
5. Assessment feedback to the couple • Therapist’s conceptualization of presenting
concerns, including developmental course
and strengths/resources used in the past
• Realistic goals for intervention
• Decision of whether to proceed with couple
therapy
listening skills) are evaluated. Both environmental stressors and resources should be
assessed, as well as how the couple has coped with environmental demands in the past.
Areas to consider include relations with the extended family network, work demands,
neighborhood and economic stresses, and experiences of discrimination (e.g., based
on race or sexual orientation).
Assessment Methods
Strategies we typically employ in our assessment for CBCT include self-report ques-
tionnaires, conjoint and individual clinical interviews, and direct observation of the
couple’s communication patterns. During the initial joint interview, the therapist
orients the couple to the process of therapy and provides the rationale for CBCT, as
well as the role of the therapist and the couple. A developmental relationship history
is obtained (e.g., what initially attracted them to each other, how the relationship
progressed toward deeper involvement and commitment, significant positive or neg-
ative life events and their effect on the relationship, any prior therapy experiences),
which helps the therapist to place the couple’s current concerns into a broader con-
text and sometimes brings positive aspects of the relationship back to the couple’s
attention. Sexual satisfaction and any problems due to sexual dysfunctions should also
be assessed. Influences of race, ethnicity, religion, sexual orientation, socioeconomic
status, and other factors are explored as well, along with potential differences between
the partners. In addition to historical factors, the therapist assesses current relationship
concerns and strengths in the relationship.
During the individual interviews, the therapist gathers more historical and current
information about each partner as an individual. In addition, the therapist elicits
information about relevant environmental factors and the individual’s perception of
the current relationship and the presenting concerns. The interviews focus on early
relationship models and other relevant factors that the individual was exposed to
within his or her family of origin (e.g., history of psychopathology in the family),
other significant past relationships, educational and employment history, physical
and mental health, and areas of personal strengths (Epstein & Baucom, 2002;
Schindler et al., 2006). The therapist gathers information about individual, dyadic,
and environmental factors in a similar fashion as in the joint interview. Because a
detailed assessment of all aspects would be too time-consuming, the therapist guides
the interview by focusing on factors that likely influence the individual as a romantic
partner in the current relationship.
During the initial joint interview, we explain to couples how confidentiality of
the information shared during individual sessions will be handled. We keep this
information confidential, although we encourage each person to tell their partner
about past experiences or current functioning that may have an influence at present in
a joint session if such information comes up (e.g., infidelity of a past romantic partner).
However, if we become aware of recent physical abuse resulting in injury and/or
the individual being afraid to live with their partner, we will keep such information
confidential. Disclosing that the individual shared such information with the therapist
may put him or her at risk for further abuse. Under such circumstances, it must be
determined whether conjoint sessions are too risky, in which case we give feedback to
Couple Therapy 709
the couple that based on our observation and their reports of conflict management,
we believe couple therapy is not the best plan of action for them at this point. We then
discuss an alternative plan with the partners, such as providing referrals for individual
therapy. Despite the complications of such situations, protection of the physical and
psychological well-being of each partner should take priority in determining the most
appropriate intervention (e.g., Holtzworth-Munroe, Meehan, Rehman, & Marshall,
2002).
A communication sample is also routinely obtained as part of the assessment process.
Ideally, a videotaped structured discussion with the therapist leaving the room for
about 10 minutes allows for a more naturalistic observation of the couple’s interaction
patterns. For example, the therapist may ask the couple to have a problem-solving
discussion or share their thoughts and feelings about a topic of moderate concern in
their relationship, or may ask one partner to describe a topic of individual concern
while the other partner responds as he or she usually would (observing social support
interactions).
Self-report questionnaires are a helpful adjunct in the assessment process. They
provide information in structured way, and some measures are also well suited to
monitor treatment progress. We usually ask couples to complete a set of questionnaires
that assess general relationship satisfaction (e.g., Dyadic Adjustment; Spanier, 1976),
as well as a number of specific areas relevant to relationship functioning (e.g., Revised
Conflict Tactics Scale; Straus, Hamby, Boney-McCoy, & Sugarman, 1996). Detailed
descriptions of useful measures and their effective use in the assessment in CBCT are
provided elsewhere (Epstein & Baucom, 2002). Most measures were developed in
the United States; however, several measures have been translated and are available in
other countries (e.g., in Germany; Schindler et al., 2006).
Setting Goals for Therapy
The therapist’s feedback to the couple about the case conceptualization and treatment
recommendation concludes the assessment phase. The therapist shares with the
couple his or her understanding of how individual, couple, and environmental factors
affect relationship functioning. In this discussion, the therapist integrates emotional,
behavioral, and cognitive patterns and how they relate to broader relationship themes.
After eliciting feedback from the couple about this case conceptualization, the therapist
and couple collaborate in defining goals based on the relationship problems. Goals
should be phrased as positive statements with adequate detail (e.g., instead of “too
little intimacy,” state the goal as “increasing intimacy in the relationship by spending
more time together as a couple and improving communication of thoughts and
feelings”). The therapist then discusses with the couple what types of interventions
will help the couple to achieve these goals. The therapist helps with setting realistic
goals for treatment and fosters the couple’s sense of self-efficacy and hope.
There are some general principles for the appropriate sequence of addressing
goals in therapy, which should be determined in collaboration with the couple.
First, both partners should have a sense that their most important issues are being
addressed in therapy; otherwise motivation for therapy will likely be diminished.
Second, for some couples the level of secondary distress is so high (e.g., frequent
volatile arguments, resentment about how conflict has been handled) that this needs
to be addressed first before it is possible to turn to sources of primary distress.
Third, some couples appear disengaged or uninvolved. To help such a couple actively
engage in therapy, an early goal may be to increase openness with each other and
emotional expressiveness. The therapist may also prescribe activities that foster a sense
of closeness. Last, some immediate issues, such as a recent relationship trauma or
engagement in high-risk behaviors, must be addressed right away, before other goals
can be attained.
Commonly Used Interventions in Cognitive Behavioral

Couple Therapy
Although, for practical reasons, we describe the wide variety of interventions used
by CBCT practitioners separately based on their primary area of interventions, it is
important to keep in mind that behavior, cognitions, and emotions are inherently
interrelated. Thus, changes in one area will usually also result in change in the other
domains. For example, if a couple improves their communication skills and learns
to share their thoughts and emotional experiences more openly, the partners might
develop more benign interpretations of each other’s behaviors and feel more positively
about each other. Interventions with a focus on one domain are often selected with
the explicit goal of addressing other aspects of the relationship at the same time.
Any of these interventions focused on behavioral, cognitive, or emotional factors can
be applied to address issues of the partners as individuals, the dyadic relationship,
or the couple’s interactions with the environment. For example, if a couple faces
demands from their environment, such as needing to take care of a parent after
a stroke, the therapist might address their cognitions regarding the event and the
support they wish or may be expected to provide, their emotional response to the
event and having to rearrange their daily lives to accommodate the new caretaking
role, and the specific actions they may need to take to respond effectively to the
demands. Similarly, a therapist might address issues pertaining to individual or dyadic
aspects of the relationship across all three domains of behavior, cognitions, and
emotions.
An integral part of CBCT is the collaborative designing of homework assignments,
to ensure that rehearsal of new patterns occurs frequently enough for changes in
ingrained dysfunctional patterns to occur, and to allow for a generalization of new
skills in the couple’s everyday life.
Interventions for Modifying Behavior
Interventions aimed at behavior change in order to achieve improvements in rela-

tionship satisfaction have a long history in couple therapy. In CBCT, there is still
a strong emphasis on helping couples to interact in more constructive ways, with
Couple Therapy 711
the intent simultaneously to create changes toward more positive cognitions and
emotions regarding each other as well. Although there are many specific behavioral
interventions, these interventions belong to two broader categories: guided behavior
change and skills-based interventions (Epstein & Baucom, 2002).
Guided Behavior Change

Guided behavior change interventions are strategies that aim at changing behaviors
with the explicit goal of impacting emotional and cognitive domains as well. These
interventions do not involve a skills component, but rather build on skills that a
couple already has. This also makes guided behavior change a useful strategy early
on in therapy; for example, in order to improve the overall tone in a relationship.
As opposed to behavioral exchange interventions in early BCT, we emphasize the
importance of each person taking responsibility for his or her own behaviors and
making changes regardless of the other partner’s actions (Halford, Sanders, &
Behrens, 1993), thereby moving away from earlier strictly rule-based quid pro quo
exchanges (Jacobson & Margolin, 1979). During the introduction of guided behavior
change interventions, the therapist should emphasize that each partner should think
about how they would behave if they were the kind of partner they themselves would
like to be. Partners in distressed couples often find themselves behaving in ways they
themselves do not like; thus, the goal of behavioral changes is to make the other
person happier, but also for each individual to feel better about him- or herself.
Guided behavior changes can be implemented for different reasons, and with two
levels of specificity. First, the therapist and couple may decide to decrease negative
behaviors and increase positive behaviors in order to change the overall emotional
tone in the relationship. Specific interventions of this category include “love days”
(Weiss, Hops, & Patterson, 1973) and “caring days” (Schindler et al., 2006; Stuart,
1980). These interventions generally involve each partner picking days on which he
or she will engage in a number of specific positive actions (such as making coffee
in the morning, sending a text message during the work day, getting the children
ready for bed, showing physical affection, etc.) to make the other person happier. The
other member of the couple can also be instructed to “catch” their partner doing
positive acts. Sharing with their partner what they especially appreciated helps to
further reinforce positive interactions. The couple and therapist can develop creative
ways to implement these changes if one or both of the partners are hesitant to try
new behaviors. For example, each partner might write small, positive acts that he or
she would enjoy from each other on slips of paper and put them in a “cookie jar,”
in order to help generating ideas for the “caring days” and to reduce concerns about
each other’s reactions (Weiss & Birchler, 1978). These interventions are especially
indicated for couples who no longer make much effort to show their love and care
for each other or have become preoccupied with other demands. The goal is for
the couple to regain a sense of relating to each other in a respectful, caring, and
thoughtful manner.
Second, more focal guided behavior changes are used to address key issues and
broader relationship themes that have been identified during the initial assessment.
For example, a couple might consider a number of behavior changes to allow one
partner to fulfill his or her need for autonomy (e.g., a husband might provide a wife
with opportunities to follow her interests and fulfill her autonomy needs by taking
over more responsibilities in the family). Similarly, a couple who is barely spending
any time together might make changes in each partner’s schedule to allow for more
joint dinners during the week, outings on weekends, and so on, in order to meet both
partners’ needs for affiliation and/or intimacy. Overall, focal guided behavior changes
are designed to address important needs or concerns in the relationship, rather than
shifting the overall ratio of positives compared to negatives.
Skills-Based Interventions
Skills-based interventions, such as communication training, usually involve the thera-
pist providing didactic instruction/psychoeducation about the skills and their purpose,
followed by the couple practicing the new skills. Skills-based interventions are used
with couples who appear to lack adequate skills, or with couples who struggle with
implementing skills that they already know. The therapist will inquire to what degree
the couple was able to perform in a certain skill area in the past, and what is currently
preventing them from doing so. For example, many couples struggle with constructive
communication when the level of negative emotions in their interactions has increased
over time, or they may engage in hardly any problem-solving discussions at all due
to past aversive experiences. Strong emotions such as anger or resentment might
currently lead to deficits in the performance of skills that the partners used effectively
in the past.
For all couples, discussing guidelines for constructive communication helps provide
the structure either to learn new skills or to address performance deficits. We
discuss with the couple the difference between two major types of communication:
conversations focused on sharing thoughts and feelings, and decision-making or
problem-solving conversations (Epstein & Baucom, 2002; Schindler et al., 2006).
This distinction in itself can be helpful for couples to make, in order to avoid
frustrations that occur when the two partners have a different “agenda” for a
conversation (e.g., a wife wants to vent about her boss after a long work day and is
frustrated with the problem-solving attempts of her husband, while the husband feels
rejected because his wife rejects all of his suggestions).
We provide couples with communication guidelines specific to both types of
conversations; sample handouts can be found elsewhere (e.g., Epstein & Baucom,
2002). We usually begin with discussing the guidelines for sharing thoughts and
feelings conversations, as these will also apply during decision making, and it is
important for couples to be able to understand each other’s view point before moving
into problem solving. Briefly stated, the guidelines for sharing thoughts and feelings
include skills for the speaker and the listener. The speaker is asked to express his
or her emotional experiences along with their thoughts in a subjective manner, to
include any positive feelings about the person or situation when expressing concerns,
and to make statements specific and avoid generalizations, among other guidelines.
The listener is instructed that his or her only tasks are to understand and accept the
speaker’s point of view; we emphasize that this does not mean that the partners agree.
The listener should also demonstrate that he or she is listening (e.g., through facial
Couple Therapy 713
expressions, body posture), and reflect back what he or she understood in a summary
(but not an interpretation).
For decision-making conversations, we provide couples with a five-step structure,
each with additional guidelines:
1. State the issue in clear, specific, non-blaming terms.

2. Clarify why the issue is important and what your needs are.
3. Propose and discuss possible solutions.
4. Decide on a solution that is feasible and agreeable to both of you.
5. Decide on a trial period to implement the solution if the situation will reoccur or
the solution needs to be implemented on an ongoing basis.
The guidelines are discussed as recommendations, rather than strict rules. Based on
the specific strengths and difficulties of each couple, certain points can be emphasized
or altered. For example, very intellectualized couples may benefit from heightening
the expression of emotions in order to create a stronger sense of closeness. Similarly,
different couples tend to struggle with different stages of the decision-making process
(e.g., accepting the first proposed solution, or not implementing solutions that were
reached in a constructive manner), and the therapist will focus the communication
training on those aspects needing particular attention.
The communication skills training per se focuses primarily on the process of
communication rather than the content. However, broader themes that the couple
and therapist have agreed to work on will naturally play out in conversations (such
as power distribution in the relationship, reflected by the couple quickly agreeing to
a solution proposed by the dominating partner, or a broader pattern of unresolved
issues due to avoidance of emotion-laden topics). Thus, it is important that the
therapist works with the couple to shift these broader patterns as they engage in these
conversations. In this manner of addressing both the communication process and
the important themes in the relationship, the therapist moves beyond the traditional
role as a “coach” in communication training, which allows therapy to address factors
related to a couple’s distress in a more comprehensive way. In addition, the therapist
might attend to the content by providing didactic information at different times; for
example, to provide a couple with information about alternative discipline techniques
as they engage in a decision-making discussion about how to handle a child’s
behavioral problems, or to share his or her concern if a couple decides on a solution
that appears contrary to the couple’s overall goals.
Interventions Focused on Cognitions
As for any other important area of life, members of a couple are likely to hold
strong beliefs about their relationship and have well-established patterns of cognitions
around how a partner should behave, why their partner is behaving the way he
or she does, what they expect their relationship to look like in the future, and so
on. These different types of cognitions have the capacity to strongly influence a
partner’s behavioral and emotional responses in a romantic relationship. Cognitions
can determine the meaning of a behavior, and are therefore important factors that
should not be overlooked in therapy. For example, a husband might take the children
on an afternoon outing. The wife’s emotional and behavioral response to the partner’s
behavior is likely to be influenced by the attribution she makes for her partner’s actions.
If she thinks that her husband is trying to be thoughtful and wants to allow her a
free afternoon so that she can follow some of her individual interests, she might
experience this as a positive event. If, however, she concludes that her husband does
not enjoy spending time with her and uses the outing with the children as a way
to avoid her, she might react with anger or sadness. Thus, the same relationship
event can result in entirely different responses, and cognitions need to be taken into
account to develop an adequate understanding of the couple’s patterns and select
effective interventions. We have described a number of cognitive variables that are
relevant in CBCT elsewhere (Epstein & Baucom, 2002), including selective attention
(what each individual notices about the partner and the relationship), attributions
(causal inferences about relationship events), expectancies (predictions of what will
occur in the relationship in the future), assumptions (beliefs about what people
and relationships are actually like), and standards (beliefs about what people and
relationships should be like).
As in individual cognitive therapy, CBCT practitioners pay particular attention to
cognitions that are markedly distorted, rather than addressing negative cognitions in
general. For example, an individual may have an unrealistic relationship standard that
leads to distorted attributions about his or her partner (“Partners should always desire
to talk about their innermost feelings. You don’t want to talk to me right away when
you get home from work; you must be doing that because you don’t really love me”).
Distorted assumptions (“Relationships never last; my partner is eventually going to
abandon me”) or expectancies (“Our relationship will just keep going downhill”) also
negatively influence emotions, behaviors, and other cognitions.
The therapist helps the couple to identify and reassess their cognitions, and works
with them to develop more balanced views. Many strategies used in individual cogni-
tive therapy apply here as well, such as the “downward arrow” method, evaluating the
logic behind a cognition, providing didactic information, or weighing the advantages
and disadvantages of a cognition. In addition, interventions more specific to the inter-
personal context (e.g., identifying macro patterns from interactions across situations
or past relationships, increasing relationship schematic thinking by highlighting repet-
itive cycles in couple interactions) can supplement these traditional strategies. Two
broad approaches summarize the overall strategies in these interventions: Socratic
questioning and guided discovery.
Socratic Questioning
Socratic questioning, a technique of helping an individual reevaluate the logic of his
or her thinking, explore underlying issues, and so on, by asking a series of questions,
is one of the core strategies in individual cognitive therapy. It can be effective in
couple therapy, but the different setting needs to be taken into account and the
interventions should be adapted to this context with caution. In individual therapy,
the client can explore and evaluate cognitions in a safe, supportive environment. In
Couple Therapy 715
a distressed romantic relationship, however, partners might already have criticized

or blamed each other for certain types of thinking, or make assumptions about
the other partner’s thoughts and possible distortions. As a result, with the other
partner being in the room, an individual is more likely to respond to Socratic
questioning in a defensive manner, because it does not feel like a safe space to
explore one’s cognitions and admit to distortions. Thus, Socratic questioning might
be unsuccessful or even counterproductive in a couple therapy setting, and may be
more useful with couples in which the partners are less hostile and hurtful toward
each other.
Guided Discovery
While the presence of the partner may interfere with effective use of Socratic question-
ing, couple therapy allows CBCT practitioners to use a different type of intervention
that appears to be highly effective. Guided discovery interventions have the goal of
creating experiences that allow one or both partners to question their thinking and
develop a different perspective on the partner or relationship, without raising their
defensiveness or exposing them to criticism from the other partner.
For example, an individual may interpret her partner’s withdrawal from sexual
intimacy as a sign that her partner no longer finds her attractive or does not love
her anymore. The therapist could use Socratic questioning to help the individual
consider a number of alternative interpretations for this behavior and evaluate the
logic and evidence for each of these explanations. On the other hand, the therapist
could create a guided discovery intervention that would provide the individual
with insights that might lead to a reevaluation of her attributions without directly
challenging her thoughts. The therapist might ask the couple to have a conversation
in which the man shared his perspective and what he is thinking and feeling about
their sexual interactions or the lack thereof. His own insecurity or hurt feelings
around previous sexual encounters may have led to the withdrawal, rather than a
lack of interest or caring. Disclosure of this perspective may lead the partner to
change her initial attributions for his behavior and thereby lead to different emotional
and behavioral responses to it. Similarly, the therapist and couple may collaborate
to design experiences in the couple’s everyday life that may also help alter their
assumptions about each other’s motives (e.g., rearranging the couple’s schedule
to allow for one partner to spend more time with the children and plan for the
partner to share thoughts and feelings about this experience, in order to address the
other partner’s belief that he or she is not interested in or does not enjoy family
life).
Relationship standards (beliefs about what a relationship or a partner’s behavior
should be like) is a category of cognitions that frequently surfaces in couple therapy.
What a person believes about ideal partners or relationships is not necessarily based on
logic, and problematic standards are therefore addressed by focusing on the advantages
and disadvantages of trying to adhere to these standards rather than evaluating their
logic. Standards can be about an individual (e.g., how open an individual should be
about his or her feelings), relationships (e.g., how much time a couple should spend
with each other), or appropriate interactions with the environment (e.g., in what
situations the couple should provide financial support to struggling extended family
members). Targeting standards that are factors related to relationship dysfunction
or distress for a given couple is one example of cognitive restructuring in couple
therapy that proceeds as follows. Generally, we begin with clarifying each person’s
existing standards and then discuss advantages and disadvantages of holding these
standards. If the couple and therapist conclude that a standard needs alteration, they
work together to form new standards that are acceptable to both individuals, typically
small variations from initial more extreme standards. These altered standards can be
taken into account behaviorally in specific domains, and problem-solving strategies
can be employed to facilitate this process. In some cases, the standards of the two
members of a couple might continue to differ; the intervention will then focus on the
degree to which the partners may be able to accept these differences, and discussing
the consequences if they are unable or unwilling to do so.
For example, a same-sex couple might differ on their standards for how “out”
couples should be, and to whom. One partner might believe that a gay couple
should be very open about their sexual orientation and their relationship, should be
politically active in the gay rights movement, and should not be hesitant to display
their affection publicly. On the other hand, the other partner may believe that they
should lead their lives in a way that reduces experiences of discrimination and negative
reactions from their environment, and thus only be out to their immediate friends
and family and be more restrictive in public. Once the partners have clarified each of
their standards regarding this issue, both partners are asked to describe the advantages
and disadvantages of living according to their own standard. That is, the first partner
would be asked to describe positive consequences of his or her standard as well as
possible disadvantages, and the second partner would then be asked to add his or
her perspective. The same procedure would then be repeated with the second partner
speaking about the pros and cons of his or her standard. The therapist should ensure
that each partner shares both positives and negatives about his or her own perspective
to avoid a polarization of the perspectives at this stage.
Following the discussion of the partners’ current standards, the therapist asks them
to try and find a moderated standard. Newly formulated standards should take both
partners’ perspectives into account. The therapist also clarifies that the couple should
not agree to a standard that would not be acceptable to one of the partners, as
behavioral changes based on such a standard would be unlikely to occur or lead to
new distress. After a newly developed standard is agreed upon, the couple is asked to
make decisions about specific behaviors that they each will engage in to implement
the new standard.
Interventions Focused on Emotions
One of the more recent developments in CBCT is to address emotional processes

explicitly, rather than addressing them indirectly through changing behaviors and
cognitions. Couples entering therapy often show extreme patterns in the expression
of emotions, with one or both partners either displaying restricted or minimized
emotions or excessive emotional responses. Understanding the specific difficulties
Couple Therapy 717
with emotions within these broader domains allows the therapist to select the
appropriate interventions.
Addressing Restricted or Minimized Emotions

Many individuals seem to have difficulty experiencing specific emotions or emotions
in general, or are very uncomfortable if they do. This may be due to a variety of
factors and can play out in a number of ways. First, some partners have problems
accessing emotions, which can be specific to certain emotions or a general experience,
as well as focal to the current relationship or typical for the individuals across contexts.
At times, cognitive or behavioral interventions are the strategy of choice in order
to address this issue. For example, a partner of an individual with a serious medical
condition might believe that showing sadness is a sign of weakness, and that he
needs to show strength at all times in order to support his partner, thus suppressing
the expression of the emotion. However, an ill partner might actually feel more
supported if the couple can mutually express their true feelings and join around more
vulnerable emotions. Other individuals might experience minimal amounts of certain
emotions independently of their cognitions. This might stem from the individual’s
temperament, or from growing up in a family or culture in which some emotions
were expressed infrequently or only with low intensity. Other individuals may not
have difficulty with specific emotions, but rather have a muted emotional response
regardless of the type of emotion. Partners with a very restricted range of emotions
may have difficulty fully engaging in their relationship in a rewarding way; at the
same time, their partner may not find it gratifying to live with a very limited range of
emotional responses.
Another common issue is a limited ability to differentiate among and label different
emotions, despite experiencing emotions in higher intensity. The ability to recognize
and articulate different emotions in a more detailed way than just knowing some-
thing feels “good” or “bad” can be helpful to both the individual and his or her
partner. For example, if an individual can identify that he or she is feeling sad, the
individual and/or the couple can address this particular emotion and the loss that
accompanies it. A more differentiated understanding and expression may also help
the members of a couple better understand each other and develop a greater sense of
closeness.
Aside from the ability to differentiate emotions, some individuals may have difficulty
relating their emotional responses to internal or external events. For example, a
member of a couple may be able to identify that he is very anxious but cannot relate
this to thoughts or an interaction with his partner that may be tied to the anxious
response. As a result, emotional responses seem to occur in an unpredictable manner
rather than being tied to specific events, and both the individual and the partner may
feel that they have little control over the relationship and the emotional reactions that
occur.
Finally, individuals often avoid experiencing or expressing emotions that they
perceive as dangerous or that cause them to feel vulnerable. Greenberg and Safran
(1987) referred to the former as primary emotions, which are associated with
important needs, such as being anxious that one’s partner will respond negatively
to the expression of intimacy needs. They suggested that individuals then revert to
secondary emotions instead that they experience as safer, such as experiencing or
expressing anger instead of anxiety when reacting to criticism in an interaction with
the partner. A number of strategies based on emotionally-focused couple therapy
(Johnson, 2004; Johnson & Greenberg, 1987) are used to help individuals access,
heighten, or differentiate their emotions. As a broad principle, the therapist first
creates a safe atmosphere and then intervenes to heighten the emotional experience.
Normalizing the experience of both positive and negative emotions is a first step to
promote a safe environment, and the therapist also encourages the partner to respond
to the expression of various emotions in a caring and supportive manner, which may
also be modeled by the therapist. Understandably, attempts by the individual to avoid
a new emotional experience are likely to occur, and the therapist will need to carefully
refocus the individual to emotional expression. To prevent these interventions from
creating an aversive experience, the therapist has to determine when and to what
degree to shift the attention (back) to the expression of emotions, depending on
the therapist’s understanding of the partners and at what point they might feel
overwhelmed.
A number of strategies can be used to heighten the experience of emotions once
a safe atmosphere is established, including asking an individual to recount the details
of a particular event in order to evoke the associated emotions; encouraging the
use of metaphors and images to make the description of emotions easier or less
frightening; using questions, reflections, and interpretations to draw out primary
emotions; discouraging attempts by an individual to distract him- or herself from
experiencing emotions; and facilitating the acceptance of the individual’s subjective
experience by the partner. The goal of these strategies is to help the individual to
enrich his or her emotional experience and expression, and for the partner to respond
appropriately, in a way that is useful to both the individual and the couple. However,
individual and cultural differences in the experience and expression of emotions should
be taken into account when deciding to use the above strategies. Focusing on this
area of functioning should not be based on a general assumption that an individual
should have rich emotional experiences with a full range of emotional expression.
Instead, the therapist should carefully assess if a restricted emotional experience or
expression is interfering with the individual’s or couple’s functioning and well-being.
Containing the Experience or Expression of Emotions

Other couples may have a somewhat opposite experience in terms of the intensity
of their emotional experience and expression, and their ability to regulate them
effectively. Most frequently, this becomes a concern if one or both partners are
experiencing and expressing negative emotions in high intensity or in inappropriate
settings. However, a few couples also experience difficulty if one person frequently
expresses strong positive emotions. Nevertheless, couple therapists are more likely to
encounter couples in which one or both individuals have difficulty regulating negative
emotional responses. Their lives may seem to revolve around a series of emotional
crises, strong arguments, or extreme behaviors, including partner abuse that may
result from unregulated, strong negative emotions. As a result, therapists may find
Couple Therapy 719
the work with such couples quite demanding, but a variety of strategies can assist in
such cases.
Similarly to the strategies noted above, behavioral and cognitive interventions
may be indicated to address an individual’s inappropriate behavior or a partner’s
extreme standards that hardly anyone could satisfy, all of which may lead to frequent
strong negative emotions. In addition, interventions that are more focal to extreme
emotional experiences are available to therapists. First, it may be useful for the
couple to establish scheduled times during which they discuss issues that one or both
partners are upset about, with the goal of containing the expression of strong negative
emotions to fewer instances and more appropriate settings. Some people with poor
affect regulation find it easier to refrain from expressing strong negative feelings if
they know there will be a set time to address their concerns. Thus, this intervention
can be helpful in keeping strong negative affect from intruding into all areas of life
or occurring under circumstances that would likely increase frustration or have other
negative consequences for the couple (e.g., at a family function).
The application of interventions from dialectical behavioral therapy (Linehan, 1993)
in an interpersonal context also can be helpful in addressing poorly regulated strong
negative emotions in CBCT. For example, one of these strategies involves increasing
an individual’s distress tolerance. Some individuals tend to express their emotions
and concerns immediately to their partners, which leads to frequent emotionally
driven negative interactions. Helping these individuals to become more comfortable
and accepting of being upset without expressing every concern immediately can be
helpful. In addition, teaching the individual how to focus on the current moment
can be helpful in keeping upset in one domain of the relationship from infiltrating
other aspects of their life. We discuss this “healthy compartmentalization” with the
understanding that it is important to voice negative emotions and address concerns
about a given aspect of a relationship, but to restrict the response to this issue, and
to be in the moment when positive events happen in the relationship as well and to
allow oneself to enjoy them.
Finally, it can be helpful to find alternative ways of coping with strong negative
emotions other than expressing them to one’s partner. Relying on friends for
expressing some of one’s concerns in an appropriate manner, writing about one’s
emotional experiences in a journal, or other alternatives for adaptively expressing
strong emotions can help an individual regulate his or her feelings more effectively.
At the same time, concerns should still be addressed with the partner. If the emotion
regulation difficulties of an individual are too severe to be addressed in the context
of couple therapy, or if teaching the necessary skills is not feasible for other reasons,
individual therapy for the partner with poor emotion regulation may be a helpful
addition to couple therapy.
Termination
The couple and therapist collaborate closely in determining when treatment should
be terminated. In this discussion, the degree to which initial goals and present-
ing concerns have been addressed should be considered, along with any additional
concerns or goals that have emerged over the course of therapy. In addition, the
relief of both primary and secondary distress should be taken into account. At
times, there may be concerns left to address, but the couple now has made changes
and developed skills that allow them to work on these remaining challenges with-
out the therapist’s assistance. Toward the end of therapy, the couple and therapist
also discuss how the partners will continue the necessary efforts and hold them-
selves accountable to further improve their relationship and/or maintain treatment
gains.
Considerations for Effective Treatment Application
A number of considerations can be helpful for therapists to keep in mind in order

to employ CBCT most effectively. One challenge unique to couple therapy com-
pared to individual treatment is the importance of therapists managing sessions in
a highly directive manner with highly distressed couples, who tend to experience
strong emotions in session, have conflict in the presence of the therapist, and shift
focus quickly from one problem to another. The therapist needs to be comfortable
interrupting the partners in an argument, directing their attention to a particular
topic, and thereby regulating their emotional arousal when the members of the
couple are unable to do so themselves. Although therapists may initially feel “rude”
doing so, this is actually an important contribution to creating a safe, supportive
environment, where the partners experience that they can openly address their con-
cerns without being at risk of getting into a highly aversive interaction with each
other.
Generally, the goal for therapists is to integrate the use of cognitive, behavioral,
and emotional interventions effectively, and apply them flexibly depending on the
overall needs of a couple and the demands in a given moment. At times, beginning
therapists tend to overutilize behavioral interventions, particularly communication
skills training. Although we also believe that improved communication itself can
result in progress in other areas of concern, we understand communication training
as the vehicle by which the therapist can assist the couple in more effectively
addressing major patterns and domains in their relationship. Thus, we believe that
teaching specific communication guidelines only is too simplistic and not sufficient for
effectively promoting changes in many distressed relationships. Other interventions
also bring challenges with them that are unique to the setting of couple therapy,
as previously discussed (e.g., applying cognitive restructuring interventions with the
partner present, creating a safe environment and equally supportive relationship
with both partners). We believe that intimate relationships are complex systems that
must be conceptualized in a rich manner with a thoughtful treatment plan that
integrates behavioral, cognitive, and emotional factors that can be targeted at the
individual, dyadic, and environmental levels. Being able to respond to this complexity
in a flexible manner, and confidently using a variety of interventions and stylistic
strategies to manage the demands of a session and generalize gains to the couple’s
everyday lives, provides them with the best chance to achieve their best possible
relationship.
Couple Therapy 721
Treatment Applicability, Empirical Support,

and Dissemination
Studies have consistently shown no significant differences between the effectiveness

of strictly behavioral couple therapy and broader cognitive behavioral couple therapy
approaches (Baucom, Sayers, & Sher, 1990; Christensen, Atkins, Baucom, & Yi,
2010; Halford et al., 1993). Thus, the empirical support for these interventions will
be discussed across the different types of couple therapy with roots in BCT.
CBCT has been the subject of a large number of controlled treatment outcome
studies, and meta-analyses and reviews have concluded that CBCT approaches are
efficacious in the treatment of relationship distress (e.g., Baucom, Hahlweg, &
Kuschel, 2003; Dunn & Schwebel, 1995; Shadish & Baldwin, 2005; Snyder et al.,
2006). Meta-analyses usually include both CBCT and BCT. Baucom et al. (2003)
found a mean effect size of d = 0.82 across the two main outcomes (relationship
quality and observed measures of communication) based on pre- versus posttest
scores in their meta-analysis, and a mean effect size of d = 0.72 when comparing the
treatment condition to wait-list control groups. Shadish and Baldwin (2005) included
unpublished studies and reported a smaller effect size of d = 0.59 for the effects
of the treatment versus no-treatment controls across a host of different outcome
variables (e.g., self-reported relationship quality, observational measures) at the end
of treatment. However, a notable number of couples do not maintain treatment
gains over long periods of time and deteriorate (Snyder et al., 2006), although
some couples, if they stay together, continue to improve years after termination
(Christensen et al., 2010). Thus, despite the effectiveness of couple therapy, it fails to
assist some couples, and long-term outcomes are not always favorable. In addition,
research often has found that the specific proposed mechanisms of change in different
couple therapy approaches (e.g., improved communication skills level in BCT) are
not predictive of therapy outcome, and different mechanisms may lead to the same
favorable outcome (e.g., Doss, Thum, Sevier, Atkins, & Christensen, 2005; Iverson
& Baucom, 1990). As a result, the field has turned to a discussion and investigation
of common and nonspecific factors that may be operating across different approaches,
although empirical findings are still scarce (Hahlweg, Grawe-Gerber, & Baucom,
2009; Halford & Snyder, 2011; Snyder et al., 2006; Sullivan & Baucom, 2002).
CBCT has also been adapted and applied to specific individual and relationship
problems, and has been found to be helpful in the treatment of couples after infidelity
(Baucom, Snyder, & Gordon, 2009; Plack & Kröger, 2008; Snyder, Baucom, &
Gordon, 2008), individual psychopathology (Baucom, Shoham, Mueser, Daiuto, &
Stickle, 1998; Hahlweg & Baucom, 2008; Snyder et al., 2006; Whisman & Baucom,
2012), medical problems (Baucom, Porter, Kirby, & Hudepohl, 2011; Martire,
Schulz, Helgeson, Small, & Saghafi, 2010), and sexual dysfunction (Baucom et al.,
1998; Kröger, Hahlweg, & Klann, 2007; Regev, O’Donohue, & Avina, 2003).
Despite the extensive research on couple therapy, its effectiveness, and its appli-
cations, very little attention has been paid to the dissemination of these effective
interventions in community settings (Hahlweg, Baucom, Grawe-Gerber, & Snyder,
2009). For most countries, it is unclear if and to what extent clinicians in the com-
munities utilize evidence-based interventions in the treatment of relationship distress,
and couple therapy or counseling is often not readily available, regardless of the
type of intervention offered (Hahlweg et al., 2009). Furthermore, investigations that
examine the effectiveness of couple therapy outside of controlled research settings are
rare, and when available, show smaller effect sizes than usually found in controlled
studies (Klann, Hahlweg, Baucom, & Kroeger, 2011). Hahlweg et al. (2009) discuss
the issues above in more detail and propose a framework for successful dissemination
of effective interventions in the future. Considering the high prevalence and negative
impact of relationship distress on the partners and the family, the dissemination of
these efficacious interventions should become a focus for the field.
References
Baucom, D. H., & Epstein, N. (1990). Cognitive-behavioral marital therapy. New York, NY:
Brunner/Mazel.
Baucom, D. H., Epstein, N., & Sullivan, L. J. (2004). Brief couple therapy. In M. Dewan,
B. Steenbarger, & R. P. Greenberg (Eds.), The art and science of brief therapies
(pp. 189–227). Washington, DC: American Psychiatric Publishing.
Baucom, D. H., Hahlweg, K., & Kuschel, A. (2003). Are waiting list control groups
needed in future marital therapy outcome research? Behavior Therapy, 34, 179–188.
doi:10.1016/S0005-7894(03)80012-6
Baucom, D. H., Porter, L. S., Kirby, J. S., & Hudepohl, J. (2011). Couple-based interventions
for medical problems. Behavior Therapy, 43, 61–76. doi:10.1016/j.beth.2011.01.008
Baucom, D. H., Sayers, S. L., & Sher, T. G. (1990). Supplementing behavioral mari-
tal therapy with cognitive restructuring and emotional expressiveness training: An
outcome investigation. Journal of Consulting and Clinical Psychology, 58, 636–645.
doi:10.1037/0022-006X.58.5.636
Baucom, D. H., Shoham, V., Mueser, K. T., Daiuto, A. D., & Stickle, T. R. (1998). Empirically
supported couples and family therapies for adult problems. Journal of Consulting and
Baucom, D. H., Snyder, D. K., & Gordon, K. (2009). Helping couples get past the affair: A
clinician’s guide. New York, NY: Guilford Press.
Boyd-Franklin, N., Kelly, S., & Durham, J. (2008). African American couples in therapy. In
A. S. Gurman (Ed.), Clinical handbook of couple therapy (4th ed., pp. 681–697).
Bradbury, T. N., & Karney, B. R. (2004). Understanding and altering the longitudinal course
of marriage. Journal of Marriage and the Family, 66, 862–879. doi:10.1111/j.0022-
2445.2004.00059.x
Christensen, A., Atkins, D. C., Baucom, B., & Yi, J. (2010). Marital status and satisfaction
five years following a randomized clinical trial comparing traditional versus integrative
behavioral couple therapy. Journal of Consulting and Clinical Psychology, 78, 225–235.
doi:10.1037/a0018132
Christensen, A., & Heavey, C. L. (1993). Gender differences in marital conflict: The
demand/withdraw interaction pattern. In S. Oskamp & M. Costanzo (Eds.), Gender
Couple Therapy 723
issues in contemporary society. Claremont Symposium on Applied Social Psychology (Vol. 6,

pp. 113–141). Newbury Park, CA: Sage.
Doss, B. D., Thum, Y., Sevier, M., Atkins, D. C., & Christensen, A. (2005). Improving
relationships: Mechanisms of change in couple therapy. Journal of Consulting and Clinical
Psychology, 73, 624–633. doi:10.1037/0022-006X.73.4.624
Dunn, R. L., & Schwebel, A. I. (1995). Meta-analytic review of marital therapy outcome
research. Journal of Family Psychology, 9, 58–68. doi:10.1037/0893-3200.9.1.58
Epstein, N., & Baucom, D. H. (2002). Enhanced cognitive-behavioral therapy for couples: A
contextual approach. Washington, DC: American Psychological Association.
Fiske, S. T., & Taylor, S. E. (1991). Social cognition. New York, NY: McGraw Hill.
Fletcher, G. J. O., & Fitness, J. (Eds.). (1996). Knowledge structures in close relationships: A
social psychological approach. Mahwah, NJ: Erlbaum.
Green, R., & Mitchell, V. (2008). Gay and lesbian couples in therapy: Minority stress, relational
ambiguity, and families of choice. In A. S. Gurman (Eds.), Clinical handbook of couple
therapy (4th ed., pp. 662–680). New York, NY: Guilford Press.
Greenberg, L. S., & Safran, J. D. (1987). Emotion in psychotherapy: Affect, cognition, and the
process of change. New York, NY: Guilford Press.
Hahlweg, K., & Baucom, D. H. (2008). Partnerschaft und psychische Störung. Fortschritte der
Psychotherapie. Göttingen, Germany: Hogrefe.
Hahlweg, K., Baucom, D. H., Grawe-Gerber, M., & Snyder, D. K. (2009). Strengthening
couples and families: Dissemination of interventions for the treatment and preven-
tion of couple distress. In K. Hahlweg, M. Grawe-Gerber, & D. H. Baucom (Eds.),
Enhancing couples: The shape of couple therapy to come (pp. 3–30). Göttingen, Germany:
Hogrefe.
Hahlweg, K., Grawe-Gerber, M., & Baucom, D. H. (Eds.) (2009). Enhancing couples: The
shape of couple therapy to come. Göttingen, Germany: Hogrefe.
Halford, W. K., Sanders, M. R., & Behrens, B. C. (1993). A comparison of the generalisation of
behavioral marital therapy and enhanced behavioral martial therapy. Journal of Consulting
and Clinical Psychology, 61, 51–60. doi:10.1037/0022-006X.61.1.51
Halford, W. K., & Snyder, D. K. (2011). Universal processes and common factors in couple
therapy and relationship education. Behavior Therapy, 43, 1–12. doi:10.1016/j.beth.
2011.01.007.
Hardy, K. V., & Laszloffy, T. A. (2002). Couple therapy using a multicultural perspective.
In A. S. Gurman & N. S. Jacobson (Eds.), Clinical handbook of couple therapy (3rd ed.,
Holtzworth-Munroe, A., Meehan, J. C., Rehman, U., & Marshall, A. D. (2002). Intimate
partner violence: An introduction for couple therapists. In A. S. Gurman & N. S.
Jacobson (Eds.), Clinical handbook of couple therapy (3rd ed., pp. 441–465). New York,
NY: Guilford Press.
Iverson, A., & Baucom, D. H. (1990). Behavioral marital therapy outcomes: Alternative
interpretations of the data. Behavior Therapy, 21, 129–138. doi:10.1016/S0005-
7894(05)80194-7
Jacobson, N. S., & Christensen, A. (1998). Acceptance and change in couple therapy: A
therapist’s guide to transforming relationships. New York, NY: Norton.
Jacobson, N. S., & Margolin, G. (1979). Marital therapy: Strategies based on social learning
and behavior exchange principles. New York, NY: Brunner/Mazel.
Johnson, S. M. (2004). The practice of emotionally focused couple therapy: Creating connection.
New York, NY: Brunner-Routledge.
Johnson, S. M., & Greenberg, L. S. (1987). Emotionally focused marital therapy: An

overview. [Special issue: Psychotherapy with families.] Psychotherapy, 24(3S), 552–560.
doi:10.1037/h0085753
Karney, B. R., & Bradbury, T. N. (1995). The longitudinal course of marital quality and
stability: A review of theory, methods, and research. Psychological Bulletin, 118, 3–34.
doi:10.1037/0033-2909.118.1.3
Kelly, S. (2006). Cognitive behavioral therapy with African Americans. In P. A. Hays &
G. Y. Iwamasa (Eds.), Culturally responsive cognitive-behavioral therapy: Assessment, prac-
tice, and supervision (pp. 97–116). Washington, DC: American Psychological Association.
Klann, N., Hahlweg, K., Baucom, D. H., & Kroeger, C. (2011). The effectiveness of couple
therapy in Germany: A replication study. Journal of Marital & Family Therapy, 37 ,
200–208. doi:10.1111/j.1752-0606.2009.00164.x
Kröger, C., Hahlweg, K., & Klann, N. (2007). Welche Auswirkungen hat Ehe- und Paar-
beratung auf die Sexualität und die sexuelle Zufriedenheit? Zeitschrift für Klinische
Psychologie und Psychotherapie: Forschung und Praxis, 36, 121–127. doi:10.1026/1616-
3443.36.2.121
LaTaillade, J. J. (2006). Considerations for treatment of African American couple relation-
ships. Journal of Cognitive Psychotherapy: An International Quarterly, 20, 341–358.
doi:10.1891/jcpiq-v20i4a002
Liberman, R. P. (1970). Behavioral approaches to family and couple therapy. American Journal
of Orthopsychiatry, 40, 106–118. doi:10.1111/j.1939-0025.1970.tb00683.x
Linehan, M. M. (1993). Cognitive-behavioral treatment of borderline personality disorder. New
Martire, L. M., Schulz, R., Helgeson, V. H., Small, B. J., & Saghafi, E. M. (2010). Review and
meta-analysis of couple-oriented interventions for chronic illness. Annals of Behavioral
Medicine, 40, 325–342. doi:10.1007/s12160-010-9216-2
Plack, K., & Kröger, C. (2008). Paartherapie nach außerpartnerschaftlichen Beziehungen: Ein
kognitiv-behavioraler Behandlungsansatz. Verhaltenstherapie und Verhaltensmedizin, 29,
111–121.
Regev, L. G., O’Donohue, W., & Avina, C. (2003). Sexual dysfunction. In D. K. Snyder & M.
A. Whisman (Eds.), Treating difficult couples: Helping clients with coexisting mental and
relationship disorders (pp. 181–200). New York, NY: Guilford Press.
Schindler, L., Hahlweg, K., & Revenstorf, D. (2006). Partnerschaftsprobleme Therapiemanual.
(2nd ed.). Berlin, Germany: Springer.
Shadish, W. R., & Baldwin, S. A. (2005). Effects of behavioral marital therapy: A meta-analysis
of randomized controlled trials. Journal of Consulting and Clinical Psychology, 73, 6–14.
doi:10.1037/0022-006X.73.1.6
Snyder, D. K., Baucom, D. H., & Gordon, K. C. (2008). An integrative approach to treating
infidelity. Family Journal, 16, 300–307. doi:10.1177/1066480708323200
Snyder, D. K., Castellani, A. M., & Whisman, M. A. (2006). Current status and
future directions in couple therapy. Annual Review of Psychology, 57 , 317–344.
doi:10.1146/annurev.psych.56.091103.070154
Spanier, G. B. (1976). Measuring dyadic adjustment: New scales for assessing the qual-
ity of marriage and similar dyads. Journal of Marriage and the Family, 38, 15–28.
doi:10.2307/350547
Straus, M. A., Hamby, S. L., Boney-McCoy, S., & Sugarman, D. B. (1996). The Revised
Conflict Tactics Scales (CTS2): Development and preliminary psychometric data. Journal
of Family Issues, 17 , 283–316. doi:10.1177/019251396017003001
Stuart, R. B. (1969). Operant interpersonal treatment for marital discord. Journal of Consulting
and Clinical Psychology, 33, 675–682. doi:10.1037/h0028475
Couple Therapy 725
Stuart, R. B. (1980). Helping couples change: A social learning approach to marital therapy.
Sullivan, L. J., & Baucom, D. H. (2002, November). Relationship-schematic processing and
matching couples to treatment intervention. Paper presented at the Annual Meeting of the
Association for Advancement of Behavior Therapy, Reno, NV.
Weiss, R. L., & Birchler, G. R. (1978). Adults with marital dysfunction. In M. Hersen and A.
Bellack (Eds.), Behavior therapy in the psychiatric setting (pp. 331–364). Baltimore, MD:
Williams & Williams.
Weiss, R. L., Hops, H., & Patterson, G. R. (1973). A framework for conceptualizing marital
conflict, a technology for altering it, some data for evaluating it. In M. Hersen &
A. S. Bellack (Eds.), Behavior change: Methodology, concepts and practice (pp. 309–342).
Champaign, IL: Research Press.
Whisman, M. A., & Baucom, D. H. (2012). Intimate relationships and psychopathology.
Clinical Child and Family Psychology Review, 15, 4–13. doi:10.1007/s10567-011-
0107-2
Wood, L. F., & Jacobson, N. S. (1985). Marital distress. In D. H. Barlow (Ed.), Clinical
handbook of psychological disorders (pp. 344–416). New York, NY: Guilford Press.
31
Family Therapy
Frank M. Dattilio
Background of Cognitive Behavioral Family Therapy
Cognitive behavioral family therapy (CBFT) has now entered the mainstream of
contemporary family therapy and appears prominently in the vast majority of major
textbooks in the field (Becvar & Becvar, 2009; Bitter, 2009; Goldenberg & Golden-
berg, 2008; Nichols & Schwartz, 2012; Sexton, Weeks, & Robbins, 2003).
CBFT has its roots in the major development of psychotherapy that spawned
during the 1960s and 1970s, involving behavior therapists’ utilization of learning
theory principles to address various problematic behaviors with children and adults.
The behavioral principles and techniques that were used successfully in the treatment
of individuals were later applied to families. Patterson, McNeal, Hawkins, and Phelps
(1967) and others (e.g., Lebow, 1976; Wahler, Winkel, Peterson, & Morrison, 1971)
applied operant conditioning and contingency-contracting procedures to help parents
control the behavior of aggressive children. This operant approach offered solid
empirical support and became popular among behaviorally-oriented therapists. This
was later integrated into work with families.
It was not until the end of the 1980s that the late Ian Falloon (1988) encouraged
behavioral family therapists to adopt an open-systems approach that examined the
multiplicity of forces that might operate within the family constellation. Falloon
stressed the need to focus on the physiological status of the individual, as well as
his or her cognitive, behavioral, and emotional responses. This was in addition to
considering the interpersonal transactions that occur within the family, work, social,
and cultural-political networks. Falloon advocated for a more contextual approach,
whereby each potentially causative factor was considered in relation to other factors.
The contextual approach was elaborated on by an earlier theorist, Arnold Lazarus
(1976), in his multimodal assessment approach. The goal of behavioral analysis became

DOI: 10.1002/9781118528563.wbcbt31
involved with exploring all systems operating on each spouse or family member that
contributed to the presenting problem. It is for this reason that pioneering behavior
family therapist Gerald Patterson (1971) stressed the need for assessment to occur in
different settings, such as the adjunctive agencies in school and work environments.
One of the hallmarks of behaviorally-oriented family therapies was the addition of
components of communication and problem-solving skills training to interventions
(Falloon, 1988; Falloon, Boyd, & McGill, 1984).
Over time, as behaviorally-oriented therapists developed more comprehensive
approaches to modifying family interactions that contribute to distressed relationship,
their methods became more appealing to family therapists in general whose work was
guided by systems theory (Dattilio, 2010). Nevertheless, schools of family therapy that
have emphasized the modification of behavior patterns (e.g., the structural-strategic
and solution-focused approaches) typically continue to use interventions that are
different from those used by behavioral family therapists (e.g., directives, paradoxical
prescriptions, and unbalancing interventions, such as temporarily siding with one
family member).
Cognitive Therapy Principles
It was also in the late 1980s that cognition was introduced as a component of
treatment within the specific behavioral paradigm of couples and family therapy
(Dattilio, 1983, 1989; Ellis, 1982; Epstein, Schlesinger, & Dryden, 1988). Family
members’ thought processes had always been considered important in a variety of
family therapy theoretical orientations (e.g., reframing and the strategic approach,
“problem-talk” in solution-focused therapy, and life stories in narrative therapy).
However, none of the original mainstream family therapy approaches employed
the concept and systemic methods of CBT to assess and intervene with thought
processes and perceptions of family relationships. Traditional family therapists did
consider cognition, but only in a very simplistic manner, such as addressing the
specific thoughts that family members expressed in their obvious conscious attitudes.
However, cognitive therapists were busy developing more thorough and complex
ways to deal with family members’ underlying belief systems that contributed to their
interactions with one another.
It was also during the 1980s that established cognitive assessment and intervention
methods were derived from individual therapy and adapted by cognitive behavioral
therapists for use in family therapy. These interventions were used to identify and
modify distorted cognitions that family members experienced about each other
(P. C. Alexander, 1988; J. F. Alexander & Parsons, 1982; Bedrosian, 1983). As
with individual psychotherapy, cognitive behavioral interventions with families were
designed to enhance the family members’ skills for evaluating and modifying their
own problematic cognitions, as well as skills for communicating and solving problems
constructively. Bedrosian (1983) specifically applied Beck’s model to cognitive therapy
to understanding and treating dysfunctional dynamics, as did Barton and Alexander
(1981). This evolved into what later became known as “functional family therapy”
(J. F. Alexander & Parsons, 1982).
Family Therapy 729
During the same decade, the model saw a rapid expansion into what constitutes
contemporary CBFT (P. C. Alexander, 1988; Dattilio, 1993; Epstein & Schlesinger,
1996; Epstein et al., 1988; Falloon et al., 1984; Schwebel & Fine, 1994; Teichman,
1981, 1992). In this chapter, I will focus on CBFT that has a strong rapport
with systemic approaches, and emphasizes the role of family schemas—those jointly
held beliefs among the family members that have formed as a result of years of
integrated interaction within the family unit. Other CBFT approaches have been
developed as well, frequently focusing on a special clinical problem; for example,
CBFT for abdominal pain in children (Sanders, Shepherd, Cleghorn, & Woolford,
1994), family intervention in psychosis (Bird et al., 2010), family-focused therapy
for anxiety disorders (Chambless, 2012), family interventions in the case of suicidal
children (Wells & Heilbron, 2012), and structured family CBT for children with
obsessive-compulsive disorder (Piacentini et al., 2011).
More recently, the triple p-positive parenting program has been widely disseminated
as a family support strategy. This is a five-level program that aims to prevent severe
behavioral, emotional, and developmental problems in children by enhancing the
knowledge, skills, and confidence of parents. Randomized efficacy trials have yielded
very favorable results (Sanders, 2012). However, to underline the specificities of the
family approach, I will exemplify schema-based CBFT.
Empirical Support for Cognitive Behavioral Family Therapy
Due to the fact that CBFT is a limited approach, the empirical literature is somewhat
lean. Faulkner, Klock, and Gale (2002) conducted a content analysis on articles
published in the marital/couple and family therapy literature from 1980 to 1999. The
American Journal of Family Therapy, Contemporary Family Therapy, Family Process,
and the Journal of Marital and Family Therapy were among the top journals from
which 131 articles that used quantitative research methodology were examined. Of
these 131 articles, fewer than half involved outcome studies. Unfortunately, none of
the studies that were reviewed considered CBFT.
One of the reasons for this may be the fact that research in family therapy is more
arduous than couple and individual therapy in that there are multiple dynamics in
the case of families. Much of the dynamics involved with CBFT draws from cognitive
behavioral couple therapy, for which there are a number of substantial controlled
outcome studies (see Dattilio, 2010, for an extensive review). These studies indicate
the effectiveness of cognitive behavioral therapy for relationships, although the
majority of the studies have primarily focused on the behavioral interventions of
communications training, problem-solving training, and behavioral contracts, with
only a handful examining the impact of cognitive restructuring procedures. This
would indicate that additional studies are certainly necessary to enable conclusions
to be drawn about the relative efficacies of the empirically supported treatments
with families using a cognitive behavioral approach. However, there is encouraging
support for CBFT as a treatment mode that can be helpful to many distressed families
(Dattilio, 1998, 2005b; Dattilio & Epstein, 2005).
Outcome studies have demonstrated the effectiveness of behaviorally-oriented

family interventions, namely psychoeducation and training in communications and
problem-solving skills. There has also been additional research conducted on the
straight behavioral approach for cases of aggressive behavior (Patterson, 1982) and
the application of operant principles to parent–child interactive therapies for conduct
problems (Sanders & Dadds, 1993; Webster-Stratton & Hancock, 1998), as well as
for child anxiety and aggression (Dadds, Barrett, Rapee, & Ryan, 1996), depression
(Birmaher, Brent, & Kolko, 2000; Brent, Holder, & Kolko, 1997), eating disorders
(Wardle et al., 2003), as well as psychiatric disorders (Mueser & Glynn, 1995).
Dadds and Salmon (2003) also proposed a transactional model addressing the
theoretical construct of punishment insensitivity, which makes predictions about the
manner in which children with particular traits respond to, as well as influence,
parenting practices.
The application of behavioral family therapy has also been studied in the treatment
of schizophrenia (Falloon et al., 1984). A focus has been placed on reducing relapse
rates and improving patient social functioning in an attempt to reduce the family
burden (Hahlweg & Wiedemann, 1999). Effective parenting strategies have also been
used successfully in the treatment of attention-deficit/hyperactivity disorder (Barkley,
1997; Chronis, Chacko, Fabiano, Wymbs, & Pelham, 2004).
As increasing emphasis has been placed on empirically validated treatments in the
mental health field, the cognitive behavioral approach in general has gained popularity
and respect among clinicians, including family therapists of various modalities (Davis
& Piercy, 2007).
Sprenkle (2003) noted the application of more rigorous outcome criteria and
research on couple and family therapy, and the movement of the field in general
toward a more evidenced-based discipline. In addition, there appears to be more
attention given to case-based reports within the family therapy literature. Traditionally,
case-based research has not been considered as scientific by many in the field, owing
to the lack of controlled conditions and objectivity. However, case study material
can serve as the basis for drawing causal inferences in properly designed clinical
cases (Dattilio, 2006a) and, in many ways, seems to be preferred among students
and trainees (Dattilio, Edwards, & Fishman, 2010; Edwards, Dattilio, & Bromley,
2004).
Relationship Schemas in Family Therapy
Consistent and compatible with systems theory, the cognitive behavioral approach
to families is based on the premise that members of the family simultaneously
influence and are influenced by each other’s thoughts, emotions, and behaviors
(Dattilio, 2001a; Leslie, 1988). In essence, to know the entire family system is to
know the individual parts and the manner in which they interact. As each family
member observes his or her own cognitions, behaviors, and emotions regarding
family interactions, as well as cues regarding the responses of other family members,
these perceptions lead to the formation of assumptions about family dynamics, which
then develop into relatively stable schemas, or what are referred to as “cognitive
Family Therapy 731
structures.” These cognitions, emotions, and behaviors may elicit responses from
some members that can constitute much of the moment-to-moment interaction with
other family members. This interplay stems from the more stable schemas that serve
as the foundation for the family’s functioning (Dattilio, 2010). When this cycle
involves negative content that affects cognitive, emotional, and behavioral responses,
the volatility of the family’s dynamics tends to escalate, rendering family members
vulnerable to a negative spiral of conflict. As the number of family members increases,
so does the complexity of the dynamics, adding more fuel and intensity to the
escalation process.
One of the important aspects of cognition with families pertains to the concept
of schema. The concept of schema has become the cornerstone of contemporary
CBFT (Dattilio, 1993, 2001a, 2005a, 2010). Family members’ perceptions of each
other’s interactions provide the information that shapes the development of their
family schemas, especially when an individual member observes such interactions
repeatedly. The pattern deduced by an individual from such observation serves as
a basis to form a schema, or a template, that is subsequently used to understand
the world of family relations and to anticipate future events. Family schemas are a
subset of a broad range of schemas that individuals develop about many aspects of life
experiences.
The Development of Family Schemas
The development and operation of schemas in family systems are similar to those
in individuals and couples and are predicated on prior and current life experiences
as perceived by each family member. It was the pioneering family therapist Virginia
Satir (1967) who wrote years ago that, “The parents are the architects of the family”
(p. 83). CBFT embraces the concept and posits that the schemas and life experiences
that a couple brings to a relationship are transmitted to their offspring and shape
the family constellation (Dattilio, 1998). For example, a couple who share the belief
that “parents should never argue in front of the children for fear of the negative
effect it may cause” may contribute to a child’s belief that parents should rarely
experience conflict. Parents’ beliefs certainly have an effect on how their offspring
perceive and interpret various life events, and they contribute greatly to a child’s
conceptualization of the world. The notion of schema, as applied to families, may
explain some of the dynamics that constitute core beliefs and how these beliefs
affect emotion and behavioral patterns with family interactions (Dattilio, 1993).
The term “family schema” is highlighted more clearly in the recent literature by
Dattilio (1998, 2001a). The concept entails stable, entrenched longstanding beliefs
that family members jointly hold about family life. Shared schemas evolve within the
marital relationship and eventually contribute to what Dattilio (1993, 1998) refers
to as “joint family schema.” It is these schemas that serve as a template for family
members in their functioning within the family unit. Schemas can be a helpful guide
for family members in navigating complex aspects of family life, but when they are
extreme or distorted, they can contribute to family conflict. In essence, elements such
as core and basic beliefs are structures that are contained within schemas that give rise
to one’s assumptions, perceptions, and personal theories of life. Myths emerge out of
schemas that individuals develop, as well as certain standards and attributions made
about self and others and expectations. In a sense, schema becomes a superordinate
or umbrella construct that comprises all of the above.
Some schemas are based on misperception since sometimes perceptual bias may
occur, depending on the course of the person’s experience with his or her family
members. These biases include:
1. selective attention: the tendency of family members to notice only certain aspects
of the events occurring in relationships and to overlook others (e.g., a sister
focusing on her brother’s statements and ignoring his actions);
2. attributions: inferences about the factors that have influenced a family member’s
actions (e.g., concluding that a parent failed to respond to a question because he
or she wants to control the relationship);
3. expectancies: predictions about the likelihood that particular events will occur in
the relationship (e.g., that expressing feelings to one’s family members will result
in the parents becoming angry);
4. assumptions: beliefs about the general characteristics of people and relationships
(e.g., a mother’s assumption that her children never respect authority);
5. standards: beliefs about the characteristics that people and relationships “should”
have (e.g., a parent’s belief that families should have no boundaries between
them, sharing all of their thoughts and emotions with each other).
To the extent that the family schema involves cognitive distortions, it may result
in dysfunctional interactions. Schemas further influence how family members sub-
sequently process information in new situations. For example, they may influence
what the individual selectively perceives, the inferences he or she makes about
the causes of another’s behavior, and whether he or she is pleased or displeased
with the family relationship. Existing schemas may often be difficult to modify and
require a great deal of effort in restructuring. Schemas usually only change when
there is enough new powerful information that serves to modify a family member’s
beliefs.
Cognitive Distortions with Family Members
Just as in the case of individuals, families are prone to engaging in cognitive distortion.
These distortions typically emanate from belief systems held not only by family
members, but families as a whole. These include:
1. arbitrary inference: Conclusions are made in the absence of substantiating

evidence. For example, parents whose teenager arrives home a half-hour beyond
her curfew conclude, “She’s up to no good again.”
2. selective abstractions: Information is taken out of context and certain details are
highlighted while other important information is ignored. For example, a man
Family Therapy 733
whose wife responds to his questions with one-word answers concludes, “She’s
mad at me.”
3. overgeneralization: An isolated incident or two is allowed to serve as a represen-
tation of similar situations everywhere, related or unrelated. For example, when
a parent declines a child’s request to go out with his friends, he concludes, “You
never let me do anything.”
4. magnification and minimization: A situation is perceived as more or less
significant than is appropriate. For example, an angry husband “blows his top”
upon discovering that the checkbook is not balanced and says to his wife, “We’re
in big trouble.”
5. personalization: External events are attributed to oneself when insufficient
evidence exists to render a conclusion. For example, a mother who finds her son
adding heavy amounts of ketchup to his dinner assumes, “He hates my cooking
and has to disguise the taste.”
6. dichotomous thinking: Experiences are codified as either black or white, a
complete success or a total failure. This is otherwise known as polarized think-
ing. For example, when a mother is reorganizing her daughter’s closet and
the daughter protests, the mother thinks to herself, “She’s destined to be a
slob.”
7. labeling and mislabeling: One’s identity is portrayed on the basis of imperfections
and mistakes made in the past, and these are allowed to define oneself. For
example, subsequent to the children’s resistance to completing their chores, a
mother concludes, “These kids expect me to be their maid.”
8. tunnel vision: Sometimes family members only see what they want to see or what
fits their current state of mind. A man who believes that his wife and children
“do whatever they want” may conclude that his voice carries no weight in the
family.
9. biased explanations: This is a type of thinking that family members develop
during times of distress and automatically assume that other family members
hold a negative alternative motive behind their intent. For example, a son may
say to himself, “My parents don’t let me go out because they want me to do
their chores.”
10. mind reading: This is the magical gift of being able to know what another
person is thinking without the aid of verbal communication. Some spouses end
up ascribing unworthy intentions to each other. For example, a man may think
to himself, “I know what is going through my wife’s mind; she thinks that I am
naive about how much she is spending.”
Schema Restructuring
Schema restructuring involves the reworking of misperceptions and distorted thinking

that occur among family members. It also explores and makes use of family-of-origin
and early life experiences of parents and how this trickles down to affect the family
members in the immediate family (Dattilio, 2006b). This also involves the notion
of addressing issues of attachment and emotional regulation. Hence, maladaptive
schemas regarding issues of attachment and bonding, boundaries, fairness, power,

and control are all fair game for working with families in conflict. Many of these
maladaptive schemas develop early within the nuclear family and tend to strengthen
and become more resistant to change as time progresses.
Focus is placed on the core themes that reflect on the family relationship dynamics.
By addressing these themes in an analytic and structured fashion, family therapists
help families to make sense of conflict, marital gridlock, and dysfunctional interaction
patterns that contribute to relationship problems. The use of education and direct
confrontation helps family members to become aware of their thinking and behavior
and to take effective action toward changing them. The therapist also works as an
agent to identify enabling factors in the spouse, parents, or other family members,
that may be serving to keep these behavioral patterns active.
Identifying Automatic Thoughts and Cognitive Distortions
Automatic thoughts are another form of cognition in CBFT that is sometimes

confused with schema. This is particularly since there is some overlap between the two
terms. Identifying automatic thoughts with families involves superficial or moment-
to-moment thoughts that family members present during the course of assessment
and treatment. These conscious automatic thoughts provide a pathway to uncover
underlying beliefs and schemas that carry more significant weight with regard to
family conflicts. Therefore, a parent who may have difficulty tolerating expressions
of disregard by his or her children might experience the automatic thought, “These
kids just don’t care about anything.” This may stem from an underlying belief or
schema that children of today have an air of entitlement and, consequently, maintain
a carefree attitude about life in general.
Sometimes cognitions can also occur beyond an individual’s level of conscious
awareness. The more expansive underlying schemas are typically revealed through
a family member’s automatic thoughts. However, not all automatic thoughts are
expressions of schemas. Some automatic thoughts may express a family member’s
attributions about causes of an event that he or she has observed (e.g., “My daughter
didn’t bother to call home and inform me that she would be late. Her friends are
more important than the family”).
Undoubtedly, schemas are essential in the application of CBFT. They tend to
be stable cognitive structures as opposed to fleeting inferences or perceptions.
Consequently, they are typically more difficult to modify and are differentiated
from perceptions (what one notices or overlooks in the environment) and from
inferences (attributions and expectancies) that a family member draws from the event
that he or she notices. While dealing with individual family members’ thoughts is
central to cognitive behavioral therapy, dealing with the joint family schemas is crucial
as well. It should be mentioned, however, that the cognitive behavioral theory does
not suggest that cognitions cause all family members’ behavior; however, it does
stress that the cognitive appraisal significantly influences family members’ behaviors,
interactions, and emotional responses to one another (Epstein et al., 1988; Wright &
Beck, 1993).
Family Therapy 735
Addressing Family-of-Origin Schemas
While individual family members maintain their own basic beliefs about themselves,
the world, and their future, they also develop schemas about characteristics of their
family-of-origin, which are commonly generalized to some degree to conceptions
about other close relationships. It has been suggested in the past that greater
emphasis should be placed on examining not only cognitions of individual family
members, but also the family schema (Bedrosian & Bozicas, 1994; Dattilio, 1993,
2005a). Many of these schemas trickle down from the parents’ families-of-origin
and it is important to investigate, particularly when underlining the strength of such
schemas to family members. Although family schemas typically constitute jointly held
beliefs about most family phenomena, such as day-to-day dilemmas and interactions,
they may also pertain to nonfamily phenomena, as well as other issues, such as cultural
and spiritual matters. Most family schemas are shared; however, individual family
members may sometimes deviate from the joint schema.
The family-of-origin of each parent in the family relationship plays a crucial role
in the shaping of the current shared family schema (Dattilio, 1993). The beliefs
developed in each parent’s family-of-origin may be either conscious or beyond a
conscious awareness, and whether or not they are explicitly expressed suggests how
they may contribute to the joint family schema (see Dattilio, 2010, for a more
expansive discussion).
Schemas are often at the heart of family conflicts (Dattilio, 2005a). It is for this
reason that they should be addressed during the early phase of treatment while the
assessment phase is still ongoing. One of the guidelines used for assessing schema
from family-of-origin is Richard Stuart’s Family of Origin Inventory (1995). This
will be discussed in more detail under the section heading of “Clinical Assessment
of the Family.” These schemas may be ingrained because they are deeply rooted in
experiences from one’s family-of-origin, depending on the circumstance and these
schemas pose as a significant challenge for therapists in treatment. They are also likely
to be culturally based and imposed early in one’s formative years, rendering them
more resistant to modification and change (Dattilio & Bahadur, 2005).
Belief systems that hail from one’s family-of-origin have usually been strongly and
consistently reinforced and have been internalized during key formative periods of
life (Dattilio, 2006b). A classic example is a father whose schema from his family-of-
origin is that fighting and arguing among parents leads to separation and divorce and,
therefore, must be avoided at all costs. Consequently, he may bend over backwards
to appease his wife and child in order to avoid intrafamilial conflict for fear that
this will break up the family. This has a trickle-down effect to the offspring who
views the father’s role as passive and may respond in one of two ways. The child
may respond to overcompensate for father’s passivity by being more aggressive and
arguing with his mother. On the other hand, this child could choose a different
posture and remain passive, much like his father, but then resent it and engage
in passive-aggressive behaviors, or even develop depression, which may cause other
problems in the family. Therefore, addressing such schemas and modifying behaviors
within the family dynamics is essential in order to incur change.
Parents and other primary caregivers have a very powerful effect on the development
of children’s belief systems, particularly when these beliefs are conveyed in the
context of strong cultural underpinnings. Such schemas, as mentioned above, may be
communicated from parents to children in a variety of ways, either directly via specific
statements or more subtly through children’s observations of interactions within the
family dynamics.
Clinical Assessment of the Family
One of the most critical aspects in assessing family dysfunctioning is case conceptual-
ization. Much of the success of treatment rests on the accuracy of careful investigation
and assessment procedures. Therefore, the use of extensive interviewing, self-report
questionnaires, and the therapist’s behavioral observation of family interactions and
dynamics are essential modes of clinical assessments (Schwebel & Fine, 1994; Dattilio,
2005b). The more specific goals of assessment are to identify strength and problem-
atic characteristics of the family and the environment, as well as to place current
family functioning in the context of its developmental stages and changes. Addition-
ally, identifying cognitive, affective, and behavioral aspects of family interactions is
essential, particularly in determining targets of intervention. While the description
of assessment in this chapter is limited, the reader is directed to a more extensive
coverage of procedures in Schwebel and Fine (1994) and Dattilio (2010).
Unlike when working with couples, family therapists typically do not separate family
members unless there are specific reasons. For example, sometimes families enter into
treatment circuitously, in which parents will come to a therapist’s office because they
are experiencing difficulty with their teenage son or daughter who refuses to submit
for therapy. Therefore, in such cases exceptions have to be made; however, most of
the time it is advantageous for therapists to see families together. It should be noted
that cognitive behavioral therapists deviate from traditional therapists who insist that
everyone attends in order for therapy to begin. Sometimes this simply is not realistic
and modifications have to be made. The therapist can focus on engaging with those
members who are motivated to attend and later work with engaging absent members.
Cognitive behavioral therapists make the assumption that the difficulties that a family
presents in ensuring all members’ attendance may be a sample of broader problematic
dynamics. Thus, from the initial contact, a therapist is observing the family process
and formulating a hypothesis about patterns that may be contributing to the family’s
overall dysfunction.
Traditionally, family therapy has been characterized by a noted division between
assessment and the actual delivery of therapy (Cierpka, 2005). Traditional family
therapy involves basic information gathering and only a superficial understanding of
the relationship dynamics.
During the initial family interview, therapists may begin to probe family members’
cognitions regarding the reasons for seeking assistance at this particular time and
whether or not a crisis may have brought them into therapy. The therapist should
probe each family member about their individual perspective on the particular concerns
Family Therapy 737
and about any changes that each member believes should be made in order to make
family functioning more satisfying.
Another area to focus on is what works well in the family functioning and what
might account for times when the family functions in a productive, cohesive fashion.
Learning about what works in the family often provides the family therapist with
vital information about what does not work well. In addition, therapists should also
familiarize themselves with the family members’ “dance,” or as the systems theorists
say, “obtaining a good handle on how the systems function within this particular
family structure and how power and control are balanced.” Developing insight into
what makes the family “tick” and how they deal with crisis and conflict are all grist for
the therapeutic mill, allowing us to see what contributes to the system’s dysfunction.
It is also very important to note that the assessment actually continues throughout
the course of treatment and is not limited to the initial visit. Even though an initial
phase of assessment may appear to be the formal inquiry, the assessment continues,
even until the end of the treatment process, since the therapist will always be
discovering new information about the family and this may change or modify the
course of therapy. Consequently, a good clinician continues to reappraise the situation
long after treatment is underway.
The Use of Inventories and Questionnaires

One of the aspects of CBFT that sets it aside from other family therapies is the use
of standardized questionnaires in gathering information on family members and their
relationships. This is often particularly helpful to a therapist who may be limited in
time; but, more importantly, it is helpful in many ways since it provides structured
questions about aspects of the family dynamics about which the therapist may not
think to ask. These questionnaires and inventories may be distributed during the initial
meeting and family members may be asked to complete them without collaborating.
There are a variety of measures that have been developed specifically to provide
an overview of key aspects of family functioning, particularly in the areas of overall
satisfaction, family cohesion, quality of communication, decision-making values, and
level of conflict. Some examples include, as mentioned earlier, the Family of Origin
Inventory (Stuart, 1995), which is a comprehensive inventory that allows parents to
describe how the experiences of their respective families-of-origin influenced their
lives, marriages, and immediate family. Other measures include the Family Environ-
ment Scale (Moos & Moos, 1986), the Family Assessment Device (Epstein, Baldwin,
& Bishop, 1983), and the Self-Report Family Inventory (Beavers, Hampson, &
Hulgus, 1985). Since items on some of these scales do not provide specific infor-
mation about each family member’s cognitions, emotions, and behavioral responses
regarding the relationship problems in the family, the therapist must inquire further
about this aspect during interviews. These inventories may serve as something of a
guideline for gathering more accurate information. It can also help to identify areas of
strength and concern, and to understand types of positive and negative interactions
that affect the family’s functioning. It should also be noted that some family members
may be more likely to report concerns on questionnaires as opposed to doing so
verbally during the family interviews.
Behavioral Observations and Change

Due to the limitations of self-report inventories, it is extremely important for family
therapists to observe samples of family members’ interactions directly. Joining the
family is a very important aspect for therapists in that they become intrinsically
involved with the family process, even during the course of therapy. The therapist
may become adept at noticing the process of verbal and nonverbal behaviors between
family members as they talk to one another and to the therapist. Part of the goal of
behavioral observation is to identify specific behavioral patterns by each individual
family member and the sequence of acts among the family as a whole that are either
constructive and pleasing or destructive and aversive. The identification of family
members who tend to be more spontaneous, as opposed to others who fade into the
background, is often quite telling with regard to family dynamics. One of the benefits
of imposing very little structure in family therapy is the ability to sample the family’s
communication in natural ways within the office setting. In this manner, the therapist
can pinpoint where a significant amount of dysfunction may be occurring. Therapists
may also elect to use some behavioral rating scales if they feel that it is important to
track family members’ interaction in a more analytic fashion.
One excellent way to observe what happens within families is to instruct the mem-
bers to engage in problem-solving discussions during the course of a session. During
such discussions, the therapist can actually observe the difficulties in communication,
as well as problem solving. Depending on the posture that the therapist chooses, he
or she may become more directive in the process and focus on certain interventions or
remain more passive in his or her observation. A good example of this is that parents
may complain that a teenage child rarely expresses his or her feelings; but, through
observation, the clinician may notice that whenever the child does express his or her
feelings, the parents either turn away or overtly cut him or her off and deny the child’s
feelings by making a disparaging comment. Such circular causal processes in family
interactions are obviously observed when a clinician notes how one family member’s
behavior provokes the others and vice versa. This clearly has a noticeable effect on the
family’s dynamics. Hence, the therapist can then acknowledge destructive patterns
that may be contributing to the problems in the family.
Assessing Cognitions
Family interviews also involve providing opportunities to elicit idiosyncratic cog-

nitions and to track influential processes that cannot be assessed by standardized
questionnaires. Socratic questioning is one method that involves a series of systematic
questions that are used to chip away at individual family members’ defenses during
both the exploration and/or assessment phase and at the beginning of treatment. This
technique helps the family therapist to piece together a chain of thoughts that medi-
ate between events and relationships and each individual’s emotional and behavioral
responses. An approach that uses Socratic questioning involves a technique known
as the “downward arrow,” developed by Beck, Rush, Shaw, and Emery (1979). This
technique was developed to uncover the underlying assumption of a family member
Family Therapy 739
that generates dysfunction or distorted thoughts. The downward arrow technique

identifies the initial thought and then follows it with questions, such as, “If so, then
what?” Assessing cognitions of this type is very important in family treatment. Also,
aiding them in determining distortions in their thoughts and labeling them, as men-
tioned earlier in this chapter, is essential. Teaching family members how to identify
automatic thoughts and associated emotions and behavior is a crucial requisite for
modifying family members’ distortions and extreme cognitions about themselves and
their family.
After a period of psychoeducation, in which the therapist educates families about
the model of treatment, the concept of automatic thoughts is addressed, along with
coaching family members in observing their own patterns of thought during sessions
that are associated with negative emotional and behavioral responses to one another.
Monitoring one’s subjective experiences is a skill that can be acquired and improved
with assistance from the therapist. In order to achieve this goal, family members
are typically asked to keep small notebooks handy between sessions and jot down
brief descriptions of circumstances in which they feel distressed about their family
relationship or conflict. In today’s age, members may be more inclined to rely on
their smartphones or MP3 players in order to keep this log, along with the description
of automatic thoughts that enter their minds, as well as the resulting emotional and
behavioral response toward one another. A modified version of the Daily Record of
Dysfunctional Thoughts (Beck et al., 1979) is utilized for this purpose. This can also
be uploaded into their smartphones or MP3 players.
Through this type of record keeping, the family therapist is able to demonstrate to
family members how their automatic thoughts are linked to emotional and behavioral
responses and to help them concentrate on specific themes, such as boundary issues
or other misperceptions that upset them in the relationship. This procedure also
increases awareness that negative emotions and behavioral responses that family
members have toward each other are controllable through systematic examination of
the cognition associated with them. Having family members review their logs and
identify the links among thoughts, emotions, and behaviors can be quite helpful.
Asking each family member then to explore alternative cognitions that might produce
different emotional and behavioral responses gives rise to discussion about these
aspects.
Identifying Cognitive Distortions and Documenting Them
Family members are eventually trained to become adept at identifying the types
of cognitive distortions involved in their automatic thoughts that create difficulties
for them. A primary exercise is to have each family member refer to the list of
cognitive distortions and labeling, along with any automatic thoughts that they
experienced during the past week. The therapist can discuss with family members
any aspects of the thoughts that were inappropriate or extreme, and whether the
distortion contributed to any negative emotions and behaviors at the time. Doing
this in session and reviewing the written logs over the course of time can increase
awareness, along with their skills, in identifying and evaluating such distorted beliefs
and correcting them.
In the event that the family therapist believes that the family members’ cognitive
distortions are associated with any form of specific psychopathology, such as depression
or a thought disorder, this can be addressed further and a referral can be made for
individual treatment.
Testing and Reinterpreting Automatic Thoughts
The process of restructuring automatic thoughts involves the individual considering

alternative explanations. Examining evidence concerning the validity of a thought,
its appropriateness for his or her family situation, or both, is an essential part of
the treatment process, and may contribute to different emotional and behavioral
responses to other family members. The following questions, taken from Dattilio and
Epstein (2005), are commonly used as a guideline for family members in examining
their thoughts:
• From your past experiences or the events occurring recently in your family, what
evidence exists that supports this thought? How could you get some additional
information to help you judge whether or not your thought is accurate?
• What might be an alternative explanation for your family member’s behavior?
What else might have led your family member to behave that way?
• We have reviewed several types of cognitive distortions that can influence a
person’s views of other family members and can contribute to getting upset with
them. Which cognitive distortions, if any, can you see in the automatic thoughts
that you just experienced? (p. 35)
An example of this might be an adolescent girl who believes that her older sister
who refuses to lend her one of her outfits is jealous of her and enjoys restricting her,
not allowing her to gain attention from her peers. An automatic thought might be,
“She is too conceited to let me use any of her things, but yet she always wants to
borrow my stuff. She doesn’t care how I feel.”
The therapist may subsequently coach her in identifying that she might have been
engaging in the “mind reading” distortion and that it might be important for her to
gather more information from her sister by addressing the issue in a nonemotional
way in order to see whether that is really her sister’s intention or whether there is
something else going on. Gathering and weighing the evidence for one’s thoughts is
an integral part of the work done in family therapy. Family members are able to provide
valuable feedback that will help each other evaluate the validity or appropriateness of
their cognitions as long as they use good communication skills, which are described
later in this chapter. After a family member challenges his or her thoughts or beliefs,
he or she is then asked to rate his or her belief from 0 to 100 on the “Alternative
Explanations” section of the Dysfunctional Thought Record. Often, revised thoughts
may not become assimilated unless they are considered credible and implemented by
family members.
Family Therapy 741
Behavioral Experiments
The use of behavioral experiments is a very popular concept in CBFT in that it

allows family members frequently to test predictions that might not be true. The
use of logical analysis to reduce family members’ expectancies concerning certain
events may not be forceful unless they have firsthand evidence to substantiate it.
Consequently, cognitive behavioral therapists often guide family members in devising
what are referred to as “behavioral experiments” in which they test their predictions
that a particular action will lead to certain responses from other family members. An
example of this might be a youth who holds the expectancy that his parents and
siblings will think that his suggestion for a family vacation will be viewed as stupid
and be rejected by other family members might try to make plans to bring this up
during a family mealtime and see what happens. When these plans are devised during
joint family therapy sessions, the therapist can ask the other family members what
they predict the responses might be during such an experiment. Family members
can anticipate potential obstacles to the success of the experiment and appropriate
adjustments can be made. In addition, the therapist can examine what evidence the
youth had for anticipating that his idea may be rejected.
Role Play Techniques
Family members sometimes also find it helpful to switch roles during role playing
exercises in order to increase empathy for each other’s experiences within the family.
Sometimes, having an adolescent play the role of his parent, and allowing him to
express how he feels the parent should handle certain things, may help the family
gain greater insight into his perceptions and why they are or are not inappropriate or
unrealistic. Having fun with techniques like this often lightens the family atmosphere
and allows family members to see their roles from different perspectives. This technique
should not be used until the therapist feels confident that the family members will be
able to process their strong emotional responses and refrain from abusive behaviors
toward each other.
Interventions Used to Modify Behavioral Patterns
There are a number of interventions that are used to modify family members’
behavioral patterns. The most common include communications training, problem-
solving strategies, and behavioral change agreements.
Communications Training
Communications training and the improvement of family members’ skills in expressing
thoughts and emotions, as well as learning to listen effectively to each other, are
very important aspects of family therapy. This intervention can have an indelible
impact on problematic behavioral interactions, reduce family members’ distorted

cognitions about one another, and contribute to regulated experiences and expression
of emotions. Presentation of specific instructions to family members about the specific
behaviors in each type of expressive and reflective skill is part of the didactic aspect
of therapy. Guidelines for speakers and listeners are provided and may involve
specific training during family sessions. The use of such strategies as the “Pad and
Pencil Technique” (as described in detail later) may be very helpful to limit the
amount that family members interrupt each other during heated exchanges (Dattilio,
2001b).
The therapist him- or herself may serve as a good role model for expressive and
reflective skills. Coaching family members in using these guidelines, beginning with
discussions or relatively benign topics and working their way up to more substantive
topics, is part of the process. It is important to start with more benign topics so that
negative emotions do not interfere with the constructive development of skills and,
as the family members improve their skills, more emotionally charged issues can be
addressed and processed.
Family members are also asked to practice these skills as homework assignments
with increasingly conflictual topics. As these communication skills are practiced and
more information surfaces about family members’ motives and desires, important
issues can be processed during the course of treatment. Following such guidelines
also increases family members’ perceptions that the others are more respectful and
have better intentions than might have been expected.
Reducing interruptions in communications among family members is often an area
that therapists need to address directly in treatment. Therapists are almost certain to
encounter family members who aggressively interrupt each other as they attempt to
tell their own versions of a particular incident or express their emotions. While such
interruptions are not necessarily all bad, sometimes they can be very intrusive and
prevent progress being made during the course of treatment. For this reason, such
techniques as the “Pad-and-Pencil Technique,” developed by Dattilio (2001b), may
be extremely helpful. This involves providing each family member with a pen and
a notepad and asking them to write down their automatic thought or their urge to
interfere when another family member is speaking. In this manner, they can record
the automatic thought and accompanying emotion and refer to it later when their
turn comes to constructively confront the other family member. This intervention is
often successful in helping each family member remain occupied and engaged as each
silently listens to the other members speak. This also dramatically reduces the amount
of disruption during the course of the sessions.
Problem-Solving Training
The use of verbal and written instructions for problem-solving training, along with
modeling and behavioral rehearsal and coaching, can facilitate effective problem
solving with family members. There are a number of steps that can be followed in
problem-solving training. These steps are outlined in more detail in Dattilio (2010).
It is essential to agree on a trial period for implementing designated solutions
and assessing their effectiveness. Once again, the use of homework practice for the
Family Therapy 743
development of problem-solving skills is important (Kazantzis, Deane, Ronan, &

L’Abate, 2005).
Behavior Change Agreements

Sometimes the use of contracts is necessary in order to agree the exchange of desired
behavior among family members. Every attempt is made to avoid making one family
member’s behavior change contingent on the others. However, the more realistic goal
may be for each person to identify and enact specific behaviors that would be likely
to please other family members regardless of what actions the other members take.
Sometimes, however, this cannot be avoided and the mere agreement of exchange may
be crucial in facilitating the modification of conflict. Every attempt should be made,
however, to avoid encouraging family members to “stand on ceremony” and wait for
others to behave positively before they engage in positive behaviors themselves. Such
agreements may be helpful in reducing propensities for family members to engage in
standoffs with each other.
De-escalation and Time Out
Teaching family members to de-escalate potentially volatile situations is often a very

difficult, yet important task for the family therapist. Many members find themselves in
the throes of emotionally charged situations in which they act out behaviorally. The
use of deep breathing techniques and restructuring exercises as a means of inoculating
themselves against future outbursts can be extremely helpful. “Time out” procedures
can be very effective. Having family members remove themselves and then return and
address the issue can sometimes make a huge difference. For example, the therapist
could suggest that family members make the sign of a “T” with both hands to indicate
that they need a “time out.” They should also all agree in advance that no one will
exploit the use of the time out procedure, but will use it only when legitimately
needed as a reprieve. This often helps to break up the momentum of an agitated
exchange that could, in some cases, lead to a very destructive interaction.
Behavioral Rehearsal
Subsequent to training and feedback from the therapist, family members often need to
refer to specific skills. This can initially occur through verbal coaching and modeling
during the therapy process. Such practice sessions have traditionally been referred to
as “behavioral rehearsal,” which starts in the therapy session and gradually generalizes
to the family’s environment. This is typically one of the most essential aspects of the
treatment sequence because it provides feedback to the therapist regarding the extent
to which couples and family members have understood what they have learned and
can demonstrate how it should be implemented. The actual practice is what galvanizes
the change and contributes to becoming a permanent fixture. Behavioral rehearsal
can be considered, in one sense, a “shaping process” in which both the therapist and
family members learn to adopt a new way of interaction. This is often considered a
form of enactment in which the change process occurs directly in a therapy session
and then, of course, is encouraged to continue outside of the session.
Homework Assignments
The use of homework, or out-of-session assignments, is not a new development in

the field of psychotherapy and has been used by other modalities for years. Home-
work assignments are a major part of the armamentaria of therapeutic techniques,
particularly when working with families. In fact, cognitive behavioral family therapists
have identified homework assignments as a cornerstone of treatment in family therapy
(Dattilio, 1998, 2002; Schwebel & Fine, 1994). Research in family therapy has also
indicated that homework assignments are crucial for change in this context (Dattilio,
Kazantzis, Shinkfield, & Carr, 2011). Homework serves to keep the therapy session
alive during the interim period and promotes a transfer from therapy sessions to
day-to-day living. In essence, homework helps to galvanize what is learned during the
therapy process.
Practice serves to heighten awareness of various issues that have unfolded during
the course of treatment. These assignments can increase the expectations for family
members to follow through with making changes rather than simply discussing change
during the course of therapy and then not following through at home.
There are various types of homework assignments used with families. Some of
the more common involve activities scheduling, biblio- or video therapy assign-
ments, self-monitoring, behavioral task assignments, and/or cognitive restructuring
of dysfunctional thoughts.
Interventions for Deficits and Excesses in Emotional

Responses
Despite the fact that CBT is sometimes characterized as neglecting or downplaying

the emotional component of treatment, this is actually misleading. There are a
variety of interventions that can be used either to enhance the emotional experience
of inhibited family members or to moderate extreme responses. Family members
sometimes report experiencing little emotion. In these cases, the therapist may want
to set clear guidelines for behavior within and outside of the therapy sessions for
family members to express themselves in a way that will not lead to recrimination by
other members.
Some of the techniques mentioned previously, such as downward arrow ques-
tioning, may be used to inquire about underlying emotions, as well as cognitions.
Coaching family members in noticing internal cues to their emotional states is
also helpful, along with repeating phrases that have an emotional impact on family
members. Helping family members refocus their attention on emotional aspects is
Family Therapy 745
often extremely important during the course of treatment. Engaging family members
in role play concerning important relationship issues in order to elicit emotional
responses is sometimes crucial in encouraging emotions to flow appropriately in
therapy.
Sometimes family members will experience intense emotions that affect them and
significant others adversely. In this manner, the therapist can help them compartmen-
talize emotional responses by scheduling specific times to discuss distressing topics
and coach them in self-soothing activities such as relaxation techniques. These activ-
ities help to improve family members’ abilities to monitor and challenge upsetting
automatic thoughts. They also help to encourage family members to seek social sup-
port from family and others and develop their ability to tolerate distressing feelings.
Enhancing a family member’s skills in expressing emotions constructively so that
others will notice is also an important aspect of treatment. Training techniques and
emotional regulation, as well as tolerance building, are also significantly helpful when
working with particularly volatile families.
The Effectiveness of Cognitive Behavioral Therapy with

Families
CBFT has grown exponentially within the past several decades among family therapists
who use it as either a straightforward approach within a system perspective or
integrated into other approaches with couples and family therapy. While in the past
the CBFT approach has focused mostly on the treatment of specific disorders in
individual members rather than on alleviating general conflicts and distress in family
constellations, it has more recently been used as a general approach to treating
families. Forms of CBFT have chosen to highlight some of the demonstrated efficacy
of the behavioral aspect, which involves training parents in behavioral interventions
for their children’s anxiety or conduct disorders, or addressing issues of attention-
deficit/hyperactivity disorder, as well as other behavioral problems. These problems
may involve addressing core symptoms of inattention, impulsivity, hyperactivity, and
even psychiatric conditions.
As noted earlier, methods of CBFT have been used in conjunction with other
interventions, particularly in addressing the issue of schema and restructuring thought
processes among family members who are in conflict. Results of various studies that
have been conducted indicate that CBFT interventions are very effective in improving
family functioning.
The CBFT approach has gained widespread adoption among family therapists
across the globe who have found the basic approach to be easily integrated with other
modalities, and also to provide an effective mechanism for restructuring maladaptive
thinking patterns and dysfunctional behaviors. The unique aspect of CBFT is that it
clearly embraces issues of attachment and emotional regulation, as well as maintaining
an overall respect for the neurobiological functioning of human beings. CBFT is
featured in all of the primary family therapy textbooks used within university graduate
school training programs, as well as in medical school residency curriculums.
It should also be noted that in some of the more recent surveys conducted among
couples and family therapists, clinicians have designated their primary treatment
modality as being CBFT, while respondents who use other approaches have stated
that they use cognitive behavioral techniques in combination with other methods
of treatment (Psychotherapy Networker, 2007; Northey, 2002). As a result, the
cognitive behavioral approach, in one form or another, will likely continue to
be one of the more espoused treatment modalities among couples and family
therapy.
References
Alexander, J. F., & Parsons, B. V. (1982). Functional family therapy. Monterey, CA:
Brooks/Cole.
Alexander, P. C. (1988). The therapeutic implications of family cognitions and constructs.
Journal of Cognitive Psychotherapy, 2, 219–236.
Barkley, R. A. (1997). ADHD and the nature of self-control. New York, NY: Guilford Press.
Barton, C., & Alexander, J. F. (1981). Functional family therapy. In A. S. Gurman &
D. P. Kniskern (Eds.), Handbook of family therapy (pp. 403–443). New York, NY:
Brunner/Mazel.
Beavers, W. R., Hampson, R. B., & Hulgus, Y. F. (1985). The Beavers systems approach to
family assessment. Family Process, 24, 398–405.
Becvar, D. S., & Becvar, R. J. (2009). Family therapy: A systemic integration (7th ed.). Boston,
MA: Allyn & Bacon.
Bedrosian, R. C. (1983). Cognitive therapy in the family system. In A. Freeman (Ed.), Cognitive
therapy with couples and groups (pp. 95–106). New York, NY: Plenum Press.
Bedrosian, R. C., & Bozicas, G. D. (1994). Treating family of origin problems: A cognitive
Bird, V., Premkumar, P., Kendall, T., Whittington, C., Mitchell, J., & Kuipers, E.
(2010). Early intervention services, cognitive-behavioural therapy and family inter-
vention in early psychosis: Systematic review. British Journal of Psychiatry, 197 ,
350–356.
Birmaher, B., Brent, D. A., & Kolko, D. (2000). Clinical outcome after short-term psychother-
apy for adolescents with major depressive disorder. Archives of General Psychiatry, 57 ,
29–36.
Bitter, J. M. (2009). Theory and practice of family therapy and counseling. Belmont, CA:
Brooks/Cole, Cengage Learning.
Brent, D. A., Holder, D., & Kolko, D. (1997). A clinical psychotherapy trial for adolescent
depression comparing cognitive, family and supportive therapy. Archives of General
Chambless, D. L. (2012). Adjunctive couple and family intervention for patients with anxiety
disorders. Journal of Clinical Psychology, 68, 548–560.
Chronis, A. M., Chacko, A., Fabiano, G. A., Wymbs, B. T., & Pelham, W. E., Jr., (2004).
Enhancements to the behavioral parent training paradigm for families of children with
ADHD: Review and future directions. Clinical Child and Family Psychology Review, 7 ,
1–27.
Family Therapy 747
Cierpka, M. (2005). Introduction to family assessment. In M. Cierpka, V. Thomas, & D. H.

Sprenkle (Eds.), Family assessment: Integrating multiple clinical perspectives (pp. 3–14).
Cambridge, MA: Hogrefe.
Dadds, M. R., Barrett, P. M., Rapee, R. M., & Ryan, S. (1996). Family process and child
anxiety and aggression: An observational analysis. Journal of Abnormal Child Psychology,
24, 715–734.
Dadds, M. R., & Salmon, K. (2003). Punishment insensitivity and parenting: Temperament
and learning as interacting risks for antisocial behaviour. Clinical Child and Family
Dattilio, F. M. (1983). The use of operant techniques and parental control in the treatment
of pediatric headache complaints: Case report. Pennsylvania Journal of Counseling, 1,
Winter, 55–58.
Dattilio, F. M. (1989). A guide to cognitive marital therapy. In P. A. Keller & S. F. Heyman
(Eds.), Innovations in clinical practice: A source book (Vol. 8, pp. 27–42). Sarasota, FL:
Professional Resource Exchange.
Dattilio, F. M. (1993). Cognitive techniques with couples and families. Family Journal, 1,
51–56.
Dattilio, F. M. (1998). Case studies in couples and family therapy: Systemic and cognitive
perspectives. New York, NY: Guilford Press.
Dattilio, F. M. (2001a). Cognitive-behavior family therapy: Contemporary myths and miscon-
ceptions. Contemporary Family Therapy, 23, 3–18.
Dattilio, F. M. (2001b). The pad and pencil technique. In R. E. Watts (Ed.), Favorite
counseling techniques with couples and families (Vol. 2, pp. 45–47). Alexandria, VA:
American Counseling Association.
Dattilio, F. M. (2002). Homework assignments in couple and family therapy. Journal of
Dattilio, F. M. (2005a). Restructuring family schemas: A cognitive behavioral perspective.
Journal of Marital and Family Therapy, 32, 15–30.
Dattilio, F. M. (2005b). Clinical perspectives on involving the family in treatment. In J. L.
Hudson & R. M. Rapee (Eds.), Psychopathology and the family (pp. 301–321). London,
England: Elsevier.
Dattilio, F. M. (2006a). Case-based research in family therapy. Australian and New Zealand
Journal of Family Therapy, 27 , 208–213.
Dattilio, F. M. (2006b). Restructuring schemata from family-of-origin couple therapy. Journal
of Cognitive Psychotherapy, 20, 359–373.
Dattilio, F. M. (2010). Cognitive-behavioral therapy with couples and families: A comprehensive
guide for clinicians. New York, NY: Guilford Press.
Dattilio, F. M., & Bahadur, M. (2005). Cognitive-behavior therapy with an East Indian family.
Contemporary Family Therapy, 27 , 137–160.
Dattilio, F. M., Edwards, D. J. A., & Fishman, D. N. (2010). Case studies within a mixed
methods paradigm: Towards the resolution of the alienation between researcher and
practitioner in psychotherapy research. Psychotherapy, 47 , 427–441.
Dattilio, F. M., & Epstein, N. B. (2005). Introduction to the special section: The role of
cognitive-behavioral interventions in couple and family therapy. Journal of Marital and
Family Therapy, 31, 7–13.
Dattilio, F. M., Kazantzis, N., Shinkfield, G., & Carr, A. G. (2011). Survey of homework use
and barriers impeding homework completion in couples and family therapy. Journal of
Marital and Family Therapy, 37 , 121–136.
Davis, S. D., & Piercy, F. P. (2007). What clients of couple therapy model developers and their
former students say about change, part 1: Model dependent common factors across three
models. Journal of Marital and Family Therapy, 33, 318–343.
Edwards, D., Dattilio, F. M., & Bromley, D. B. (2004). Developing evidence based practice:
The role of case based research. Professional Psychology: Research and Practice, 35,
589–597.
Ellis, A. (1982). Rational-emotive family therapy. In A. M. Home & M. M. Ohlsen (Eds.),
Family counseling and therapy (pp. 302–328). Itasca, IL: Peacock.
Epstein, N. B., Baldwin, L. M., & Bishop, D. S. (1983). The MacMaster Family Assessment
Device. Journal of Marital and Family Therapy, 9, 171–180.
Epstein, N., & Schlesinger, S. E. (1996). Treatment of family problems. In M. A. Reinecke,
F. M. Dattilio, & A. Freeman (Eds.), Cognitive therapy with children and adolescents: A
casebook for clinical practice (pp. 299–326). New York, NY: Guilford Press.
Epstein, N., Schlesinger, S. E., & Dryden, W. (1988). Concepts and methods of cognitive-
behavior family treatment. In N. Epstein, S. E. Schlesinger, & W. Dryden (Eds.),
Cognitive-behavior therapy with families (pp. 5–48). New York, NY: Brunner/Mazel.
Falloon, I. R. H. (Ed.) (1988). Handbook of behavioral family therapy. New York, NY: Guilford
Press.
Falloon, I. R. H., Boyd, J. L., & McGill, C. W. (1984). Family care of schizophrenia. New
Faulkner, R. A., Klock, K., & Gale, J. E. (2002). Qualitative research in family therapy:
Publication trends from 1980 to 1999. Journal of Marital and Family Therapy, 28,
69–74.
Goldenberg, I., & Goldenberg, H. (2008). Family therapy: An overview (8th ed.). Belmont,
CA: Brooks/Cole.
Hahlweg, K., & Wiedemann, G. (1999). Principles and results of family therapy in
schizophrenia. European Archives of Psychiatry and Clinical Neuroscience, 249(Suppl.4),
IV/108–IV/115.
Kazantzis, N., Deane, F. P., Ronan, K. R., & L’Abate, L. L. (Eds.) (2005). Using homework
assignments in cognitive-behavior therapy. New York, NY: Routledge.
Lazarus, A. A. (1976). Multimodal behavior therapy. New York, NY: Springer.
Lebow, M. D. (1976). Behavior modification for the family. In G. D. Erickson & T. P. Hogan
(Eds.), Family therapy: An introduction to theory and technique (pp. 347–376). New York,
NY: Jason Aronson.
Leslie, L. A. (1988). Cognitive-behavioral and systems models of family therapy: How compat-
ible are they? In N. B. Epstein, S. E. Schlesinger, & W. Dryden (Eds.), Cognitive-behavior
therapy with families (pp. 49–83). New York, NY: Brunner/Mazel.
Moos, R. H., & Moos, B. H. (1986). Family environment scale manual (2nd ed.). Palo Alto,
CA: Consulting Psychologists Press.
Mueser, K. T., & Glynn, S. M. (1995). Behavioral family therapy for psychiatric disorders.
Boston, MA: Allyn and Bacon.
Nichols, M. P., & Schwartz, R. C. (2012). Family therapy: Concepts and methods (9th ed.).
Boston, MA: Allyn and Bacon.
Northey, W. F. (2002). Characteristics and clinical practices of marriage and family therapists:
A national survey. Journal of Marital and Family Therapy, 28, 487–494.
Patterson, G. R. (1971). Families: Applications of social learning to family life. Champagne, IL:
Research Press.
Patterson, G. R. (1982). Coercive family process. Eugene, OR: Castalia Press.
Patterson, G. R., McNeal, S., Hawkins, N., & Phelps. R. (1967). Reprogramming the social
environment. Journal of Child Psychology and Psychiatry, 8, 181–195.
Family Therapy 749
Piacentini, J., Bergman, R. L., Chang, S., Langley, A., Peris, T., Wood, J. J., & McCracken, J.
(2011). Controlled comparison of family cognitive behavioral therapy and psychoeduca-
tion/relaxation training for child obsessive-compulsive disorder. Journal of the American
Academy of Child and Adolescent Psychiatry, 50, 1149–1161.
Psychotherapy Networker. (2007). The top 10: The most influential therapist of the past
quarter-century. Psychotherapy Networker, 31, 24–68.
Sanders, M. R. (2012). Development, evaluation, and multinational dissemination of the Triple
P-Positive Parenting Program. Annual Review of Clinical Psychology, 8, 345–379.
Sanders, M. R., & Dadds, M. R. (1993). Behavioral family intervention. Boston, MA: Allyn &
Bacon.
Sanders, M. R., Shepherd, R. W., Cleghorn, G. & Woolford, H. (1994). The treatment of
recurrent abdominal pain in children: A controlled comparison of cognitive-behavioral
family intervention and standard pediatric care. Journal of Consulting and Clinical
Satir, V. M. (1967). Conjoint family therapy (rev. ed.). Palo Alto, CA: Science and Behavioral
Books.
Schwebel, A. I., & Fine, M. A. (1994). Understanding and helping families: A cognitive-behavior
approach. Hillsdale, NJ: Erlbaum.
Sexton, T. L., Weeks, G. R., & Robbins, M. S. (2003) (Eds.). Handbook of family therapy.
New York, NY: Brunner-Routledge.
Sprenkle, D. H. (2003). Effectiveness research in marriage and family therapy: Introduction.
Journal of Marital and Family Therapy, 29, 85–96.
Stuart, R. B. (1995). Family of origin history. New York, NY: Guilford Press.
Teichman, Y. (1981). Family therapy with adolescents. Journal of Adolescence, 4, 87–92.
Teichman, Y. (1992). Family treatment with an acting-out adolescent. In A. Freeman & F. M.
Dattilio (Eds.), Comprehensive casebook of cognitive therapy (pp. 331–346). New York,
NY: Plenum Press.
Wahler, R. G., Winkel, G. H., Peterson, R. F., & Morrison, D. C. (1971). Mothers as behavior
therapists for their own children. In A. M. Graziano (Ed.), Behavior therapy with children
(pp. 388–403). Chicago, IL: Aldine.
Wardle, J., Cooke, L. J., Gibson, E. L., Sapochnik, M., Sheiham, A., & Lawson, M. (2003).
Increasing children’s acceptance of vegetables: A randomized trial of parent-led exposure.
Appetite, 40, 155–162.
Webster-Stratton, D., & Hancock, L. (1998). Parent training for young children with con-
duct problems: Content, methods, and therapeutic processes. In C. E. Schaefer (Ed.),
Handbook of parent training (pp. 98–152). New York, NY: John Wiley & Sons, Inc.
Wells, K. C., & Heilbron, N. (2012). Family-based cognitive-behavioral treatments for suicidal
adolescents and their integration with individual treatment. Cognitive and Behavioral
Practice, 19, 301–314.
Wright, J. H., & Beck, A. T. (1993). Family cognitive therapy with inpatients. In J. H. Wright,
M. E. Thase, A. T. Beck, & J. W. Ludgate (Eds.), Cognitive therapy with inpatients
32
Attention-Deficit/Hyperactivity
Disorder in Adults
Laura E. Knouse
University of Richmond, United States
Steven A. Safren
Massachusetts General Hospital and Harvard Medical School, United States
Attention-deficit/hyperactivity disorder (ADHD) is characterized by developmen-

tally inappropriate levels of inattention and hyperactivity-impulsivity that contribute
to cross-domain functional impairment (American Psychiatric Association, 2000).
Although in the past it was generally assumed that children with ADHD “grow
out of” the condition, empirical studies document persistence of symptoms and
impairment into adulthood in approximately two-thirds of cases diagnosed in child-
hood (Barkley, Murphy, & Fischer, 2008a) with adult prevalence estimated at 3–4%
(Fayyad et al., 2007; Kessler et al., 2006). ADHD in adulthood has been associated
with impairment in nearly every domain of functioning studied (see Table 32.1) and
confers increased risk for psychiatric comorbidity (T. W. Miller, Nigg, & Faraone,
2007). The disorder is also associated with deficits in executive functioning (EF)
linked to structural and functional variation in the prefrontal cortex and networks
that underlie working memory and behavioral inhibition (Barkley, 1997b; Nigg,
2006; Rapport et al., 2008). Difficulties with tasks requiring goal-directed activity
across time are particularly evident when these difficulties are measured with respect
to “real-world” contexts and are predictive of impairment across multiple domains
(Barkley & Fischer, 2011; Barkley & Murphy, 2010).
Adults with ADHD are often motivated to seek treatment because of pervasive
functional impairments rather than specific ADHD symptoms per se, including
difficulty completing academic programs, maintaining satisfactory performance at
work, sustaining reciprocal relationships, and simply keeping up with everyday tasks
such as paying bills, attending appointments, keeping commitments to others, and
working toward modest personal goals. Table 32.1 depicts a subset of findings from
one of the largest, most comprehensive studies comparing clinic-referred adults with

DOI: 10.1002/9781118528563.wbcbt32
Table 32.1 Clinic-Referred Adults with ADHD: Selected Domains of Impairment
Compared to community controls
Higher rates of:

• Lifetime major depression and dysthymia
• Lifetime generalized anxiety disorder
• Lifetime alcohol and marijuana use disorders
• Lifetime treatment for alcohol and drug use disorders
• Suicidal ideation and attempts in adulthood
Compared to clinical and community controls
• Greater number of impaired domains by self- and other-report; for example:

Education
• More educational problems by self- and other-report
• Fewer years of education
• Less likely to have a college degree
• Lower college grade point average (for those attending college)
• Lower math and spelling achievement scores
Work
• More likely to have been disciplined at work
• More likely to have been fired from a job
• Lower overall employer-rated job performance
Money and self-management
• More problems managing daily responsibilities by self- and other-report
• More money management problems by self- and other-report
• More likely to have had utilities turned off
• More self-reported problems with impulse buying
• More likely to smoke cigarettes
Legal problems and driving
• More likely to have been arrested and jailed in the past
• Poorer self-reported motor vehicle safety
• More likely to have license suspended or revoked (self- and DMV-report)
• More speeding citations (self- and DMV-report)
• More self-reported crashes where he or she was at fault
Parenting
• More severe overall parenting stress
Notes. Selected findings summarized from chapters 6, 8, 9, 10, 11, and 12 of Barkley, Murphy, & Fischer
(2008a), reporting on data from 146 clinic-referred adults diagnosed with ADHD, 97 clinical controls
referred to the same clinic but not diagnosed with ADHD, and 109 community controls. DMV =
Department of Motor Vehicles.
Attention-Deficit/Hyperactivity Disorder in Adults 753
ADHD to community and clinical controls (Barkley et al., 2008a) and illustrates the
range of functional impairments and comorbidity associated with the disorder. In
particular, comparisons with clinical controls highlight the magnitude of treatment
needs in this population.
While medication is a crucial intervention for many patients because it provides
more direct reduction in core neurobiological symptoms, psychosocial treatment is
also recognized as a necessary component for many patients. Some patients may be
unable or unwilling to take medications, others may be medication nonresponders,
and many experience some symptom reduction from medications but continue to
experience residual symptoms, skill deficits, symptoms of comorbid disorders, and
ongoing functional impairments. Indeed, the proliferation of self-help books on
adult ADHD and commercially available treatment approaches over the past 10
years demonstrates increasing demand for psychosocial approaches to management of
ADHD in adults.
Several individual and group cognitive behavioral approaches have been developed
and tested in the last 10 to 15 years and, while enthusiasm for novel approaches is
certainly warranted, there is also a need for critical evaluation of both efficacy and
“active ingredients” in the context of evidence-based practice. Programs that carry
the CBT label can vary in content and in presumed mechanisms of change (Knouse &
Safren, 2010). Fortunately, recent clinical trials in this emerging area provide an
empirical basis—albeit a small one relative to other longer-studied disorders—for the
use of particular cognitive behavioral approaches for adult ADHD.
Adult ADHD can be a particularly challenging condition to treat using standard
cognitive and behavioral strategies due to potential interference from the core
symptoms of the disorder itself and the didactic nature of skills training in cognitive
behavioral therapy (CBT) (Ramsay, 2010). The very nature of the disorder, with its
difficulties in executive functioning, is likely to interfere with a client’s ability to access
a standard CBT intervention. Attending sessions regularly and on time, processing and
recalling session content, completing homework assignments, and bringing important
skills and concepts to mind when needed in one’s daily life are all processes that might
be particularly difficult for an adult with ADHD. In one of the first studies to describe
a large group of adults with ADHD presenting for treatment, Ratey, Greenberg,
Bemporad, and Lindem (1992) noted that many of their patients diagnosed with
adult ADHD were treatment failures referred by clinicians using insight-oriented
approaches, where patients’ lack of progress was interpreted as resistance. They
also observed that structured short-term approaches were often hindered by the
patients’ difficulties “maintaining the focused commitment” necessary for success
(Ratey et al., 1992, p. 270). For this reason, successful approaches purposefully
incorporate treatment strategies that can address these difficulties (Ramsay, 2010;
Ramsay & Rostain, 2008).
Efficacious CBT for adult ADHD focuses on helping patients not only to acquire
strategies but also to implement them consistently (Knouse & Safren, 2010, 2011;
Ramsay, 2010). Compensatory skills practice can directly address therapy-interfering
behavior. For example, a client learning to consistently use a calendar system with
reminders might choose an initial goal of using these tools to arrive on time for
therapy appointments. The therapy context has provided an opportunity for clients to
practice implementation of skills. Thus, the application of skills to therapy-interfering

behaviors serves a dual purpose in CBT for adult ADHD—improving access to the
intervention while providing an opportunity for skills practice.
Brief History and Review of Open Trials
Isolated research studies of adults with “minimal brain dysfunction” (as ADHD
was then known) began to appear in the literature in the 1960s and 1970s, but
ADHD in adults did not receive widespread recognition in the clinical research
literature until the mid-1990s (Barkley, Murphy, & Fischer, 2008b). Although
recommendations for nonmedication treatments based on clinical anecdote appeared
earlier, the first outcome data for a psychosocial treatment for adult ADHD appeared
when Wilens et al. (1999) published a retrospective chart review of 26 cases treated
with a combination of cognitive therapy adapted for ADHD (McDermott, 2000)
and stimulant medication. Patient clinical global impression (CGI) scores for ADHD
symptoms decreased significantly from baseline to medication stabilization and then
again significantly decreased from that point to the endpoint of cognitive therapy.
Although limited by its methodology, the study was the first to provide data in
support of the idea that cognitive behavioral methods could be successfully applied to
the treatment of adult ADHD. That same year Wiggins, Singh, Getz, and Hutchins
(1999) published a small wait-list-controlled trial (N = 17) of four sessions of “group
psychoeducation” showing decreases in self-reported inattention and disorganization
at posttreatment. Sessions covered specific skills that patients could use to improve
goal setting, time management, and task completion.
Soon after, three other research groups began publishing on modifications of exist-
ing cognitive and behavioral paradigms to suit the needs of adults with ADHD. In
Germany, Hesslinger et al. (2002) adapted dialectical behavior therapy (DBT) skills
groups (Linehan, 1993) for use with adults with ADHD. In a small nonrandomized
controlled trial (N = 15) the treatment group self-reported significant improvements
in depression and ADHD symptoms compared to no changes in the wait-list control
group. This research team later published a larger open trial (N = 72) wherein
patients receiving modified DBT self-reported significant pre-to-post reductions in
ADHD symptoms and depressive symptoms (Philipsen et al., 2007). A multisite,
randomized controlled trial (RCT) of this treatment program alone and in combina-
tion with medication treatment has recently completed data collection and results are
forthcoming (A. Philipsen, personal communication, January 10, 2012). A different
research group recently published an RCT of DBT for adult ADHD compared to an
active control condition (Hirvikoski et al., 2011). These results are detailed later in
this chapter.
In Australia, Stevenson, Whitmont, Bornholt, Livesey, and Stevenson (2002) took
a cognitive remediation approach and developed a group treatment designed to
“retrain cognitive functions,” followed soon after by individual cognitive behavioral
treatment for patients taking medication but experiencing residual symptoms by
Safren, Otto, et al. (2005). Both of these approaches are discussed in detail below.
Weiss and Hechtman (2006) reported on a multisite placebo-controlled study of
dextroamphetamine versus paroxetine for adults with ADHD in which eight sessions
of problem-focused therapy were provided to all patients. Although patients receiving
active medications generally fared better than those receiving placebo, 16% of the
placebo plus problem-focused therapy group showed a treatment response for ADHD
symptoms and 28% showed a response in their overall CGI. It is not possible, however,
to tease apart the effects of problem-focused therapy versus pill placebo as there was
not a “therapy-only” group. Also in this period, one of the most prolific teams of
scientist-practitioners in psychosocial treatment for adult ADHD, J. Russell Ramsay
and Anthony Rostain, began publishing descriptions of a direct modification of
cognitive behavioral therapy for adults with ADHD (Ramsay, 2002; Ramsay &
Rostain, 2003), culminating in an open trial of 43 patients treated with CBT and
medication (Rostain & Ramsay, 2006). Treatment consisted of 16 sessions of CBT
(Ramsay & Rostain, 2008) over 6 months combined with up to 20 mg of Adderall
twice a day. From pre-to-post, significant decreases in self-reported and investigator-
rated ADHD symptoms were observed as well as reductions in anxiety and depression
symptoms, with generally large effect sizes.
Virta and colleagues (Salakari et al., 2009; Virta et al., 2010; Virta et al., 2008)
published two small studies that employed group or individual versions of “cognitive
behaviorally oriented rehabilitation.” This treatment approach covered a wide variety
of topics across 10–11 sessions. In an open trial (Virta et al., 2008) (N = 29), they
obtained significant but small effects on one self-report ADHD symptom checklist but
not on the DSM-IV based checklist. In a follow-up study (Salakari et al., 2009), the 11
participants defined as responders (with at least a 30% mean reduction in symptoms
across two self-report checklists) maintained their gains at 3 and 6 months. This group
(Virta et al., 2010) more recently published a small (N = 29) randomized controlled
pilot study testing individual rehabilitation against computerized cognitive training
and against wait-list control. Compared to wait-list, the individual rehabilitation did
not demonstrate significant effects on any measures administered by investigators
blind to treatment condition or on a DSM-IV based self-report checklist, but did
show reductions on some subscales of another ADHD self-report measure. None of
the comparisons between rehabilitation and cognitive training were significant.
Following the general trend in CBT toward integration of acceptance and
mindfulness-based techniques, as well as dovetailing with the aforementioned appli-
cations of DBT, Zylowska et al. (2008) conducted an open feasibility trial (N = 30)
to examine the effects of mindfulness meditation training on self-reported symptoms
and cognitive measures. Self-reported ADHD symptoms were significantly reduced
pre-to-post with a medium to large effect size and improvements were observed on
several cognitive measures including the Stroop task and measures of task switching.
Controlled studies will be needed to increase internal validity and, in particular, to
rule out practice effects in accounting for changes on the cognitive measures. As we
have discussed elsewhere (Knouse & Safren, 2010), this treatment approach is unique
among CBT approaches in that it purports to more directly alter the deficient cogni-
tive functions associated with ADHD rather than helping patients to learn strategies
to work around them. In this same year, Solanto, Marks, Mitchell, Wasserstein, and
Kofman (2008) published an open trial of their group “metacognitive therapy,”
discussed in detail later in this chapter.
As evidenced by the pilot studies and open trials described above, clinical innovations
in psychosocial treatment for adult ADHD have accelerated over the past 10 years.
Fortunately, this has also been accompanied by increasingly rigorous research trials
to establish the efficacy of these approaches. While this literature is still small, it
has been growing at an encouraging rate. Just a few years ago (Knouse & Safren,
2010), we reviewed the literature and identified three published RCTs—at the time
of writing, that number has doubled, with the largest, most rigorous trials to date
published in 2010 (Safren et al., 2010; Solanto et al., 2010). Next, we review RCTs
with wait-list or treatment-as-usual controls followed by those with active control
groups.
Efficacy of Cognitive Behavioral Therapy: Randomized

Controlled Trials
The American Psychological Association (APA) has codified its support of Evidence-
Based Practice in Psychology in its recent policy statement (APA Presidential Task
Force on Evidence-Based Practice, 2006), supporting systematic review of RCTs as
the highest-quality evidence of clinical efficacy. In this section, we review RCTs of
cognitive behavioral therapy for adult ADHD, first focusing on studies using wait-list
or treatment-as-usual control groups and then studies with active, attention-matched
controls. This method is also consistent with APA Division 12’s criteria for Empirically
Supported Treatments (Chambless, 1998). For each trial we report between-groups
effect sizes (Cohen’s d) at posttreatment for ADHD symptoms either reported by the
authors or computed from reported means and standard deviations.
Randomized Controlled Trials with Wait-List or Treatment-as-Usual

Controls
Stevenson et al. (2002) published the first RCT of a program training cognitive
and behavioral strategies for adults with ADHD. The group cognitive remediation
program was designed to help patients develop coping strategies, retrain cognitive
functions, and structure the environment to support coping. Treatment consisted
of eight 2-hour group sessions led by a clinical psychologist and included the
assistance of an individual coach for each patient who took notes during sessions and
had weekly between-session supportive telephone contacts with patients. At acute
outcome, patients in the treatment group (N = 22) self-reported significantly greater
reductions in ADHD symptoms (d = −1.72) and improvements in organizational
skills (d = 1.21) than the wait-list control group (N = 21). The treatment group also
reported significantly greater reductions in state anger and increases in self-esteem.
The treatment group continued to report these significant changes at 2-month and
1-year follow-ups. Stevenson, Stevenson, and Whitmont (2003) went on to obtain
promising results from a version of this treatment with “minimal therapist contact,”
which included only three clinician-led sessions, the supportive coach, and client
completion of self-guided exercises using a workbook.
Safren, Otto, et al. (2005) conducted an RCT (N = 31) of their individual

cognitive behavioral therapy designed for adults with ADHD who were taking
medications but still experiencing residual symptoms. The treatment approach and
the results of a larger RCT are described in detail in the next section. At the
outcome assessment, patients randomized to CBT (N = 16) had significantly greater
reductions in ADHD symptoms (d = 1.2) and global severity (CGI; d = 1.4) as
rated by an evaluator blinded to treatment condition than those randomized to
continued psychopharmacology alone (N = 15). Patients in the CBT group self-
reported significantly greater reductions in ADHD symptoms (d = 1.7) and anxiety.
The CBT group also showed reductions in independent evaluator-rated anxiety and
depression. Using a conservative threshold for responder status (CGI score reduction
of at least 2 points), significantly more patients were treatment responders in the CBT
group (56%) compared to the control group (13%).
Most recently, Emilsson et al. (2011) employed a very similar research design to the
Safren, Otto, et al. (2005) study, evaluating the Reasoning and Rehabilitation 2 for
ADHD (R&R2ADHD) group cognitive behavioral program for adults with ADHD
taking medication but experiencing significant residual symptoms. R&R2ADHD
was adapted from a group treatment aimed at improving prosocial competencies in
individuals in correctional facilities (Young, Chick, & Gudjonsson, 2010). Goals of the
treatment included decreasing the impairment resulting from core ADHD symptoms
and improving problem-solving, social, and organizational skills. Treatment consisted
of 15 group sessions taking place twice per week combined with between-session
contact with individual coaches who supported the patients in application of skills.
In this study, trained undergraduates served as coaches. The use of individual
coaches providing between-session skills support appears similar to the program
developed by Stevenson et al. (2002) and described earlier. Seventeen patients in each
group received an independent evaluation at posttreatment of 27 patients originally
randomized to each group. At posttreatment, the group receiving R&R2ADHD
showed significantly greater reductions in evaluator-rated ADHD symptoms (d =
1.03) but not in overall clinical global impressions compared to the wait-list controls
with continued medication. The treatment group also reported significantly greater
reductions in self-reported total ADHD symptoms (d = 0.76) and antisocial behaviors
but not in anxiety or depression symptoms. The authors also report 3-month follow-
up data from a subset of patients (CBT N = 8, control N = 13) demonstrating
significantly greater effects on all measures from baseline to follow-up for the treatment
group compared to the control group with generally large effect sizes. This may reflect
a lag in treatment-related improvements in functioning, although the rate of attrition
from the groups from posttreatment to follow-up makes these findings difficult to
interpret.
Randomized Controlled Trials with Active Controls

Three randomized trials with active, attention-matched, psychological placebo con-
ditions appear in the literature. Two of these trials (Safren et al., 2010; Solanto
et al., 2010) also employed larger sample sizes and gathered outcome data using
independent evaluators blinded to treatment status, qualifying them as the most
rigorous efficacy studies of CBT for adult ADHD to date. As a result, we outline these
treatment approaches and findings in some detail concluding with a recent RCT of
group DBT skills training for adult ADHD compared to support group (Hirvikoski
et al., 2011).
Metacognitive group therapy. Solanto and colleagues (Solanto, 2011; Solanto et al.,
2008; Solanto et al., 2010) developed a group treatment for adults with ADHD called
metacognitive therapy. Their use of the term “metacognitive” reflects the focus of the
treatment on helping patients develop executive self-management skills and routines
to compensate for core neuropsychological deficits. The treatment specifically aims to
help patients cope with the inattentive symptoms of ADHD by developing their time
management and organizational skills. Importantly, the treatment heavily emphasizes
implementation and maintenance of these skills in patients’ daily lives. Practice and
repetition of skills in sessions and during homework assignments is employed so
that they will become automatic, habitual behaviors. Self-instructional phrases are
rehearsed to increase the likelihood that patients will recognize cues indicating the
need for skill implementation. Patients also learn to challenge maladaptive cognitions
that may arise. Skill modules are arranged hierarchically and include time and task
management skills, followed by organization of physical space, and planning. During
weekly 2-hour sessions, group members first discuss at-home application of skills,
receive feedback from group members, and are then given new skill information and
homework assignments from group leaders with anticipatory troubleshooting.
Solanto et al. (2008) first obtained promising results from an open trial with 30
adults diagnosed with ADHD completing either an 8- or a 12-session version of
the treatment. After treatment, patients showed significant and sizeable reductions
in inattentive symptoms as measured by the Conners’ Adult ADHD Rating Scale
(CAARS) and the Brown ADD Scales, with 47% falling below the clinical cutoff for
inattentive symptoms on the CAARS.
In an RCT, Solanto et al. (2010) compared metacognitive group therapy to a
group supportive therapy, randomizing 88 patients stratified by medication status.
Patients were rigorously diagnosed with either inattentive or combined-type ADHD
and, other than active substance use disorders and pervasive developmental disorders,
patients with other Axis I disorders were included. Over half of each treatment group
was diagnosed with a current anxiety disorder and about one-third was diagnosed
with a current mood disorder using the Structured Clinical Interview for DSM-IV
Axis I Disorders (SCID-I; Spitzer, Williams, Gibbon, & First, 1995). Metacognitive
and supportive therapy groups were run concurrently 2 hours per week for 12
weeks and used the same therapists. Supportive therapy was described to patients
as a way to provide education, share experiences, and provide support. Group
members identified specific goals for the treatment period and each session focused
on reviewing the events of the previous week and having group members provide
support and troubleshooting. Therapists also led discussion on psychoeducational
themes suggested by group members.
Compared to supportive therapy, metacognitive therapy resulted in significantly
greater reductions in independent evaluator-rated inattentive symptoms as measured
by the Adult ADHD Investigator Symptom Rating Scale (Spencer et al., 2010)
and as measured by the CAARS (Conners, Erhardt, & Sparrow, 1999) completed
by a significant other with medium effect sizes (d = 0.55; 0.57). Response to
treatment measured by self-reported inattention symptoms on the CAARS showed an
interaction between treatment condition and baseline scores, such that patients with
higher baseline symptom scores showed larger differential benefit of metacognitive
therapy. In the supportive therapy group, the magnitude of symptom reduction was
relatively flat across levels of baseline symptom severity. Metacognitive therapy also had
more treatment responders (at least 30% reduction in symptoms) measured by blinded
investigator ratings (42% vs. 12%) and self-report (reduction of at least one standard
deviation; 53% vs. 28%) of inattentive symptoms. Treatment group was not associated
with changes in comorbid anxiety and depressive symptoms. Patients in both treatment
groups who were diagnosed with a depressive disorder showed significant reductions
in self-reported depression symptoms from pre- to posttreatment. In summary,
metacognitive therapy was associated with ADHD inattentive symptom reduction
over and above the nonspecific elements of group therapy, and treatment-related
change was large for patients with more severe symptoms.
Cognitive behavioral therapy for medication-treated adults with attention-

deficit/hyperactivity disorder and residual symptoms. This treatment is based upon
a cognitive behavioral model of the consequences of ADHD across development,
as depicted in Figure 32.1 (Safren, Perlman, Sprich, & Otto, 2005; Safren, Sprich,
Chulvick, & Otto, 2004). The available evidence supports a strong neurobiological
basis for ADHD and thus the cognitive behavioral model begins with neuropsychiatric
impairments at the core of the disorder. In this treatment approach, the core
deficits are directly addressed by ongoing adherence to medications while cognitive
and behavioral skills address the consequences of a lifetime of ADHD symptoms.
Theories of ADHD emphasize deficits in executive functions including sustained
attention, inhibitory control, working memory, and motivation that underlie the
DSM-IV symptoms (Barkley, 1997b; Nigg, 2006; Rapport et al., 2008). Present
from childhood, these core impairments are hypothesized to confer a vulnerability
for chronic functional impairment in adulthood via two pathways—behavioral and
cognitive. First, core neuropsychiatric impairments interfere with the development
and maintenance of self-management skills such as organization, planning, time
management, and self-motivation. Unfortunately, these are the same adaptive,
compensatory behaviors that might ameliorate symptom-related difficulties, the lack
of which contribute to symptom maintenance and further functional impairment.
To address this pathway, Safren, Perlman, et al. (2005) emphasize the acquisition
and implementation of key compensatory behaviors including organization and
planning skills and strategies to manage distractibility. Because the very nature
of ADHD makes maintaining these adaptive behaviors difficult for patients, the
treatment approach emphasizes simple systems practiced repeatedly until they
become habitual and automatic. Via a second pathway in the model, individuals
with ADHD develop maladaptive patterns of thoughts and beliefs in response to
multiple failure experiences and ongoing negative social feedback from parents,
teachers, and peers. These thinking patterns are associated with decreased motivation,
increased avoidance, mood disturbance, and a decreased likelihood of persistence
Core
(Neuropsychiatric)
Impairments in
Attention
Inhibition
Self-Regulation
History of Failure to utilize
(impulsivity)
Failure compensatory
Underachievement strategies – examples:
Relationship problems Organizing
Planning
(i.e., task list)
Managing
procrastination,
Mood avoidance,
Dysfunctional disturbance distractibility
cognitions and beliefs Depression
Guilt
Anxiety
Anger
Functional
impairment
Figure 32.1 Cognitive behavioral model of ADHD. From Safren, Sprich, Chulvick, & Otto
(2004), p. 351.
in acquiring and using compensatory strategies. To address this pathway, Safren,

Perlman, et al. (2005) include cognitive restructuring to help patients become aware
of the relationship between thoughts and maladaptive behaviors and to disengage
from automatic, avoidant ways of coping. Thus, although the core symptoms of
ADHD are neurobiological in nature, CBT can help to break the link between core
symptoms and continued functional impairment.
This manualized treatment (Safren, Perlman, et al., 2005) and accompanying client
workbook (Safren, Sprich, Perlman, & Otto, 2005) consists of three core modules
and two optional modules. We describe the treatment elements of each module
below. For additional details and a more practice-focused discussion of CBT for adult
ADHD, we refer readers to the aforementioned manuals and to two recent practice-
oriented chapters (Knouse & Safren, 2011, 2013). Each session begins with a review
of medication adherence and of self-report ratings of ADHD symptoms experienced
in the past week. After setting the session agenda, therapist and patient discuss
homework (skills practice) from the previous week and engage in troubleshooting
as necessary. Next, the rationale and techniques for new skills are introduced and
therapist and patient discuss where, when, and how to practice as well as anticipated
barriers to skills implementation before setting the homework for the following week.
Throughout the treatment, the active and repeated practice of skills is emphasized
along with assessing and addressing barriers to implementation, both behavioral and
cognitive.
The first core module of the treatment, psychoeducation/organization and plan-
ning skills, begins with an introduction to the CBT model of ADHD described
above. Next, the patient’s treatment goals are discussed and motivational interviewing
strategies (W. R. Miller & Rollnick, 2002) are employed to enhance motivation for
behavior change. In subsequent sessions, the therapist guides the patient in choosing
and implementing a calendar for all appointments and a task list for all to-do items.
These compensatory tools are considered foundational for subsequent skills and so
considerable time and attention are devoted to helping the patient choose a calendar
and task list system that is effective yet simple enough to maintain. Throughout the
program, the emphasis is on choosing simple systems and using them consistently
until they become habit. Patients often come to CBT having tried numerous times to
develop organizational systems only to “fail” at them when they have chosen overly
complicated systems that are far too unwieldy to maintain, or when they have not
practiced the system long enough for it to become habitual. The therapist pays close
attention to other aspects of implementation, such where the calendar/task list will
be kept, when the patient will use it, and whether the patient needs external cues to
remember to use the system.
Next, strategies for prioritization and breaking down overwhelming tasks are
introduced. The patient uses a simple prioritization system to label items in his or
her task list and is taught to break a large task list item down until the first “chunk”
no longer seems prohibitively overwhelming. These skills are followed by training
in traditional problem-solving skills including identifying the problem, generating
possible solutions, evaluating the alternatives, and forming an action plan. The
organization and planning module concludes with a session on creating filing systems
and organizing mail.
The second module focuses on strategies to help patients manage distractibility.
They first engage in an exercise to become more aware of their attention span and
then practice breaking down tasks to fit within this time window. For example, if
a patient finds that she can only work on organizing papers in her filing system for
10 minutes at a time before becoming distracted, then she would proactively assign
herself this type of task in 10-minute “chunks.” The following session focuses on
setting up the environment to reduce sources of distraction. The client and therapist
go through an inventory of possible distractions in the work environment and employ
stimulus control strategies to reduce distractions. For example, a patient might find
that turning off audible “new email” alerts while working on a long, boring, or
difficult-to-complete task results in reduced distractibility.
The third module focuses on adaptive thinking and uses traditional cognitive
therapy techniques including a thought record, identification of cognitive errors, and
formulation of rational responses (Beck, 1995). In particular, the goal is to increase
the patient’s awareness of thoughts that occur in the context of negative emotion,
avoidance, or failure to use a compensatory skill. The patient can then use rational
responses, including recalling past instances of successful skill use, to increase adaptive
coping and decrease avoidance. For example, a patient might figure out that the
thought, “I’ll just do it later,” often precedes avoidance and, with practice, he or she
is able to stop and reevaluate the situation whenever this “red flag” thought occurs.
Following the main modules, an optional one-session module focuses on applying
previously learned skills to the problem of procrastination. Another optional one-
session module involves meeting with the patient and a significant person in his or
her life to provide psychoeducation and recruit the person’s support for the patient’s
behavior-change efforts.
Following promising results in the aforementioned trial comparing CBT to

treatment-as-usual (Safren, Otto, et al., 2005), Safren et al. (2010) conducted an RCT
that compared this CBT to an active condition—relaxation training with educational
support. These control group patients were trained in progressive muscle relaxation
applied to ADHD symptoms and also received ongoing psychoeducation and sup-
portive therapy. Both treatments consisted of 12 weekly 50-minute individual sessions
and the same therapists were used across conditions. Safren et al. (2010) conducted
an intent-to-treat analysis of 43 patients randomized to CBT and 43 randomized to
active control. All patients were taking medications for ADHD but still experienced
significant residual symptoms. At acute outcome, patients who received CBT showed
significantly greater reductions in independent (blinded) evaluator ratings of overall
symptom severity (CGI; d = 0.60) and ADHD symptoms (ADHD Rating Scale
[DuPaul, Power, Anastopoulos, & Reid, 1998]; d = 0.53) with medium effect sizes.
CBT had more treatment responders according to the independent evaluation as
measured by CGI (2-point reduction on CGI of 1 or 2 posttreatment; 53% vs. 23%)
and ADHD symptom checklist (reduction of at least 30%; 67% vs. 33%). Self-reported
weekly ADHD symptoms showed a significantly steeper decline in the CBT group
across the treatment period. Assessments at 6- and 12-month follow-up indicated
that patients who had a response or partial response to CBT maintained their gains
as evidenced by the absence of a significant change in slope for any of the three
main outcome measures. Compared to an active, attention-control condition, this
CBT for medication-treated adults with residual symptoms demonstrated superior
symptom reduction and a greater proportion of treatment responders who went on
to maintain their treatment-related gains across 12 months. This study represents the
most rigorous test of CBT for adult ADHD to date in that it included follow-up
assessments to examine the durability of treatment-related change. It provides com-
pelling evidence that symptom reduction can be attributed to the specific cognitive
and behavioral elements targeting ADHD symptoms and not just supportive elements
or the teaching and application of skills in general.
Dialectical behavior therapy group for adult attention-deficit/hyperactivity disorder. In

the third RCT to date that employed an active, attention-matched control group, a
research group in Sweden (Hirvikoski et al., 2011) tested the modified DBT skills
group developed by Hesslinger et al. (2002) against supportive group therapy. This
treatment approach, originally developed for the treatment of borderline personality
disorder, combines traditional change-oriented CBT skills with acceptance-based
mindfulness skills. Hesslinger et al. (2002) note that ADHD shares many overlapping
features with borderline personality disorder including difficulties with impulsivity,
emotion regulation, and interpersonal functioning. In addition to mindfulness skills,
DBT for adult ADHD incorporates training in behavior analysis and specific behavioral
coping skills, as well as psychoeducation about a variety of topics relevant to ADHD
including depression, stress, substance use, and relationships. As described earlier,
two open trials have been conducted using this approach and, averaging across these
studies, a large pre-to-post effect size on self-reported ADHD symptoms was obtained
(Knouse & Safren, 2010).
Hirvikoski et al. (2011) randomized 51 adults with ADHD to either a DBT skills
group or a supportive discussion group. Nineteen DBT group participants and 18
support group participants were analyzed per protocol, with subjects who made
changes to their medications during the trial excluded. Outcomes were based on
self-report and showed a significantly greater reduction in ADHD symptoms for the
DBT group (d = 0.57). They report that responders with at least a 30% reduction
in symptoms represented 32% of the DBT group and 0% of the support group.
None of the comorbid symptoms measures showed significantly greater change in the
DBT group. A strength of this study is that it employed more inclusive entry criteria
than has been the case for past studies such that 75% of individuals screened were
eligible to participate. The authors caution, however, that four participants in the
groups reported worsening anxiety at the end of the trial due to apprehension about
separation from the group. When these participants were included in the analyses
along with participants who had dropped out or changed medications (intent-to-
treat), the effect of DBT on ADHD symptoms was not significant. Clinicians using
group treatments must be sensitive to the way patients respond to the loss of this
form of support and should work to ease this transition.
DBT for adult ADHD is currently being tested in a multimodal, multisite treatment
study in Germany where it is being compared alone and in combination with medica-
tion to medication alone. Results of this trial are forthcoming (A. Philipsen, personal
communication, January 10, 2012) and comparison among emerging treatment
approaches will be important as the field continues to develop.
Summary evaluation of randomized controlled trials. Investigations of cognitive

behavioral treatments for adult ADHD have proceeded from open trials to wait-
list and treatment-as-usual controlled trials to the more rigorous active control group
designs, showing promising effect sizes along the way (Knouse & Safren, 2010).
In addition, using blinded evaluators in measurement of outcomes and follow-up
assessment periods to establish durability of gains are also important steps. Empiri-
cally supported treatments (ESTs) are those interventions with demonstrated efficacy
in treatment outcome studies with high internal validity—a highly valuable type
of scientific evidence in the provision of Evidence-Based Practice in Psychology
(APA Presidential Task Force on Evidence-Based Practice, 2006). From this review,
both metacognitive group therapy (Solanto et al., 2010) and individual CBT for
medication-treated adults with ADHD and residual symptoms (Safren et al., 2010)
appear to meet criteria as “probably efficacious” treatments according to the criteria
set forth by APA Division 12 (Chambless, 1998). That is, both studies show that
the treatment in question is statistically superior to a psychological placebo or active
treatment, were conducted with treatment manuals, and clearly specified their par-
ticipant samples. Another such successful treatment trial by an independent research
group would be required for either of these treatments to qualify as “empirically
supported.” In addition, the study by Hirvikoski et al. (2011) may move DBT for
adult ADHD closer to achieving this status, although the smaller sample size, reliance
on self-report, and lack of significant findings using intent-to-treat analysis suggest
that data from the larger DBT trial will be needed to further evaluate this treatment.
Clearly, rigorous replications of these results are needed, as well as additional

data on the durability of treatment effects. Researchers, however, must also begin
to move beyond straightforward efficacy studies and examine treatment moderators,
mechanisms of action, and implementation.
Moderators, Active Ingredients, and Dissemination
Despite these promising results, far more questions about CBT for adult ADHD
remain than these studies have answered. As would be expected, effect size estimates
in these trials have tended to decrease as the integrity of the comparison group
improves and response rates to CBT are far from 100%. Thus, further investigation of
“what works for whom” in the form of moderator analyses is needed, some of which
are described below. In particular, participant samples in these initial research trials
have been (understandably for this stage of development) relatively homogeneous
and high functioning and thus the limits of generalizability of these findings are
not known. Additional data on the effect of education level, comorbidity, and
symptom severity on response to CBT are needed. This information will be crucial
in tailoring the treatment to the needs of particular patients and settings, improving
the utility of CBT for this population. A second compelling question concerns active
ingredients or underlying mechanisms of change that may be operating within and
across studies. The treatment packages described here contain multiple components
and it is not yet clear which elements are necessary or sufficient for helping adults with
ADHD improve. Identifying the most critical elements through mediation analyses
and dismantling studies—as has been undertaken for other forms of CBT (Dimidjian
et al., 2006)—may improve the efficiency and cost-effectiveness of these interventions,
facilitating dissemination and reducing patient burden. Finally, a host of questions
related to dissemination and implementation of CBT for adults with ADHD remain
to be answered, including how to adapt the treatment to other settings (primary
care, universities, prison systems, child clinics), how much and by what methods to
train therapists, and whether novel delivery methods are feasible and effective (e.g.,
self-help format, Internet delivery). In the following sections, we outline existing data
on these questions and future directions.
Moderators of Cognitive Behavioral Therapy for Adult

Attention-Deficit/Hyperactivity Disorder: What Works for Whom?
As for most psychotherapies, response rates in clinical trials are far from 100%,
prompting questions about predictors of treatment response. Identifying moderators
of treatment outcome would inform treatment planning in the clinic and treatment
innovation in clinical research programs. We consider potential moderators of treat-
ment outcome with the caveats that the data are limited and that participants in these
studies are unlikely to be representative of the entire population of adults with ADHD
(Knouse & Safren, 2011), limiting our ability fully to assess predictors of treatment
success in practice.
Medication status. Clinical intuition might suggest that most adults with
ADHD—due to their core symptoms and impairments in executive functioning—are
likely to need some form of medication treatment to help control their symptoms
and facilitate the acquisition of behavioral and cognitive skills. Treatment approaches
such as that of Safren, Perlman, et al. (2005) have been specifically developed for
and tested with adults who are already receiving ongoing medication treatment.
However, the CBT outcome studies that have examined medication status as a
moderator have not found support for this hypothesis (Philipsen et al., 2007; Solanto
et al., 2008; Solanto et al., 2010; Stevenson et al., 2003; Stevenson et al., 2002;
Zylowska et al., 2008). For example, in their RCT, Solanto et al. (2010) did not
find that medication status predicted treatment response. In addition, medication
status was not associated with baseline symptom severity—an important piece of
information given that medication status and symptom severity might be confounded
with one another, that is, clients with more severe symptoms are more likely to seek
medication treatment. Ramsay and Rostain (2011) recently reported the results of
a small pilot study of individual CBT for adults with ADHD who were not taking
medication (N = 5). The authors describe their sample as relatively high functioning
and uncomplicated. Nevertheless, nonparametric tests showed significant pre-to-post
reductions in total clinician-rated ADHD with a large effect size (d = 0.83). Changes
in CGI score did not reach significance but also demonstrated a large effect size
(d = 0.85) and internalizing symptoms showed significant and sizeable reductions
(e.g., Beck Depression Inventory d = 1.17). These results must be interpreted
with caution, however, and the most responsible interpretation is probably that
for adults with ADHD who cannot or are unwilling to take medication, CBT is
not contraindicated. Medication remains a critical treatment component for many
patients and multimodal treatment is likely to be associated with the best outcomes
for adults. As described earlier, the forthcoming results of the study by Philipsen and
colleagues will directly test this hypothesis.
Comorbid symptoms. Comorbidity may complicate the treatment of adult ADHD and
few empirical data exist to guide clinicians in treatment planning for the many adults
with ADHD and other disorders (Knouse & Safren, 2011). Is there any evidence that
comorbid symptoms moderate the effects of CBT? During their open trial, Solanto
et al. (2008) reported that depressive symptoms at baseline did not predict changes
in any of the primary outcome measures. In their RCT, Solanto et al. (2010) did not
find that comorbid anxiety or depressive diagnoses predicted differential treatment
response. Philipsen et al. (2007) found that DBT group participants with more severe
depressive symptoms at baseline had greater reductions in depressive symptoms and
in ADHD symptoms as measured by one self-report measure. Zylowska et al. (2008)
found that baseline severity score on symptom measures showing pre-to-post changes
predicted the magnitude of those changes with more severe symptoms at baseline
leading to greater magnitude of improvement. Likewise, Stevenson et al. (2002)
did not find that comorbid anxiety problems predicted effects of group CBT, and
change scores in the minimal therapist contact version of the treatment (Stevenson
et al., 2003) were not correlated with depression, anxiety, stress, intellectual ability,
or spelling or reading ability. Again, results must be interpreted with caution due to
the likelihood that these samples had lower rates and severity of comorbidity than
adults with ADHD in general. Furthermore, patients with externalizing problems
such as substance abuse were frequently excluded from study. However, none of the
available data suggest that comorbid internalizing symptoms at a mild to moderate
level reduce the efficacy of CBT for adult ADHD. Treatment of ADHD may even
be associated with reductions in mild comorbid symptoms (e.g., Safren, Otto, et al.,
2005).
Moderators for future study. There is currently no evidence that gender moderates
the effects of CBT for adult ADHD (Rostain & Ramsay, 2006; Solanto et al., 2010;
Zylowska et al., 2008) but conclusions about other moderators including education
level, socioeconomic status, race/ethnicity, and intellectual functioning cannot be
adequately assessed given the available data and the nature of the samples examined.
Future effectiveness studies of CBT for adults with ADHD will be needed to test the
boundary conditions of these promising efficacy results.
Active Ingredients
What are the “active ingredients” or critical behavior change processes in CBT
for adult ADHD? The answer to this question is not clear. An analogy might be
drawn between the current state of this young field and the state of treatments for
anxiety disorders in the 1960s and 1970s. Up to that point, a variety of behavioral
methods for the treatment of anxiety disorders—systematic desensitization, implosive
therapy, flooding, in vivo exposure—had proliferated and it took an intensive series
of comparative and dismantling studies to determine that exposure was the “active
ingredient” of these various approaches (McNally, 2007). Similarly, one might
ask whether current CBT approaches for adult ADHD are converging around
common change processes. Identifying features of efficacious approaches and critically
appraising treatment elements that are not sufficient for efficacy will result in better
“adult ADHD CBT 2.0.”
From the preceding review, we have observed a variety of goals, techniques,
and strategies that appear within treatments described as being based on CBT.
Some treatments focus mainly on helping the client develop organizational and
motivational systems and habits to compensate for their ADHD-related deficits.
Many incorporate concepts from cognitive therapy, wherein habitual patterns of
thinking that contribute to avoidance and emotional distress are examined and
modified. Other interventions appear to be primarily psychoeducational in nature,
covering a broad range of topics associated with ADHD in adults with less emphasis
on specific compensatory and implementation strategies. Finally, a few treatment
approaches incorporate mindfulness-based skills designed to improve clients’ ability
to focus their attention in the moment.
In a previous review of the literature where we examined effect sizes of trials
published to that point (Knouse & Safren, 2010), we hypothesized that the most
critical element in successful CBT for adult ADHD is “the introduction and, most
importantly, the repetition and reinforcement of compensatory skills that target core
symptoms” (p. 507). We also noted that the most efficacious treatments included
elements to deal with motivational difficulties including awareness of and coping

with thinking patterns associated with avoidance. Based on the additional data now
available—particularly larger controlled trials of treatments that emphasize these
elements (Safren et al., 2010; Solanto et al., 2010) and encouraging results from
another structured, skills-based treatment including these elements (Emilsson et al.,
2011)—we maintain this hypothesis.
Our conclusions dovetail with a recent analysis by Ramsay (2010) of possible
mechanisms of change based on an executive dysfunction model of ADHD. His anal-
ysis emphasizes skills training and cognitive and behavioral implementation strategies
including scaffolding, environmental modification, cognitive modification, and plac-
ing interventions at the “point of performance” (Ingersoll & Goldstein, 1993).
The prediction that predominantly psychoeducational and supportive approaches are
unlikely to be effective can be derived from the fact that ADHD is not an issue of
deficient knowledge but of problems implementing that knowledge and translating
it into action (Barkley, 1997a; Ramsay, 2010). Thus, while psychoeducation and
support are necessary elements of successful CBT for adult ADHD, they are not
sufficient. We recommend that the next generation of CBT approaches continue to
focus on techniques to enhance the implementation of compensatory skills (Knouse
& Safren, 2011).
Mediator analyses support the idea that one method of enhancing skill
implementation—homework assignments—is associated with greater improvements
in CBT. Solanto et al. (2010) examined homework completion as a potential
mediator of response to their metacognitive group therapy and found that it was
significantly related to change in investigator-rated inattentive symptoms, while
frequency of session attendance was not a significant predictor of treatment response.
This suggests that implementation of skills in daily life may be a stronger predictor
of improvement than the amount of material to which a patient is exposed. Yovel
and Safren (2007) examined a novel homework-related measure—homework
utility—in the 16 adults with ADHD who received CBT in the Safren, Otto, et al.
(2005) study. Homework utility is an index of the relationship between homework
adherence and session-by-session symptom change over time. Homework utility
significantly predicted improvements in functioning and in investigator-rated CGI
over time in this small sample, whereas overall homework adherence did not. These
findings suggest that the most powerful homework assignments are those that are
both directly relevant to the patient’s functional impairments and implemented
consistently by the patient. A careful functional analysis of a patient’s most impairing
problems can increase the correspondence between skills introduced in CBT and the
patient’s needs (Knouse & Safren, 2013).
Dissemination and Implementation

To make a meaningful impact, CBT for adult ADHD needs to go where the patients
and the clinicians who treat them are. Careful scientific evaluation of delivery and
therapist training methods is necessary to ensure effectiveness. Although large-scale
advances in this area may need to wait for further efficacy data to emerge, smaller-scale
next-step studies informing dissemination should be on the minds of researchers.
CBT for adult ADHD could be adapted for and exported to specialized settings
where people with ADHD are likely to present with unique challenges. For example,
ADHD is highly heritable and thus children with ADHD who are referred for
treatment often have parents who meet criteria for the disorder as well. Behavioral
treatments involving parents are considered first-line interventions for children with
ADHD, especially for young children (American Academy of Pediatrics, 2011). Given
that behavioral parent training interventions require parents to learn and implement
new skills requiring significant self-regulation, skills-based CBT for adults with ADHD
could be adapted to meet the needs of parents with ADHD and could further improve
child outcomes (Chronis-Tuscano et al., 2011). University and community college
settings, including counseling centers and disability services offices, are another setting
in which the unique needs of adults with ADHD could be met with a modified CBT
intervention. For example, in these settings, specific interventions to improve self-
guided study and memory strategies could be incorporated into “standard” CBT
(Knouse, Anastopoulos, & Dunlosky, 2011). People with ADHD in correctional
facilities and chemical dependency units are also in acute need of specialized treatment
approaches (Chan, Dennis, & Funk, 2008; Rösler et al., 2004).
Following the recent work of Craske et al. (2009) on dissemination and imple-
mentation of CBT for anxiety disorders in primary care, there are certainly similar
opportunities for innovation in delivery of adult ADHD treatment. Possible direc-
tions include lower-intensity versions of treatment delivered in a doctor’s office by
paraprofessionals, on-site computer-assisted delivery methods, and online self-help
versions of treatment. The use of paraprofessional “coaches” to augment group CBT
for adult ADHD (e.g., Emilsson et al., 2011; Stevenson et al., 2003) has the potential
to increase both efficacy and cost-effectiveness and should be studied more closely.
Several treatment manuals for CBT approaches outlined in this chapter are now
published (Ramsay & Rostain, 2008; Safren, Perlman, et al., 2005; Solanto, 2011)
and the effects of these manuals on therapist practice and patient outcomes could also
be studied systematically. Importantly, as outlined by McHugh and Barlow (2010),
studies of dissemination strategies must examine two critical issues—how much and
what type of therapist training is needed to ensure competency and positive patient
outcomes, and how should such outcomes be measured? As this field moves forward,
clinical researchers must attend to and build upon dissemination knowledge and
models developed for the exporting of other efficacious CBTs.
Conclusion
CBT for adult ADHD is designed to ameliorate the significant functional impairments
experienced by people with the disorder that are not addressed by medication
alone. Group and individual CBT approaches have recently received support in
larger and more rigorous efficacy studies (Safren et al., 2010; Solanto et al., 2010)
with medium effect sizes compared to active-treatment control groups. The most
efficacious approaches to date focus on helping adults with ADHD acquire and—most
importantly—implement compensatory strategies that ameliorate core symptoms and
deficits in executive functioning. Available evidence to date suggests that CBT may
be useful in treating adults with ADHD who are not taking medication and who
have mild to moderate comorbid internalizing symptoms, but additional studies of
moderators and mediators of treatment outcome are needed. Future critical research
directions also include additional rigorous efficacy studies, adaptation of the treatment
for specialized populations, and evaluation of dissemination and implementation
strategies that should be informed by prior CBT research. Considerable progress has
been made in the last 15 years and yet considerable work remains to provide every
adult with ADHD access to high-quality, evidence-based psychosocial treatment.
References
American Academy of Pediatrics. (2011). ADHD: Clinical practice guideline for the diagnosis,
evaluation, and treatment of attention-deficit/hyperactivity disorder in children and
adolescents. Pediatrics, 128, 1007–1022. doi:10.1542/peds.2011–2654
American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorder
American Psychological Association Presidential Task Force on Evidence-Based Practice.
(2006). Evidence-based practice in psychology. American Psychologist, 61, 271–285.
doi:10.1037/0003-066x.61.4.271
Barkley, R. A. (1997a). ADHD and the nature of self control. New York, NY: Guilford Press.
Barkley, R. A. (1997b). Behavioral inhibition, sustained attention, and executive functions:
Constructing a unifying theory of ADHD. Psychological Bulletin, 121, 65–94.
Barkley, R. A., & Fischer, M. (2011). Predicting impairment in major life activities and
occupational functioning in hyperactive children as adults: Self-reported executive
function (EF) deficits versus EF tests. Developmental Neuropsychology, 36, 137–161.
doi:10.1080/87565641.2010.549877
Barkley, R. A., & Murphy, K. R. (2010). Impairment in occupational functioning and adult
ADHD: The predictive utility of executive function (EF) ratings versus EF tests. Archives
of Clinical Neuropsychology, 25, 157–173. doi:10.1093/arclin/acq014
Barkley, R. A., Murphy, K. R., & Fischer, M. (2008a). ADHD in adults: What the science says.
Barkley, R. A., Murphy, K. R., & Fischer, M. (2008b). History and prevalence of ADHD in
adults. In R. A. Barkley, K. R. Murphy, & M. Fischer, ADHD in adults: What the science
says (pp. 9–25). New York, NY: Guilford Press.
Beck, J. S. (1995). Cognitive therapy: basics and beyond. New York, NY: Guilford Press.
Chambless, D. L. (1998). Update on empirically validated therapies, II. Clinical Psychologist,
51, 3.
Chan, Y.-F., Dennis, M. L., & Funk, R. R. (2008). Prevalence and comorbidity of
major internalizing and externalizing problems among adolescents and adults present-
ing to substance abuse treatment. Journal of Substance Abuse Treatment, 34, 14–24.
doi:10.1016/j.jsat.2006.12.031
Chronis-Tuscano, A., O’Brien, K., Johnston, C., Jones, H., Clarke, T., Raggi, V., …
Seymour, K. (2011). The relation between maternal ADHD symptoms & improvement in
child behavior following brief behavioral parent training is mediated by change in negative
parenting. Journal of Abnormal Child Psychology, 39, 1047–1057. doi:10.1007/s10802-
011-9518-2
Conners, C. K., Erhardt, D., & Sparrow, E. (1999). Conners’ Adult ADHD Rating Scales:
Technical manual. Toronto, Canada: Multi-Health Systems.
Craske, M. G., Roy-Byrne, P. P., Stein, M. B., Sullivan, G., Sherbourne, C., & Bystritsky, A.
(2009). Treatment for anxiety disorders: Efficacy to effectiveness to implementation.
Behaviour Research and Therapy, 47 , 931–937. doi:10.1016/j.brat.2009.07.012
Dimidjian, S., Hollon, S. D., Dobson, K. S., Schmaling, K. B., Kohlenberg, R. J.,
Addis, M. E., … Jacobson, N. S. (2006). Randomized trial of behavioral activation,
cognitive therapy, and antidepressant medication in the acute treatment of adults with
DuPaul, G. J., Power, T. J., Anastopoulos, A. D., & Reid, R. (1998). ADHD Rating Scale-IV:
Checklists, norms, and clinical interpretation. New York, NY: Guilford Press.
Emilsson, B., Gudjonsson, G., Sigurdsson, J., Baldursson, G., Einarsson, E., Olafsdottir, H., &
Young, S. (2011). Cognitive behaviour therapy in medication-treated adults with ADHD
and persistent symptoms: A randomized controlled trial. BMC Psychiatry, 11, 116.
Fayyad, J., de Graaf, R., Kessler, R., Alonso, J., Angermeyer, M., Demyttenaere, K., … Jin, R.
(2007). Cross-national prevalence and correlates of adult attention-deficit hyperactivity
disorder. British Journal of Psychiatry, 190, 402–409.
Hesslinger, B., Tebartz van Elst, L., Nyberg, E., Dykierek, P., Richter, H., Berner, M., &
Ebert, D. (2002). Psychotherapy of attention deficit hyperactivity disorder in adults: A
pilot study using a structured skills training program. European Archives of Psychiatry and
Clinical Neuroscience, 252, 177–184.
Hirvikoski, T., Waaler, E., Alfredsson, J., Pihlgren, C., Holmström, A., Johnson, A., …
Nordström, A.-L. (2011). Reduced ADHD symptoms in adults with ADHD after
structured skills training group: Results from a randomized controlled trial. Behaviour
Research and Therapy, 49, 175–185. doi: 10.1016/j.brat.2011.01.001
Ingersoll, B. D., & Goldstein, S. (1993). Attention deficit disorder and learning disabilities:
Realities, myths, and controversial treatments. New York, NY: Doubleday.
Kessler, R. C., Adler, L., Barkley, R. A., Biederman, J., Conners, C. K., Demler, O., …
Zaslavsky, A. M. (2006). The prevalence and correlates of adult ADHD in the United
States: Results from the National Comorbidity Survey Replication. American Journal of
Knouse, L. E., Anastopoulos, A. D., & Dunlosky, J. (2011). Isolating metamemory deficits
in the self-regulated learning of adults with ADHD. Journal of Attention Disorders, 16,
650–660. doi:10.1177/1087054711417231
Knouse, L. E., & Safren, S. A. (2010). Current status of cognitive behavioral therapy for
adult attention-deficit hyperactivity disorder. Psychiatric Clinics of North America, 33,
497–509.
Knouse, L. E., & Safren, S. A. (2011). Psychosocial treatment of adults with attention-
deficit/hyperactivity disorder. In S. W. Evans & B. Hoza (Eds.), Treating attention deficit
hyperactivity disorder (pp. 12-2–12-7). Kingston, NJ: Civic Research Institute.
Knouse, L. E., & Safren, S. A. (2013). Psychosocial treatment for adult ADHD. In C. B.
Surman (Ed.), ADHD in adults: A practical guide to evaluation and management. New
York, NY: Humana Press.
Linehan, M. M. (1993). Skills training manual for treating borderline personality disorder. New
McDermott, S. P. (2000). Cognitive therapy for adults with attention-deficit/hyperactivity
disorder. In T. E. Brown (Ed.), Attention-deficit disorders and comorbidities in children,
adolescents, and adults (pp. 569–607). Washington, DC: American Psychiatric Press.
McHugh, R. K., & Barlow, D. H. (2010). The dissemination and implementation of evidence-
based psychological treatments: A review of current efforts. American Psychologist, 65,
73–84.
McNally, R. J. (2007). Mechanisms of exposure therapy: How neuroscience can improve

psychological treatments for anxiety disorders. Clinical Psychology Review, 27 , 750–759.
doi:10.1016/j.cpr.2007.01.003
Miller, T. W., Nigg, J. T., & Faraone, S. V. (2007). Axis I and II comorbidity in adults with
ADHD. Journal of Abnormal Psychology, 116, 519–528.
Nigg, J. T. (2006). What causes ADHD? New York, NY: Guilford Press.
Philipsen, A., Richter, H., Peters, J., Alm, B., Sobanski, E., Colla, M., … Hesslinger, B.
(2007). Structured group psychotherapy in adults with attention deficit hyperactivity
disorder: Results of an open multicentre study. Journal of Nervous and Mental Disease,
195, 1013–1019.
Ramsay, J. R. (2002). A cognitive therapy approach for treating chronic procrastination
and avoidance: Behavioral activation interventions. Journal of Group Psychotherapy, Psy-
chodrama & Sociometry, 55, 79–92.
Ramsay, J. R. (2010). CBT for adult ADHD: Adaptations and hypothesized mechanisms of
change. Journal of Cognitive Psychotherapy, 24, 37–45. doi:10.1891/0889-8391.24.1.37
Ramsay, J. R., & Rostain, A. L. (2003). A cognitive therapy approach for adult atten-
tion deficit/hyperactivity disorder. Journal of Cognitive Psychotherapy, 17 , 319–334.
doi:10.1891/jcop.17.4.319.52537
Ramsay, J. R., & Rostain, A. (2008). Cognitive-behavioral therapy for adult ADHD: An
integrative psychosocial and medical approach. New York, NY: Routledge/Taylor &
Francis.
Ramsay, J. R., & Rostain, A. L. (2011). CBT without medications for adult ADHD: An
open pilot study of five patients. Journal of Cognitive Psychotherapy, 25, 277–286.
doi:10.1891/0889-8391.25.4.277
Rapport, M. D., Alderson, R. M., Kofler, M. J., Sarver, D. E., Bolden, J., & Sims, V. (2008).
Working memory deficits in boys with attention-deficit/hyperactivity disorder (ADHD):
The contribution of central executive and subsystem processes. Journal of Abnormal Child
Ratey, J. J., Greenberg, M. S., Bemporad, J. R., & Lindem, K. J. (1992). Unrecognized
attention-deficit hyperactivity disorder in adults presenting for outpatient psychotherapy.
Journal of Child & Adolescent Psychopharmacology, 2, 267–275.
Rösler, M., Retz, W., Retz-Junginger, P., Hengesch, G., Schneider, M., Supprian, T., …
Thome, J. (2004). Prevalence of attention deficit-/hyperactivity disorder (ADHD) and
comorbid disorders in young male prison inmates. European Archives of Psychiatry and
Clinical Neuroscience, 254, 365–371. doi:10.1007/s00406-004-0516-z
Rostain, A. L., & Ramsay, J. R. (2006). A combined treatment approach for adults with
ADHD: Results of an open study of 43 patients. Journal of Attention Disorders, 10,
150–159.
Safren, S. A., Otto, M. W., Sprich, S., Winett, C. L., Wilens, T., & Biederman, J. (2005).
Cognitive-behavioral therapy for ADHD in medication-treated adults with continued
symptoms. Behavior Research and Therapy, 43, 831–842.
Safren, S. A., Perlman, C. A., Sprich, S., & Otto, M. W. (2005). Mastering your adult ADHD:
A cognitive-behavioral therapy approach. New York, NY: Oxford University Press.
Safren, S. A., Sprich, S., Chulvick, S., & Otto, M. W. (2004). Psychosocial treatments for
adults with ADHD. Psychiatric Clinics of North America, 27 , 349–360.
Safren, S. A., Sprich, S., Mimiaga, M. J., Surman, C., Knouse, L. E., Groves, M., & Otto,
M. W. (2010). Cognitive behavioral therapy vs. relaxation with educational support for
medication-treated adults with ADHD and persistent symptoms. JAMA, 304, 857–880.
Safren, S. A., Sprich, S., Perlman, C. A., & Otto, M. W. (2005). Mastering your adult ADHD: A
cognitive-behavioral treatment program client workbook. New York, NY: Oxford University
Press.
Salakari, A., Virta, M., Gronroos, N., Chydenius, E., Partinen, M., Vataja, R., … Iivanainen,
M. (2009). Cognitive-behaviorally-oriented group rehabilitation of adults with ADHD:
Results of a 6-month follow-up study. Journal of Attention Disorders, 13, 516–523.
doi:10.1016/j.psc.2010.04.001
Solanto, M. V. (2011). Cognitive-behavioral therapy for adult ADHD: Targeting executive
dysfunction. New York, NY: Guilford Press.
Solanto, M. V., Marks, D. J., Mitchell, K. J., Wasserstein, J., & Kofman, M. (2008).
Development of a new psychosocial treatment for adult ADHD. Journal of Attention
Disorders, 11, 728–736.
Solanto, M. V., Marks, D. J., Wasserstein, J., Mitchell, K., Abikoff, H., Alvir, J., & Kofman,
M. D. (2010). Efficacy of metacognitive therapy for adult ADHD. American Journal of
Psychiatry, 167 , 958–968.
Spencer, T. J., Adler, L. A., Meihua Qiao, Saylor, K. E., Brown, T. E., Holdnack, J. A., …
Kelsey, D. K. (2010). Validation of the Adult ADHD Investigator Symptom Rating Scale
(AISRS). Journal of Attention Disorders, 14, 57–68. doi:10.1177/1087054709347435
Spitzer, R. L., Williams, J., Gibbon, M., & First, M. B. (1995). The Structured Clinical
Interview for DSM-IV (SCID). New York, NY: Biometric Research Department, New
York State Psychiatric Institute.
Stevenson, C. S., Stevenson, R. J., & Whitmont, S. (2003). A self-directed psychosocial
intervention with minimal therapist contact for adults with attention deficit hyperactivity
disorder. Clinical Psychology & Psychotherapy, 10, 93–101.
Stevenson, C. S., Whitmont, S., Bornholt, L., Livesey, D., & Stevenson, R. J. (2002). A
cognitive remediation programme for adults with attention deficit hyperactivity disorder.
Australian and New Zealand Journal of Psychiatry, 36, 610–616.
Virta, M., Salakari, A., Antila, M., Chydenius, E., Partinen, M., Kaski, M., …
Iivanainen, M. (2010). Short cognitive-behavioral therapy and cognitive training for
adults with ADHD: A randomized controlled pilot study. Neuropsychiatric Disease and
Treatment, 6, 443–453.
Virta, M., Vedenpää, A., Grönroos, N., Chydenius, E., Partinen, M., Vataja, R., …
Iivanainen, M. (2008). Adults with ADHD benefit from cognitive-behaviorally oriented
group rehabilitation: A study of 29 participants. Journal of Attention Disorders, 12,
218–226.
Weiss, M., & Hechtman, L. (2006). A randomized double-blind trial of paroxetine and/
or dextroamphetamine and problem-focused therapy for attention-deficit/hyperactivity
disorder in adults. Journal of Clinical Psychiatry, 67 , 611–619.
Wiggins, D., Singh, K., Getz, H. G., & Hutchins, D. E. (1999). Effects of brief group
intervention for adults with attention deficit/hyperactivity disorder. Journal of Mental
Health Counseling, 21, 82–93.
Wilens, T. E., McDermott, S. P., Biederman, J., Abrantes, A., Hahesy, A., & Spencer, T.
(1999). Cognitive therapy in the treatment of adults with ADHD: A systematic chart
review of 26 cases. Journal of Cognitive Psychotherapy, 13, 215–226.
Young, S., Chick, K., & Gudjonsson, G. (2010). A preliminary evaluation of reasoning and
rehabilitation 2 in mentally disordered offenders (R&R2M) across two secure forensic
settings in the United Kingdom. Journal of Forensic Psychiatry & Psychology, 21, 336–349.
doi:10.1080/14789940903513203
Yovel, I., & Safren, S. (2007). Measuring homework utility in psychotherapy: Cognitive-
behavioral therapy for adult attention-deficit hyperactivity disorder as an example.
Cognitive Therapy and Research, 31, 385–399. doi:10.1007/s10608-006-9065-2
Zylowska, L., Ackerman, D. L., Yang, M. H., Futrell, J. L., Horton, N. L., Hale, T. S., …
Smalley, S. L. (2008). Mindfulness meditation training in adults and adolescents with
ADHD: A feasibility study. Journal of Attention Disorders, 11, 737–746.
33
Attention-Deficit/Hyperactivity
Disorder in Children and
Adolescents
Miguel T. Villodas
University of California, San Francisco, United States
Stephen P. Hinshaw
University of California, Berkeley, United States
Linda J. Pfiffner
University of California, San Francisco, United States
Attention-deficit/hyperactivity disorder (ADHD) is one of the most frequently diag-

nosed psychiatric disorders among children and adolescents, characterized by pervasive
symptoms of inattention (e.g., difficulty completing tasks) and/or hyperactivity (e.g.,
difficulty sitting still) and impulsivity (e.g., difficulty waiting one’s turn; American
Psychiatric Association, 2000). These problems typically develop during early to mid-
dle childhood, although detection in some cases may not be until middle school, and
manifest in profound impairments in multiple contexts. Multiple etiologies may lead
to ADHD, but evidence supports neurological and genetic factors as leading causes
(Barkley, 2006). Nevertheless, it is clear that social-environmental variables can impact
symptom severity, extent and type of impairment, and the development of comorbid
disorders. At school, children with ADHD often have significant impairments in their
academic performance and are frequently cited for behavioral problems (DuPaul &
Stoner, 2003). At home, relationships with their parents are often strained and they
have difficulty managing and organizing responsibilities (Johnston & Jassy, 2007;
Langberg et al., 2011). Moreover, children’s ADHD symptoms interfere with peer
relations, as they are often perceived as uninterested and spaced out, or aggressive
and overbearing (McQuade & Hoza, 2008; Nijmeijer et al., 2008).
In consideration of the pervasive nature of this disorder, behavioral interventions
have been developed that provide parents and teachers with strategies to improve

DOI: 10.1002/9781118528563.wbcbt33
symptoms and functioning of children with ADHD across settings. Despite the
neurological and genetic underpinnings of ADHD, evidence indicates that changing
the social environment through behavioral interventions can dramatically impact
outcomes for youth with ADHD. A substantial literature supports these approaches.
Indeed, a meta-analysis reported large average effect sizes (Cohen’s ds ranging from
0.70 to 3.78 depending on study design) that were stable across demographic factors
(e.g., age, IQ, and race of children, family structure, etc.; Fabiano, Pelham, et al.,
2009).
In contrast to these approaches, early cognitive approaches attempted to address
ADHD deficits and impairments by directly teaching children to use self-instruction
and self-reinforcement in order to improve self-regulation and behavioral responses
(Baer & Nietzel, 1991; DuPaul & Eckert, 1997; Dush, Hirt, & Schroeder, 1989).
The hope was that these approaches would provide a more portable and sustainable
method for promoting behavior change than strictly behavioral approaches, which
rely on parents and teachers. Unfortunately, such strategies were not supported in
empirical studies. A combination of factors may have limited the success of self-
instruction, including the need for sufficient verbal-executive control for children
to generalize their use of the strategies outside of the therapy setting, inadequate
methods within the procedures for addressing the impulsivity and affective instability
characteristics of ADHD, and a failure to address potential skill deficits (Pfiffner,
Calzada, & McBurnett, 2000).
Despite the shortcomings of stand-alone cognitive interventions, a growing evi-
dence base supports psychosocial intervention strategies that include cognitive and
behavioral approaches. For the purposes of this chapter, we will define cognitive
behavioral interventions broadly, with a focus on psychosocial interventions, including
those with cognitive behavioral elements, which have been empirically demonstrated
to improve symptom and functioning deficits in children and adolescents with ADHD.
ADHD symptoms are frequently comorbid with many other psychiatric disorders,
most notably disruptive behavior problems; a number of interventions have been
developed to address both sets of problems (Barkley, 2006). Although this chapter
will primarily focus on interventions with evidence for treating ADHD-related prob-
lems, many of the outcomes will also apply to the comorbid externalizing problems.
Frequently comorbid internalizing problems (e.g., anxiety, depression) may require
additional strategies (MTA Cooperative Group, 1999b).
Behavioral Interventions
Behavioral interventions are the most consistently researched and implemented psy-
chosocial interventions for ADHD (Pelham & Fabiano, 2008). Rooted in social
learning theory (Bandura, 1977), behavioral interventions for this population are
supported by empirical evidence of efficacy across multiple implementation settings.
Although effect sizes vary depending on the outcome of interest and the method of
assessment, results of a key meta-analysis (Fabiano, Pelham, et al., 2009) indicated
medium to large average effect sizes for improvements in parent-reported parenting
practices, direct observations of parenting practices and children’s behaviors, and
Attention-deficit/Hyperactivity Disorder in Children 777
parent and teacher reports of children’s ADHD symptoms, externalizing behaviors,

and impaired functioning. Average effect sizes for academic outcomes were more
variable, generally small to medium for measures of academic achievement.
Behavioral interventions typically begin with a functional behavioral analysis, in
which treatment targets are identified (Pfiffner & Kaiser, 2010). Specifically, positive
and negative behaviors are chosen as targets to increase or decrease, respectively, the
antecedents and consequences of the identified behaviors. Based on this analysis, a
structured system of contingencies (i.e., immediate incentives and consequences) is
developed and is directly linked to the target behaviors. The utility of these approaches
for ADHD is underscored by studies showing that children with ADHD lack
responsivity to partial reinforcement (Parry & Douglas, 1983), delayed reinforcement
(Sonuga-Barke, 2005), and signs of punishments or loss of rewards (Quay, 1997).
They may also have elevated reward thresholds (Haenlein & Caul, 1987). Such
reward-related deficits may relate, at a neural level, to an inherent lack of crucial
receptors for dopamine in key brain tracts (Volkow et al., 2009). Based on these
findings, it would appear that children with ADHD are ideal candidates for behavioral
interventions, which stress immediate, expectable, and salient rewards, appropriate
consequences, consistent routines, and clearly structured rules and expectations.
Behavioral programs have been adapted to target children and adolescents of all
ages in either the home or school setting using behavioral parent training (BPT),
behavioral classroom management (BCM), or a combination of the two. Although
for younger children the primary focus is on training parents and teachers, as children
get older and become more autonomous it becomes increasingly important to involve
them directly in treatment (Pfiffner & Kaiser, 2010). This is often accomplished
by including child skills training components for elementary school-aged children, as
discussed below, or directly including adolescents in the problem-solving process used
to identify target behaviors and contingencies. Adolescents and their parents may also
benefit from interventions that include components of communication skills training.
Behavioral Parent Training

BPT, also referred to as parent training, parent management training, or behavioral
family therapy, focuses on reshaping the “coercive” parent–child interaction process,
as described by Patterson (1982), among families with children characterized by
behavior problems. In this process, parents and their children struggle to control one
another’s behaviors through negative reinforcement (Pfiffner & Kaiser, 2010). For
example, a child may learn to avert parental demands (e.g., chores) by engaging in
increasingly undesirable behavior (e.g., argumentativeness, aggression) until his or
her parents withdraw their demands. Conversely, parents may learn that they can
achieve compliance from their children by engaging in extremely aversive or punitive
behaviors (e.g., yelling, slapping). Among children with ADHD in particular, the early
emergence of behaviors related to core ADHD symptoms has been found to increase
the use of negative parenting practices, which in turn increases the problematic
behaviors in a transactional manner (Johnston & Jassy, 2007). Thus, teaching parents
of children with ADHD to implement effective behavior management techniques is
particularly appropriate.
Versions of BPT have been designed for children and adolescents of all ages
with ADHD (Pfiffner & Kaiser, 2010). BPT is often included in multicomponent
treatments but has also been shown to be effective as a stand-alone treatment for
symptoms and impairments related to ADHD (Fabiano, Pelham, et al., 2009). When
implemented alone, BPT is typically 8–16 sessions and can be administered in a parent
group format or to individual parents/families (Pelham & Fabiano, 2008), or as a
mixture of group and individual sessions (Wells et al., 2000). Most BPT programs for
ADHD include education about ADHD symptoms and impairments plus common
social-learning-theory derived elements that teach parents the following:
• to give short, clear, and effective instructions;

• to develop a structured routine with consistent rules and expectations;
• to reward appropriate behaviors with praise, attention, and incentives;
• to develop a token-economy system to reinforce appropriate home behaviors;
• to extend this system to manage school behaviors (e.g., using daily report cards);
• to actively ignore negative behaviors;
• to effectively use time-out when the child is noncompliant and/or aggressive;
• to effectively manage noncompliant and/or aggressive behaviors in public places;
• to apply the skills to future challenging situations.
Furthermore, many BPT programs are combined with specific skills training for
children, discussed in further detail below.
A variant of BPT is parent–child interaction therapy (PCIT; Zisser & Eyberg,
2010). Although not designed specifically for ADHD, PCIT is an evidence-based
intervention that has been shown to be effective with young children (aged 2–7)
with ADHD. PCIT focuses on restructuring dyadic interactions between parents and
their children in the context of structured play in order to create a context in which
behavior can be managed effectively. In the first phase, child-directed interaction,
children lead play while parents learn to praise enthusiastically, reflect, imitate, and
describe the child’s actions. During the second phase, parent-directed interaction,
parents direct the child to complete tasks using behavioral strategies like those taught
in BPT, such as effectively giving commands and implementing time-out when the
child is noncompliant. Parents learn and practice skills in session with live coaching
from a therapist.
Mediators and moderators of behavioral parent training. Despite the success of BPT,
researchers have identified important factors related to implementation that influence
the impact of this intervention on children with ADHD (Pelham & Fabiano, 2008).
For example, researchers have found that the match between parental treatment
preferences, such as program times, locations, activities, and advertised benefits of the
treatment in which parents participated, influenced their utilization of BPT programs
(Cunningham et al., 2008). Moreover, positive parental expectations prior to and
throughout treatment have been found to predict better treatment engagement in
BPT and better child outcomes (Kaiser, Hinshaw, & Pfiffner, 2010). Similarly, based
on a review of the relevant literature, Mah and Johnston (2008) recommended that
parental social cognitions, such as attributions and parenting efficacy, may be crucial
targets for increasing acceptability of and engagement in BPT, particularly during the
early stages of the treatment.
Researchers have found that factors related to family socioeconomic status may
influence the impact of BPT for children with ADHD and their families because
of barriers to treatment engagement (Lundahl, Risser, & Lovejoy, 2006), such as
attrition, low income, parent education level, single motherhood, and a lack of
father involvement (Chronis, Chacko, Fabiano, Wymbs, & Pelham, 2004; Pelham &
Fabiano, 2008). In response to concerns about the barriers faced by single mothers,
Chacko et al. (2009) developed the Strategies to Enhance Positive Parenting (STEPP)
program. This program enhances BPT by integrating it with a group-based supportive
problem-solving format that follows a manualized approach to common burdens of
single motherhood. In order to increase engagement in treatment among fathers,
Fabiano, Chacko, et al. (2009) developed the Coaching Our Acting-out Children:
Heightened Essential Skills (COACHES) program. This program facilitated the
acquisition of behavioral management techniques among fathers in the context of
sports activities, and found that it increased father involvement in treatment. Atkins
et al. (2006) recruited respected parents from the African American community to
serve as community consultants in a partnership with providers and school personnel
as part of the Positive Attitudes for Learning in Schools (PALS) program in order
to increase engagement in BPT among low-income African American families. Based
on input from these community consultants, the program improved engagement in
BPT by framing sessions as “parent parties” rather than training sessions, emphasizing
social support and community building, and having a community consultant co-lead
groups with a therapist.
Given the strong heritability of ADHD and the risk for a variety of psychopathol-
ogy among parents of youth with ADHD, researchers have begun developing BPT
protocols that include cognitive behavioral therapy (CBT) elements for parents. For
example, in response to the finding that maternal depression may limit the impact of
BPT on child outcomes (Owens et al., 2003), an integrated treatment protocol that
combines BPT and an adjunctive CBT treatment for maternal depression, the Coping
with Depression Course for mothers of children with ADHD, is being developed
and evaluated (e.g., Chronis-Tuscano & Clarke, 2008). Similarly, researchers have
identified that maternal ADHD symptoms attenuate the impact of BPT on child out-
comes because mothers with ADHD often have difficulty adopting and implementing
the new parenting practices (Chronis-Tuscano et al., 2011; Sonuga-Barke, Daley, &
Thompson, 2002). However, a combined treatment for parents and children who
each have ADHD has not yet been developed.
Behavioral Classroom Management

BCM is analogous to BPT and aims to train teachers in behavioral principles that
can be implemented in the classroom setting (DuPaul & Eckert, 1997; Pelham &
Fabiano, 2008). In this intervention model, mental health professionals train teachers
in empirically supported behavior management techniques and provide regular con-
sultation (e.g., DuPaul et al., 2006). Strategies include the use of token-economies
(Pfiffner, Barkley, & DuPaul, 2006) and a mix of positive reinforcement (e.g.,
praise) and prudent negative consequences (e.g., response cost; Pfiffner, O’Leary,
Rosen, & Sanderson, 1985; Pfiffner, Rosen, & O’Leary, 1987) for managing the
behavior problems of children with ADHD. These approaches have been found to
improve academic achievement and behaviors that facilitate academic productivity
(e.g., motivation, engagement, etc.; DuPaul et al., 2006). A variant of a token
economy is the use of a daily report card, on which the child is rated each day
on his or her performance in a number of prespecified domains of behavior that
require improvement—and rewarded for performance (Fabiano et al., 2010). Daily
report cards have been found to improve observed classroom functioning, attainment
of individualized education plan goals, and teacher-rated academic productivity and
disruptive behaviors (Fabiano et al., 2010). Daily report cards also facilitate commu-
nication between teachers and parents and allow for the coordination of school and
home behavioral targets.
Mediators and moderators of behavioral classroom management. Few studies have

examined specific mediators and moderators of BCM, but as with BPT, it is likely
that implementation factors such as engagement, fidelity, and intervention inten-
sity/dosage are important considerations (Pelham & Fabiano, 2008). For example,
although evidence supports the utility of specific interventions, such as daily report
cards, recent studies have demonstrated that these strategies are more likely to be
implemented adequately if conjoint parent–teacher consultation meetings are held
at the child’s school (Murray, Rabiner, Schulte, & Newitt, 2008) and if existing
school personnel substitute for teachers so that they can attend consultation meetings
(Owens, Murphy, Richerson, Girio, & Himawan, 2008). Pfiffner et al. (2011) trained
existing school mental health personnel, learning support professionals, to schedule
conjoint sessions at school with teachers, parents, and their children in order to
develop and manage home and school daily report cards as part of a multicomponent
intervention. In these examples, the use of existing school infrastructure may result in
sustainable implementation of interventions. In another example, Atkins et al. (2008)
recruited influential teachers, referred to as key opinion leaders, and trained them to
implement evidence-based intervention techniques in their classrooms. This strategy
resulted in an increase in the acquisition of these techniques by other teachers in the
same school, as a result of social diffusion. These studies have demonstrated the utility
of these innovative implementation methods for children in low-income, ethnically
diverse, rural and urban communities.
Child Skills Training Interventions
Whereas the above interventions target parents and teachers in order to improve
symptoms and functioning in children with ADHD, skills training interventions that
directly address the skill deficits of these children have also been developed. These
generally include cognitive components but are differentiated from purely cognitive
interventions through their focus on specific skills for day-to-day functioning rather
than global self-instruction.
Social Skills Training

As mentioned above, ADHD in children and adolescents is often associated with
profound and enduring social impairments, many of which are the direct result of
ADHD symptoms (e.g., social unawareness; McQuade & Hoza, 2008; Nijmeijer
et al., 2008). Researchers have identified that youth with ADHD are often more
insensitive and self-centered than their peers (Normand et al., 2011) and more
likely to interrupt others, talk excessively, and behave aggressively and impulsively
(Nijmeijer et al., 2008). Symptoms of inattention may also contribute to difficulty
interpreting emotional and nonverbal cues from peers, often resulting in social
performance deficits (Semrud-Clikeman, 2010). As a result of such impairments in
social functioning, youth with ADHD are more frequently rejected by peers and have
fewer friends (Mikami, 2010; Murray-Close et al., 2010; Nijmeijer et al., 2008).
Social skills training programs have been developed for ADHD to teach a variety
of skills such as good sportsmanship, conversation and communication skills, and
handling teasing and disagreements. A challenge has been generalizing the newly
acquired skills from the treatment setting to everyday encounters at home and school
(e.g., Antshel & Remer, 2003). Programs that have focused on training children at the
point of performance, among similar-age peers, are prone to reinforce the acquisition
of skills and increase the likelihood that they will generalize beyond the treatment
context (Frankel, Myatt, Cantwell, & Feinberg, 1997; Pfiffner et al., 2000; Pfiffner &
McBurnett, 1997; Pfiffner et al., 2007). An exception to this recommendation is for
interventions targeting deviant and delinquent behaviors, in which group treatments
have been found to foster peer training in undesirable behaviors (e.g., Dishion &
Dodge, 2006). Studies have found that training parents to reinforce or coach the
skills taught in social skills training groups facilitates the acquisition of social skills and
the improvement of social outcomes, such as children’s knowledge of social skills and
parents’ and teachers’ ratings of social skill use and social functioning (Frankel et al.,
1997; Pfiffner & McBurnett, 1997; Pfiffner et al., 2007).
Despite the more promising results yielded by studies using these implementation
strategies, impact on peer acceptance and rejection is not especially strong (Mikami,
2010). In addition, it is not apparent that improvements in social skills translate to
improvements in the quality or quantity of children’s friendships. In an attempt to
better target friendship development, Mikami et al. (2010) developed an eight-session
intervention for parents of children with ADHD in which parents were trained to
coach their children in appropriate social skills as well as structure and facilitate
appropriate social interactions or play dates. The results of a pilot study revealed
that children improved on parent-reported social skills and friendship quality and
teacher-reported peer acceptance/rejection (Mikami, Lerner, et al., 2010).
Training Skills for Academic Success

Children and adolescents with ADHD are often characterized by academic problems
that result directly and indirectly from their symptoms (DuPaul & Stoner, 2003).
Specifically, they often have severe difficulties performing executive functions such
as organizing tasks, managing their time, and planning effectively (Barkley, 2006;
Langberg et al., 2011; Langberg, Epstein, Urbanowicz, Simon, & Graham, 2008;
Willcutt, Doyle, Nigg, Faraone, & Pennington, 2005). These functions are partic-
ularly impairing in the academic setting, in which children’s academic success (i.e.,
organizing and completing class work, homework, tests, and projects) is often depen-
dent on these skills. Poor organizational and study skills often translate into lower
scores on academic achievement tests, poorer class work and homework completion,
lower report card grades, and overall deficits in academic performance (Barkley,
2006; Power, Werba, Watkins, Angelucci, & Eiraldi, 2006; Schultz, Evans, & Serpell,
2009). Interventions have been developed to target the following specific skills, which
promote academic success:
• organizational skills (Abikoff et al., 2013; Evans, Langberg, Raggi, Allen, &
Buvinger, 2005; Langberg, Epstein, Urbanowicz, et al., 2008);
• self-management (Gureasko-Moore, DuPaul, & White, 2006, 2007);
• note-taking (Evans, Pelham, & Grudberg, 1995);
• homework skills (Raggi, Chronis-Tuscano, Fishbein, & Groomes, 2009).
Comprehensive programs that teach many of these skills, such as the Challenging
Horizons Program (CHP; Evans et al., 2005; Evans, Schultz, DeMars, & Davis,
2011; Langberg, Epstein, Urbanowicz, et al., 2008), have recently demonstrated
their utility for the improvement of children’s academic outcomes as well as their
organization and homework skills. CHP combines various treatment components,
which have been evaluated individually and in varying doses, into a comprehensive
after-school program involving intensive intervention 2 to 4 days each week. The
intervention can be implemented in different forms, but in general the sessions last
approximately 2 hours each and can continue for 10 weeks up to an academic year,
and can be implemented by mental health professionals or school personnel. The
most comprehensive implementations of CHP include three Family Check-Up (FCU;
Dishion, Nelson, & Kavanagh, 2003) sessions during the fall semester prior to the
start of the intervention (Evans et al., 2011). The Family Check-Up was designed as
an enhancement to more intensive interventions, in which parents are motivated and
engaged in better monitoring of their children and management of their families. The
three sessions consist of an initial interview, an assessment session, and a feedback
session, in which feedback about the assessment results is delivered using motivational
interviewing techniques.
Mediators and Moderators of Child Skills Training Interventions

As noted above, most social skills training programs are targeted for child training,
and the effects are a function of the extent to which generalization is achieved.
Recent studies have found that negative parenting practices (Kaiser, McBurnett,
& Pfiffner, 2011; Mikami, Jack, Emeh, & Stephens, 2010) and maternal ADHD
(Griggs & Mikami, 2011b; Mikami, Jack, et al., 2010) were not only related to
poor social functioning and poor peer relations among children with ADHD, but also
moderated parents’ abilities to facilitate their children’s development and maintenance
of friendships (Griggs & Mikami, 2011a). These findings highlight the importance
of combining social skills training with parent training, such as BPT. They also
underscore the importance of including parents in a complementary role in these
interventions. It is likely that social skills training will be most beneficial with ongoing
monitoring and incentives from parents and that didactic learning will be insufficient.
With regard to training skills for academic success, some important factors should
also be considered. For example, it has been estimated that approximately 30% of
children and adolescents with ADHD have a comorbid specific learning disorder
(DuPaul & Stoner, 2003). Teaching study and organizational skills may be necessary
but not sufficient for those with a specific learning disorder, which will in all prob-
ability require educational interventions in the areas of disability. Another potential
consideration for the development of academic skills interventions is the age range
of the youth who are targeted. Langberg and colleagues (Langberg, Epstein, Altaye,
et al., 2008; Langberg et al., 2011) have identified that ADHD symptoms and
impairments generally decrease as children develop, but this trend can be disrupted
by contextual shifts (e.g., the transition to more demanding academic environments).
These findings suggest that it is appropriate to tailor these interventions to meet
the needs of key transition periods. Moreover, teaching these skills in the context in
which they will be used (e.g., the school setting) may facilitate their acquisition and
application.
Cognitive Skills Training
Researchers have recently begun to investigate interventions to directly treat the

neurocognitive deficits thought to underlie many of the core symptoms and impair-
ments of children with ADHD, such as deficits in the executive functioning domains
involved with attention, planning, inhibition, and working memory (Barkley, 2006;
Willcutt et al., 2005). In response to preliminary successes in improving these exec-
utive functions among individuals who have sustained brain injuries (e.g., Sohlberg,
McLaughlin, Pavese, Heidrich, & Posner, 2000), researchers began to develop pro-
grams to target children with similar cognitive deficits that result from ADHD.
For example, investigators have developed computer-mediated programs that require
children to complete increasingly difficult working memory tasks for approximately
25 to 45 minutes daily for 4 to 6 weeks (Holmes et al., 2010; Klingberg et al.,
2005; Klingberg, Forssberg, & Westerberg, 2002; Mezzacappa & Buckner, 2010).
Although some clinical evaluations have shown promising preliminary results for
improvements on tests of verbal and visuo-spatial working memory and other execu-
tive functions (e.g., response inhibition), effects on ADHD symptoms and day-to-day
impairments have been less consistently investigated. Specifically, although one study
reported improvements in teacher ratings of ADHD symptoms (Mezzacappa & Buck-
ner, 2010), only one study used blinded ratings of such symptoms, finding significant
improvements in parent but not teacher reports (Klingberg et al., 2005).
Other similar neurocognitive training programs aim to improve the attention
deficits that are central to ADHD (Hagen, Moore, Wickman, & Maples, 2008;
Kerns, Eso, & Thomson, 1999; Semrud-Clikeman et al., 1999; Shalev, Tsal, &
Mevorach, 2007). These programs have followed a similar format, requiring varying
doses (ranging from 50 minutes to 2 hours weekly for 4 to 8 weeks) of attention

exercises of increasing difficulty, using either computer-mediated tasks (e.g., Hagen
et al., 2008; Shalev et al., 2007) or neurocognitive training administered in person
(e.g., Kerns et al., 1999; Semrud-Clikeman et al., 1999). Children received auditory
feedback based on their accuracy and reaction time, converted into points upon the
completion of each task. Evidence of improvement in attention problems has been
documented, and a randomized clinical trial reported evidence of improvements in
academic outcomes (i.e., reading comprehension and writing fluency) as well (Shalev
et al., 2007). However, significant improvements in ADHD symptoms were reported
only in this study (a randomized clinical trial) and were restricted to parent reports of
inattention symptoms (Shalev et al., 2007).
Neurofeedback, a specific type of biofeedback, which involves the use of electrodes
to measure the electrical activity of the brain in different functional states, has also been
proposed as a potential treatment for children with ADHD (Lofthouse, McBurnett,
Arnold, & Hurt, 2011; Sherlin, Arns, Lubar, & Sokhadze, 2010). Neurofeedback
uses auditory and visual feedback about changes in the brain’s electrical activity, which
allows individuals to learn to control their physiological states. Children with ADHD
in particular have been found to have low levels of arousal in frontal areas of the brain
as a result of excessive theta (slow) waves and a deficit of beta (fast) waves. Through
intensive neurofeedback training (approximately 30 to 40 hours over 2 to 3 months),
the goal is to teach children through operant and classical conditioning to increase
beta and decrease theta brain wave patterns in frontal areas. Researchers have called
for improved methodological rigor in the evaluation of these treatments, pointing
to the dearth of randomized clinical trials and studies comparing neurofeedback to
semi-active control groups and placebo treatments, such as sham neurofeedback and
cognitive skills trainings, that simulate the nonspecific effects of neurofeedback (e.g.,
therapist–client interaction, time-intensive training, etc.; Loo & Barkley, 2005).
However, recent studies have addressed these concerns and have begun to establish
evidence of the efficacy of this treatment for improving beta-theta activity as well
as symptoms of ADHD, particularly inattention, in children (Bakhshayesh, Hänsch,
Wyschkon, Rezai, & Esser, 2011; Gevensleben et al., 2009; Gevensleben et al., 2010).
Although these treatments have demonstrated some preliminary evidence for
positive effects on core neurocognitive impairments associated with ADHD, it is
unclear whether these treatments ameliorate symptoms or functional impairments.
Although it is possible that these programs could develop into important adjunctive or
complementary components to other skill remediation and behavioral interventions,
more research is needed to identify their potential efficacy, particularly given the
relative time and financial costs with which they are associated.
Multicomponent Interventions
The preponderance of contemporary intervention programs consists of combinations

of the aforementioned interventions, often including some form of BPT, BCM,
and child skills training. Although each component has been supported, in part,
by empirical evidence, the multicomponent interventions described below have
evidenced the most comprehensive impacts on the symptoms and functioning of

children with ADHD.
Child Life and Attention Skills/Collaborative Life Skills programs

The majority of interventions for children with ADHD have focused on improving
hyperactivity and impulsivity, with little emphasis on improving inattention. To
address this gap, Pfiffner et al. (2007) developed the Child Life and Attention
Skills program (CLAS), which was designed to directly address the symptoms and
impairments of elementary school-aged children with the predominantly inattentive
type of ADHD (ADHD-I). The intervention was adapted from previous evidence-
based treatments and consists of 10 sessions of concurrent BPT and child skills
training groups that are delivered in a clinic setting, as well as up to five teacher
consultation sessions in which teachers learn to implement classroom accommodations
and develop a daily report card. In the skill groups, children learn social, emotion
regulation, organizational, problem-solving, and independent living skills. Parents
learn the general principles of behavior management and develop a home daily report
card that complements the school daily report card. Delivery is coordinated so that
parents, children, and teachers are simultaneously trained, with identical terminology,
via group and individualized methods. Reinforcement contingencies are implemented
within and across settings in order to maximize the impact of the intervention
across impairment domains in an active partnership of parents, teachers, and learning
support professionals. The results of a randomized clinical trial indicate that children
who received CLAS had significant improvements in aggregate parent and teacher
ratings of ADHD symptoms and severity, as well as social and organizational skills, at
posttreatment, which were sustained at 3- to 5-month follow-up (Pfiffner et al., 2007).
A large-scale, two-site randomized clinical trial of CLAS is currently being conducted.
Based on the success of CLAS, Pfiffner et al. (2011) extended this program in order
to target the more general ADHD population, including all types, with the objective
of establishing a sustainable implementation method in a public school setting. The
adapted intervention, the Collaborative Life Skills (CLS) program, is targeted for
elementary school-aged children, but is designed to be implemented at the child’s
school by existing school mental health personnel, learning support professionals.
Implementation in the school setting also allows for intervention delivery at the point
of performance, that is, in the setting in which many of the children’s problems are
occurring. Learning support professionals are trained in the intervention by university-
based clinicians. As part of the program, learning support professionals conduct 10
weekly BPT and child skills training groups at the children’s schools, lead a 30-
to 60-minute orientation meeting for participating teachers, and coordinate two or
three meetings with teachers, parents, and their children to develop a school daily
report card to complement the home daily report card developed by the parents.
Initial pre-post results reveal that children significantly improved in parent ratings of
problem behavior, homework problems, and social skills; teacher ratings of behaviors
that enable academic success; parent and teacher ratings of ADHD symptoms and
organizational skills; and academic achievement scores, observations of classroom
behavior, and report card grades (Pfiffner et al., 2011; Pfiffner et al., 2013).
Summer Treatment Programs

Some of the most comprehensive and intensive multicomponent intervention pro-
grams are summer treatment programs, which are generally targeted for children in
grades 1–11 (e.g., Pelham, Fabiano, Gnagy, Greiner, & Hoza, 2005; Pelham et al.,
2010; Pelham & Hoza, 1996). Summer treatment programs combine BPT, child
skills training, and analogous BCM interventions in a summer-camp-like setting that
children attend for approximately 9 hours per day for 8 weeks. Trained behavioral
counselors maintain a behavior management system analogous to BCM as the children
engage in sports, art, and academic classes. Included in the regular curriculum are
child social and academic skill interventions, with individual daily report cards devel-
oped for each child. In addition, group BPT sessions and medication evaluation and
management are provided. Studies evaluating summer treatment programs have gen-
erally indicated that these programs improve symptoms and functional impairments
across a variety of domains as rated by parents, teachers, and counselors. Although
summer treatment programs provide a convenient treatment setting for families in
which children are supervised daily, these programs are labor-intensive and costly,
which may limit their feasibility. Researchers are currently exploring adaptations to
the intervention protocol that would facilitate their implementation as after-school
programs (Frazier, Cappella, & Atkins, 2007). Furthermore, there is no evidence that
summer treatment programs provide gains that fundamentally alter the trajectories
of youth with ADHD across the long term. It seems likely that ongoing, albeit less
intensive, behavioral interventions will be needed.
Programs with Partial Support for Attention-Deficit/Hyperactivity

Disorder
First steps to success. Although not specifically designed for children with ADHD, the
First Steps to Success program is another intervention in which school personnel
implement BPT and BCM in the school context in order to ameliorate children’s
externalizing behavior problems (Walker et al., 2009). The program is targeted for
children in Kindergarten to third grade and consists of 30 “program days” on which
the intervention is implemented at school, plus six home sessions in which parents learn
to implement BPT strategies. Seeley et al. (2009) conducted a randomized clinical
trial for children with ADHD and found that children assigned to the intervention
condition had significantly greater improvements in ADHD behaviors, social skills,
and academic problems at school. However, they did not find significantly greater
improvements in ADHD behaviors and social skills at home among this group, which
may indicate that the parent component of this intervention needs further adaptation
to adequately address the impairments of children with ADHD.
Incredible years. Initially designed for disruptive behavior problems in preschool chil-
dren, the Incredible Years program (Webster-Stratton & Reid, 2010) has shown
some evidence of utility for children with both comorbid and primary ADHD prob-
lems. Incredible Years is a comprehensive, multisetting program for young children
(ages 3–7) that integrates BPT, BCM, and child skills training interventions. Each
component of the program can be implemented separately, but the program is

more potent when the components are combined. The only evaluation of Incred-
ible Years for ADHD is a recent 20-week randomized clinical trial with just the
BPT and child skills training components. Results showed improvements in a
variety of child externalizing behavior problems, including inattention and hyper-
activity, by mother and father reports, but not teacher reports (Webster-Stratton,
Reid, & Beauchaine, 2011). Additional studies that include the BCM component
are needed to evaluate the effects of the intervention for key areas of ADHD
impairment.
Multimodal Treatments
The focus of this chapter has been on psychosocial interventions for ADHD, but
it is also important to consider the impact of these interventions in the context of
pharmacological approaches to treatment, given their status as an evidence-based
treatment for ADHD (Hinshaw, Klein, & Abikoff, 2007). Stimulant medication in
particular has a strong evidence base supporting its efficacy for ADHD and is widely
used by pediatricians and psychiatrists for managing ADHD symptoms in children
and adolescents. Additionally, medication and behavioral interventions in combination
appear to form an especially potent treatment. The largest and most renowned study
of medication and behavioral treatments was the Multimodal Treatment Study of
ADHD (MTA), a six-site collaborative effort designed to rigorously evaluate the
effects of pharmacological, behavioral, and combined intervention approaches for the
treatment of ADHD (MTA Cooperative Group, 1999a; Pelham et al., 2000; Swanson
et al., 2008a, 2008b). The behavioral treatment included 35 BPT sessions for parents,
both group and individual; therapist-facilitated consultation and coordination with
the children’s teachers; an 8-week summer treatment program; and paraprofessional
aide involvement in the classroom for 3 months following the summer treatment
program. These treatments were faded toward the end of the 14-month intervention
period.
Although initial results supported the superiority of the medication and combined
treatments over behavioral treatment alone for ADHD symptom reduction, (a) com-
bination treatment was superior with regard to academic, social, and parenting-related
impairments (e.g., Connors et al., 2001); and (b) after the active intervention period,
medication benefits fell off more sharply than those from behavioral intervention
(e.g., Molina et al., 2009). Furthermore, during the summer treatment program, a
comparison of differences between the behavioral and combined treatment groups
across three sites revealed few differences between them while both treatments were
active (Pelham et al., 2000). Moreover, subsequent analyses have revealed important
and positive impacts of the behavioral treatment on parent–child interactions (Wells
et al., 2006) and homework success (Langberg et al., 2010). Finally, combination
treatment, when associated with improved parenting, was prone to yield not just
improvement in behavior, but normalization of such behavior (Hinshaw et al., 2000).
Overall, the MTA study has demonstrated the substantial benefit of combined phar-
macological and behavioral interventions as the most potent treatment approach for
the most impaired children with ADHD. Further evidence for this treatment approach
comes from studies showing that when behavioral interventions are in place, optimal
medication dosages may be lower, with more durable and broader effects (Fabiano
et al., 2007).
Conclusions
The evidence base for behavioral interventions is longstanding, with BPT, BCM,
and intensive peer-based treatments meeting rigorous criteria for categorization as
evidence-based treatments (Pelham & Fabiano, 2008). Although initial evaluations
of cognitive interventions focused on self-instruction for children with ADHD were
discouraging, more recent psychosocial interventions that incorporate both cogni-
tive and behavioral strategies targeting specific skill development show significant
and clinically important effects on ADHD symptoms and functional impairments.
Moreover, despite evidence for individual intervention strategies such as BPT, BCM,
and child skills training, combined/multicomponent/multimodal treatment packages
have demonstrated the most consistent impact on a broader range of symptoms and
impairments among these children and adolescents. This latter finding is likely to be
the result of direct training of skills in the real-world contexts to which they apply (e.g.,
school, home, etc.) and the generalization of the structured behavioral contingencies
across these contexts. Given the potential for moderators and mediators to influence
the impact of interventions, emerging research on adaptive implementation strategies
should improve the sustainability and dissemination of interventions to populations
who were previously unable to access them. In addition, the personalization of inter-
vention packages to match the preferences and needs of specific populations should
facilitate increased treatment engagement. Also, in light of support for the incremental
impact of combined pharmacological and behavioral interventions, it is possible that
personalizing this combined treatment approach through sequencing of interventions
could provide the most potent effects. Although evidence for working memory and
attention training is still preliminary, additional research is warranted to determine
the potential benefits of these approaches for the full range of ADHD symptoms and
impairments. Finally, researchers should continue to explore and develop innovative
methods of intervention dissemination that are both sustainable and cost-effective.
References
Abikoff, H., Gallagher, R., Wells, K. C., Murray, D. W., Huang, L., Lu, F., et al. (2013)
Remediating Organizational Functioning in Children with ADHD: Immediate and Long-
Term Effects from a Randomized Controlled Trial. Journal of Consulting and Clinical
Antshel, K. M., & Remer, R. (2003). Social skills training in children with attention deficit
hyperactivity disorder: A randomized-controlled clinical trial. Journal of Clinical Child
and Adolescent Psychology, 32, 153–165. doi:10.1207/15374420360533149
Atkins, M. S., Frazier, S. L., Birman, D., Adil, J. A., Jackson, M., Graczyk, P. A., … McKay, M.
M. (2006). School-based mental health services for children living in high poverty urban
communities. Administration and Policy in Mental Health and Mental Health Services
Research, 33, 146–159.
Atkins, M. S., Frazier, S. L., Leathers, S. J., Graczyk, P. A., Talbott, E., Jakobsons, L.,
… Bell, C. C. (2008). Teacher key opinion leaders and mental health consultation in
low-income urban schools. Journal of Consulting and Clinical Psychology, 76, 905–908.
doi:10.1037/a0013036
Baer, R. A., & Nietzel, M. T. (1991). Cognitive and behavioral treatment of impulsivity in
children: A meta-analytic review of the outcome literature. Journal of Clinical Child
Psychology, 20, 400–412. doi:10.1207/s15374424jccp2004_9
Bakhshayesh, A. R., Hänsch, S., Wyschkon, A., Rezai, M. J., & Esser, G. (2011). Neurofeedback
in ADHD: A single-blind randomized controlled trial. European Child & Adolescent
Psychiatry, 20, 481–491. doi:10.1007/s00787-011-0208-y
Bandura, A. (1977). Social learning theory. Oxford, England: Prentice Hall.
Barkley, R. A. (Ed.). (2006). Attention-deficit hyperactivity disorder: A handbook for diagnosis
and treatment (3rd ed.). New York, NY: Guilford Press.
Chacko, A., Wymbs, B. T., Wymbs, F. A., Pelham, W. E., Swanger-Gagne, M. S., Girio,
E., … O’Connor, B. (2009). Enhancing traditional behavioral parent training for single
mothers of children with ADHD. Journal of Clinical Child and Adolescent Psychology, 38,
206–218.
Chronis, A. M., Chacko, A., Fabiano, G. A., Wymbs, B. T., & Pelham, W. E. (2004).
Enhancements to the behavioral parent training paradigm for families of children with
ADHD: Review and future directions. Clinical Child and Family Psychology Review, 7 ,
1–27.
Chronis-Tuscano, A., & Clarke, T. L. (2008). Behavioral skills training for depressed mothers
of children with ADHD. In L. L’Abate (Ed.), Toward a science of clinical psychology:
Laboratory evaluations and interventions (pp. 57–77). Hauppauge, NY: Nova Science.
Chronis-Tuscano, A., O’Brien, K. A., Johnston, C., Jones, H. A., Clarke, T. L., Raggi, V.
L., … Seymour, K. E. (2011). The relation between maternal ADHD symptoms and
improvement in child behavior following brief behavioral parent training is mediated by
change in negative parenting. Journal of Abnormal Child Psychology, 39, 1047–1057.
doi:10.1007/s10802-011-9518-2
Connors, C. K., Epstein, J. N., March, J. S., Angold, A., Wells, K. C., Klaric, J., … Wigal,
T. (2001). Multimodal treatment of ADHD in the MTA: An alternative outcome
analysis. Journal of the American Academy of Child & Adolescent Psychiatry, 40, 159–167.
doi:10.1097/00004583-200102000-00010
Cunningham, C. E., Deal, K., Rimas, H., Buchanan, D. H., Gold, M., Sdao-Jarvie, K., &
Boyle, M. (2008). Modeling the information preferences of parents of children with
mental health problems: A discrete choice conjoint experiment. Journal of Abnormal
Child Psychology, 36, 1123–1138.
Dishion, T. J., & Dodge, K. A. (2006). Deviant peer contagion in interventions and programs:
An ecological framework for understanding influence mechanisms. In K. A. Dodge, T. J.
Dishion, & J. E. Lansford (Eds.), Deviant peer influences in programs for youth: Problems
and solutions (pp. 14–43). New York, NY: Guilford Press.
Dishion, T. J., Nelson, S. E., & Kavanagh, K. (2003). The family check-up with high-risk
young adolescents: Preventing early-onset substance use by parent monitoring. Behavior
Therapy, 34, 553–571. doi:10.1016/s0005-7894(03)80035-7
DuPaul, G. J., & Eckert, T. L. (1997). The effects of school-based interventions for attention
deficit hyperactivity disorder: A meta-analysis. School Psychology Review, 26, 5–27.
DuPaul, G. J., Jitendra, A. K., Volpe, R. J., Tresco, K. E., Lutz, J. G., Junod, R. E. V., …
Mannella, M. C. (2006). Consultation-based academic interventions for children with
ADHD: Effects on reading and mathematics achievement. Journal of Abnormal Child
Psychology, 34, 635–648. doi:10.1007/s10802-006-9046-7
DuPaul, G. J., & Stoner, G. (2003). ADHD in the schools: Assessment and intervention strategies
Dush, D. M., Hirt, M. L., & Schroeder, H. E. (1989). Self-statement modification in
the treatment of child behavior disorders: A meta-analysis. Psychological Bulletin, 106,
97–106. doi:10.1037/0033-2909.106.1.97
Evans, S. W., Langberg, J., Raggi, V., Allen, J., & Buvinger, E. C. (2005). Development
of a school-based treatment program for middle school youth with ADHD. Journal of
Attention Disorders, 9, 343–353. doi:10.1177/1087054705279305
Evans, S. W., Pelham, W., & Grudberg, M. V. (1995). The efficacy of notetaking to improve
behavior and comprehension of adolescents with attention deficit hyperactivity disorder.
Exceptionality, 5, 1–17. doi:10.1207/s15327035ex0501_1
Evans, S. W., Schultz, B. K., DeMars, C. E., & Davis, H. (2011). Effectiveness of the
Challenging Horizons after-school program for young adolescents with ADHD. Behavior
Therapy, 42, 462–474.
Fabiano, G. A., Chacko, A., Pelham, W. E., Robb, J., Walker, K. S., Wymbs, F., … Pirvics, L.
(2009). A comparison of behavioral parent training programs for fathers of children with
attention-deficit/hyperactivity disorder. Behavior Therapy, 40, 190–204.
Fabiano, G. A., Pelham, W. E., Coles, E. K., Gnagy, E. M., Chronis-Tuscano, A., & O’Connor,
B. C. (2009). A meta-analysis of behavioral treatments for attention-deficit/hyperactivity
disorder. Clinical Psychology Review, 29, 129–140.
Fabiano, G. A., Pelham, W. E., Gnagy, E. M., Burrows-MacLean, L., Coles, E. K., Chacko,
A., … Robb, J. A. (2007). The single and combined effects of multiple intensities of
behavior modification and multiple intensities of methylphenidate in a classroom setting.
School Psychology Review, 36, 195–216.
Fabiano, G. A., Vujnovic, R. K., Pelham, W. E., Waschbusch, D. A., Massetti, G. M.,
Pariseau, M. E., … Volker, M. (2010). Enhancing the effectiveness of special education
programming for children with attention deficit hyperactivity disorder using a daily report
card. School Psychology Review, 39, 219–239.
Frankel, F., Myatt, R., Cantwell, D. P., & Feinberg, D. T. (1997). Parent-assisted transfer
of children’s social skills training: Effects on children with and without attention-deficit
hyperactivity disorder. Journal of the American Academy of Child & Adolescent Psychiatry,
36, 1056–1064. doi:10.1097/00004583-199708000-00013
Frazier, S. L., Cappella, E., & Atkins, M. S. (2007). Linking mental health and after school
systems for children in urban poverty: Preventing problems, promoting possibilities.
Administration and Policy in Mental Health and Mental Health Services Research, 34,
389–399. doi:10.1007/s10488-007-0118-y
Gevensleben, H., Holl, B., Albrecht, B., Schlamp, D., Kratz, O., Studer, P., … Heinrich, H.
(2009). Distinct EEG effects related to neurofeedback training in children with ADHD:
A randomized controlled trial. International Journal of Psychophysiology, 74, 149–157.
doi:10.1016/j.ijpsycho.2009.08.005
Gevensleben, H., Holl, B., Albrecht, B., Schlamp, D., Kratz, O., Studer, P., … Heinrich,
H. (2010). Neurofeedback training in children with ADHD: 6-month follow-up of
a randomised controlled trial. European Child & Adolescent Psychiatry, 19, 715–724.
doi:10.1007/s00787-010-0109-5
Griggs, M. S., & Mikami, A. Y. (2011a). Parental attention-deficit/hyperactivity disor-
der predicts child and parent outcomes of parental friendship coaching treatment.
Journal of the American Academy of Child & Adolescent Psychiatry, 50, 1236–1246.
doi:10.1016/j.jaac.2011.08.004
Griggs, M. S., & Mikami, A. Y. (2011b). The role of maternal and child ADHD symptoms in
shaping interpersonal relationships. Journal of Abnormal Child Psychology, 39, 437–449.
Gureasko-Moore, S., DuPaul, G. J., & White, G. P. (2006). The effects of self-management
in general education classrooms on the organizational skills of adolescents with ADHD.
Behavior Modification, 30, 159–183. doi:10.1177/0145445503259387
Gureasko-Moore, S., DuPaul, G. J., & White, G. P. (2007). Self-management of classroom
preparedness and homework: Effects on school functioning of adolescents with attention
deficit hyperactivity disorder. School Psychology Review, 36, 647–664.
Haenlein, M., & Caul, W. F. (1987). Attention deficit disorder with hyperactivity: A specific
hypothesis of reward dysfunction. Journal of the American Academy of Child & Adolescent
Psychiatry, 26, 356–362. doi:10.1097/00004583-198705000-00014
Hagen, H., Moore, K., Wickman, G., & Maples, W. C. (2008). Effect of the EYEPORT system
on visual function in ADHD children: A pilot study. Journal of Behavioral Optometry, 19,
37–41.
Hinshaw, S. P., Klein, R. G., & Abikoff, H. B. (2007). Childhood attention-
deficit/hyperactivity disorder: Nonpharmacological treatments and their combination
with medication. In P. J. Nathan & A. M. Gorman (Eds.), A guide to treatments that work
(3rd ed., pp. 3–27). New York, NY: Oxford University Press.
Hinshaw, S. P., Owens, E. B., Wells, K. C., Kraemer, H. C., Abikoff, H. B., Arnold,
L. E., … Wigal, T. (2000). Family processes and treatment outcome in the MTA:
Negative/ineffective parenting practices in relation to multimodal treatment. [Special
Issue: Child and family characteristics as predictors and outcomes in the Multimodal
Treatment Study of ADHD (MTA Study)] Journal of Abnormal Child Psychology, 28,
555–568. doi:10.1023/A:1005183115230
Holmes, J., Gathercole, S. E., Place, M., Dunning, D. L., Hilton, K. A., & Elliott, J. G.
(2010). Working memory deficits can be overcome: Impacts of training and medication
on working memory in children with ADHD. Applied Cognitive Psychology, 24, 827–836.
doi:10.1002/acp.1589
Johnston, C., & Jassy, J. S. (2007). Attention-deficit/hyperactivity disorder and opposi-
tional/conduct problems: Links to parent–child interactions. Journal of the Canadian
Kaiser, N. M., Hinshaw, S. P., & Pfiffner, L. J. (2010). Parent cognitions and behavior parent
training: Engagement and outcomes. ADHD Reports, 18, 6–12.
Kaiser, N. M., McBurnett, K., & Pfiffner, L. J. (2011). Child ADHD severity and positive and
negative parenting as predictors of child social functioning: Evaluation of three theoretical
models. Journal of Attention Disorders, 15, 193–203. doi:10.1177/1087054709356171
Kerns, K. A., Eso, K., & Thomson, J. (1999). Investigation of a direct intervention for
improving attention in young children with ADHD. Developmental Neuropsychology, 16,
273–295. doi:10.1207/s15326942dn1602_9
Klingberg, T., Fernell, E., Olesen, P. J., Johnson, M., Gustafsson, P., Dahlström, K., …
Westerberg, H. (2005). Computerized training of working memory in children with
ADHD: A randomized, controlled trial. Journal of the American Academy of Child &
Adolescent Psychiatry, 44, 177–186. doi:10.1097/00004583-200502000-00010
Klingberg, T., Forssberg, H., & Westerberg, H. (2002). Training of working memory in chil-
dren with ADHD. Journal of Clinical and Experimental Neuropsychology, 24, 781–791.
doi:10.1076/jcen.24.6.781.8395
Langberg, J. M., Arnold, L. E., Flowers, A. M., Epstein, J. N., Altaye, M., Hinshaw, S.
P., … Hechtman, L. (2010). Parent-reported homework problems in the MTA study:
Evidence for sustained improvement with behavioral treatment. Journal of Clinical Child
and Adolescent Psychology, 39, 220–233. doi:10.1080/15374410903532700
Langberg, J. M., Epstein, J. N., Altaye, M., Molina, B. S. G., Arnold, L. E., & Vitiello, B.
(2008). The transition to middle school is associated with changes in the developmental
trajectory of ADHD symptomatology in young adolescents with ADHD. Journal of
Clinical Child and Adolescent Psychology, 37 , 651–663.
Langberg, J. M., Epstein, J. N., Girio-Herrera, E., Becker, S. P., Vaughn, A. J., & Altaye,
M. (2011). Materials organization, planning, and homework completion in middle-
school students with ADHD: Impact on academic performance. School Mental Health, 3,
93–101. doi:10.1007/s12310-011-9052-y
Langberg, J. M., Epstein, J. N., Urbanowicz, C. M., Simon, J. O., & Graham, A. J. (2008).
Efficacy of an organization skills intervention to improve the academic functioning of
students with attention-deficit/hyperactivity disorder. School Psychology Quarterly, 23,
407–417. doi:10.1037/1045-3830.23.3.407
Lofthouse, N., McBurnett, K., Arnold, L. E., & Hurt, E. (2011). Biofeedback and neuro-
feedback treatment for ADHD. Psychiatric Annals, 41, 42–48. doi:10.3928/00485713-
20101221-07
Loo, S. K., & Barkley, R. A. (2005). Clinical utility of EEG in attention deficit hyperactivity
disorder. [Special Issue: Attention deficit hyperactivity disorder] Applied Neuropsychology,
12, 64–76. doi:10.1207/s15324826an1202_2
Lundahl, B., Risser, H. J., & Lovejoy, M. C. (2006). A meta-analysis of parent train-
ing: Moderators and follow-up effects. Clinical Psychology Review, 26, 86–104.
doi:10.1016/j.cpr.2005.07.004
Mah, J. W. T., & Johnston, C. (2008). Parental social cognitions: Considerations in the
acceptability of and engagement in behavioral parent training. Clinical Child and Family
Psychology Review, 11, 218–236. doi:10.1007/s10567-008-0038-8
McQuade, J. D., & Hoza, B. (2008). Peer problems in attention deficit hyperactivity disorder:
Current status and future directions. [Special Issue: ADHD and modifiers of the syndrome:
Influences on educational outcomes] Developmental Disabilities Research Reviews, 14,
320–324. doi:10.1002/ddrr.35
Mezzacappa, E., & Buckner, J. C. (2010). Working memory training for children with attention
problems or hyperactivity: A school-based pilot study. School Mental Health, 2, 202–208.
doi:10.1007/s12310-010-9030-9
Mikami, A. Y. (2010). The importance of friendship for youth with attention-
deficit/hyperactivity disorder. Clinical Child and Family Psychology Review, 13, 181–198.
doi:10.1007/s10567-010-0067-y
Mikami, A. Y., Jack, A., Emeh, C. C., & Stephens, H. F. (2010). Parental influence on
children with attention-deficit/hyperactivity disorder: I. Relationships between parent
behaviors and child peer status. Journal of Abnormal Child Psychology, 38, 721–736.
doi:10.1007/s10802-010-9393-2
Mikami, A. Y., Lerner, M. D., Griggs, M. S., McGrath, A., & Calhoun, C. D. (2010). Parental
influence on children with attention-deficit/hyperactivity disorder: II. Results of a pilot
intervention training parents as friendship coaches for children. Journal of Abnormal Child
Psychology, 38, 737–749. doi:10.1007/s10802-010-9403-4
Molina, B. S. G., Hinshaw, S. P., Swanson, J. M., Arnold, L. E., Vitiello, B., Jensen, P. S., …
Houck, P. R. (2009). The MTA at 8 years: Prospective follow-up of children treated for
combined-type ADHD in a multisite study. Journal of the American Academy of Child &
Adolescent Psychiatry, 48, 484–500. doi:10.1097/CHI.0b013e31819c23d0
MTA Cooperative Group. (1999a). A 14-month randomized clinical trial of treatment

strategies for attention-deficit/hyperactivity disorder. Archives of General Psychiatry, 56,
1073–1086. doi:10.1001/archpsyc.56.12.1073
MTA Cooperative Group. (1999b). Moderators and mediators of treatment response for
children with attention-deficit/hyperactivity disorder: The multimodal treatment study of
children with attention-deficit/hyperactivity disorder. Archives of General Psychiatry, 56,
1088–1096. doi:10.1001/archpsyc.56.12.1088
Murray, D. W., Rabiner, D., Schulte, A., & Newitt, K. (2008). Feasibility and integrity of
a parent–teacher consultation intervention for ADHD students. Child & Youth Care
Forum, 37 , 111–126.
Murray-Close, D., Hoza, B., Hinshaw, S. P., Arnold, L. E., Swanson, J., Jensen, P.
S., … Wells, K. (2010). Developmental processes in peer problems of children
with attention-deficit/hyperactivity disorder in the Multimodal Treatment Study of
Children with ADHD: Developmental cascades and vicious cycles. [Special Issue:
Developmental cascades: Part 2] Development and Psychopathology, 22, 785–802.
doi:10.1017/S0954579410000465
Nijmeijer, J. S., Minderaa, R. B., Buitelaar, J. K., Mulligan, A., Hartman, C. A., & Hoekstra,
P. J. (2008). Attention-deficit/hyperactivity disorder and social dysfunctioning. Clinical
Normand, S., Schneider, B. H., Lee, M. D., Maisonneuve, M.-F., Kuehn, S. M., & Robaey,
P. (2011). How do children with ADHD (mis)manage their real-life dyadic friendships?
A multi-method investigation. Journal of Abnormal Child Psychology, 39, 293–305.
doi:10.1007/s10802-010-9450-x
Owens, E. B., Hinshaw, S. P., Kraemer, H. C., Arnold, L. E., Abikoff, H. B., Cantwell, D. P.,
… Wigal, T. (2003). Which treatment for whom for ADHD? Moderators of treatment
response in the MTA. Journal of Consulting and Clinical Psychology, 71, 540–552.
doi:10.1037/0022-006x.71.3.540
Owens, J. S., Murphy, C. E., Richerson, L., Girio, E. L., & Himawan, L. K. (2008).
Science to practice in underserved communities: The effectiveness of school mental
health programming. Journal of Clinical Child and Adolescent Psychology, 37 , 434–447.
doi:10.1080/15374410801955912
Parry, P. A., & Douglas, V. I. (1983). Effects of reinforcement on concept identifica-
tion in hyperactive children. Journal of Abnormal Child Psychology, 11, 327–340.
doi:10.1007/bf00912095
Patterson, G. R. (1982). Coercive family process. Eugene, OR: Castalia.
Pelham, W. E., & Fabiano, G. A. (2008). Evidence-based psychosocial treatments for attention-
deficit/hyperactivity disorder [Special Issue: Evidence-based psychosocial treatments for
children and adolescents: A ten year update] Journal of Clinical Child and Adolescent
Psychology, 37 , 184–214.
Pelham, W. E., Fabiano, G. A., Gnagy, E. M., Greiner, A. R., & Hoza, B. (2005). The
role of summer treatment programs in the context of comprehensive treatment for
attention-deficit/hyperactivity disorder. In E. D. Hibbs & P. S. Jensen (Eds.), Psychosocial
treatments for child and adolescent disorders: Empirically based strategies for clinical practice
(2nd ed., pp. 377–409). Washington, DC: American Psychological Association.
Pelham, W. E., Gnagy, E. M., Greiner, A. R., Hoza, B., Hinshaw, S. P., Swanson, J. M., …
McBurnett, K. (2000). Behavioral versus behavioral and pharmacological treatment in
ADHD children attending a summer treatment program. [Special Issue: Child and family
characteristics as predictors and outcames in the Multimodal Treatment Study of ADHD]
Journal of Abnormal Child Psychology, 28, 507–525. doi:10.1023/a:1005127030251
Pelham, W. E., Gnagy, E. M., Greiner, A. R., Waschbusch, D. A., Fabiano, G. A., & Burrows-
Maclean, L. (2010). Summer treatment programs for attention-deficit/hyperactivity
disorder. In J. R. Weisz (Ed.), Evidence-based psychotherapies for children and adolescents
(2nd ed., pp. 277–292). New York, NY: Guilford Press.
Pelham, W. E., & Hoza, B. (1996). Intensive treatment: A summer treatment program for
children with ADHD. In E. Hibbs & P. Jensen (Eds.), Psychological treatments for child
and adolescent disorders: Empirically based strategies for clinical practice (pp. 311–340).
New York, NY: American Psychological Association. doi:10.1037/10196-013
Pfiffner, L. J., Barkley, R. A., & DuPaul, G. J. (2006). Treatment of ADHD in school settings.
In R. A. Barkley (Ed.), Attention-deficit hyperactivity disorder: A handbook for diagnosis
and treatment (3rd ed., pp. 547–589). New York, NY: Guilford Press.
Pfiffner, L. J., Calzada, E., & McBurnett, K. (2000). Interventions to enhance social compe-
tence. Child and Adolescent Psychiatric Clinics of North America, 9, 689–709.
Pfiffner, L. J., & Kaiser, N. M. (2010). Behavioral parent training. In M. K. Dulcan (Ed.),
Dulcan’s textbook of child and adolescent psychiatry (pp. 845–868). Arlington, VA:
American Psychiatric Publishing.
Pfiffner, L. J., Kaiser, N. M., Burner, C., Zalecki, C., Rooney, M., Setty, P., & McBurnett,
K. (2011). From clinic to school: Translating a collaborative school–home behavioral
intervention for ADHD. School Mental Health, 3, 127–142.
Pfiffner, L. J., & McBurnett, K. (1997). Social skills training with parent generalization:
Treatment effects for children with attention deficit disorder. Journal of Consulting and
Clinical Psychology, 65, 749–757. doi:10.1037/0022-006x.65.5.749
Pfiffner, L. J., Mikami, A. Y., Huang-Pollock, C., Easterlin, B., Zalecki, C., & McBurnett, K.
(2007). A randomized, controlled trial of integrated home–school behavioral treatment
for ADHD, predominantly inattentive type. Journal of the American Academy of Child &
Pfiffner, L. J., O’Leary, S. G., Rosen, L. A., & Sanderson, W. C. (1985). A comparison of
the effects of continuous and intermittent response cost and reprimands in the classroom.
Journal of Clinical Child Psychology, 14, 348–352.
Pfiffner, L. J., Rosen, L. A., & O’Leary, S. G. (1987). The efficacy of an all-positive
approach to classroom management. Journal of Applied Behavior Analysis, 18, 257–261.
doi:10.1901/jaba.1985.18-257
Pfiffner, L. J., Villodas, M., Kaiser, N., Rooney, M., McBurnett, K. (2013). Educational
Outcomes of a Collaborative School-Home Behavioral Intervention for ADHD. School
Psychology Quarterly, 28, 25–36.
Power, T. J., Werba, B. E., Watkins, M. W., Angelucci, J. G., & Eiraldi, R. B. (2006). Patterns of
parent-reported homework problems among ADHD-referred and non-referred children.
School Psychology Quarterly, 21, 13–33. doi:10.1521/scpq.2006.21.1.13
Quay, H. C. (1997). Inhibition and attention deficit hyperactivity disorder. Journal of Abnormal
Child Psychology, 25, 7–13. doi:10.1023/a:1025799122529
Raggi, V. L., Chronis-Tuscano, A., Fishbein, H., & Groomes, A. (2009). Development of
a brief, behavioral homework intervention for middle school students with attention-
deficit/hyperactivity disorder. School Mental Health, 1, 61–77. doi:10.1007/s12310-
009-9008-7
Schultz, B. K., Evans, S. W., & Serpell, Z. N. (2009). Preventing failure among middle school
students with attention deficit hyperactivity disorder: A survival analysis. [Special Issue:
Research updates on teacher consultation for students with attention deficit hyperactivity
disorder] School Psychology Review, 38, 14–27.
Seeley, J. R., Small, J. W., Walker, H. M., Feil, E. G., Severson, H. H., Golly, A. M., &
Forness, S. R. (2009). Efficacy of the “First Step to Success” intervention for students with
attention-deficit/hyperactivity disorder. School Mental Health, 1, 37–48. doi:10.1007/
s12310-008-9003-4
Semrud-Clikeman, M. (2010). The role of inattention and social perception and perfor-
mance in two subtypes of ADHD. Archives of Clinical Neuropsychology, 25, 771–780.
doi:10.1093/arclin/acq074
Semrud-Clikeman, M., Nielsen, K. H., Clinton, A., Sylvester, L., Parle, N., & Connor,
R. T. (1999). An intervention approach for children with teacher- and parent-
identified attentional difficulties. Journal of Learning Disabilities, 32, 581–590.
doi:10.1177/002221949903200609
Shalev, L., Tsal, Y., & Mevorach, C. (2007). Computerized progressive attentional train-
ing (CPAT) program: Effective direct intervention for children with ADHD. Child
Neuropsychology, 13, 382–388. doi:10.1080/09297040600770787
Sherlin, L., Arns, M., Lubar, J., & Sokhadze, E. (2010). A position paper on neu-
rofeedback for the treatment of ADHD. Journal of Neurotherapy, 14, 66–78.
doi:10.1080/10874201003773880
Sohlberg, M. M., McLaughlin, K. A., Pavese, A., Heidrich, A., & Posner, M. I. (2000).
Evaluation of attention process training and brain injury education in persons with
acquired brain injury. Journal of Clinical and Experimental Neuropsychology, 22, 656–676.
doi:10.1076/1380-3395(200010)22:5;1-9;ft656
Sonuga-Barke, E. J. S. (2005). Causal models of attention-deficit/hyperactivity disorder: From
common simple deficits to multiple developmental pathways. Biological Psychiatry, 57 ,
1231–1238. doi:10.1016/j.biopsych.2004.09.008
Sonuga-Barke, E. J. S., Daley, D., & Thompson, M. (2002). Does maternal ADHD reduce the
effectiveness of parent training for preschool children’s ADHD? Journal of the American
Academy of Child & Adolescent Psychiatry, 41, 696–702. doi:10.1097/00004583-
200206000-00009
Swanson, J., Arnold, L. E., Kraemer, H., Hechtman, L., Molina, B., Hinshaw, S., …
Wigal, T. (2008a). Evidence, interpretation, and qualification from multiple reports
of long-term outcomes in the Multimodal Treatment Study of Children with ADHD
(MTA): Part I: Executive summary. Journal of Attention Disorders, 12, 4–14.
doi:10.1177/1087054708319345
Swanson, J., Arnold, L. E., Kraemer, H., Hechtman, L., Molina, B., Hinshaw, S., …
Wigal, T. (2008b). Evidence, interpretation, and qualification from multiple reports
of long-term outcomes in the Multimodal Treatment Study of Children with ADHD
(MTA): Part II: Supporting details. Journal of Attention Disorders, 12, 15–43.
doi:10.1177/1087054708319525
Volkow, N. D., Wang, G.-J., Kollins, S. H., Wigal, T. L., Newcorn, J. H., Telang, F.,
… Swanson, J. M. (2009). Evaluating dopamine reward pathway in ADHD: Clinical
implications. JAMA, 302, 1084–1091. doi:10.1001/jama.2009.1308
Walker, H. M., Seeley, J. R., Small, J., Severson, H. H., Graham, B. A., Feil, E. G., … Forness,
S. R. (2009). A randomized controlled trial of the first step to success early intervention:
Demonstration of program efficacy outcomes in a diverse, urban school district. Journal
of Emotional and Behavioral Disorders, 17 , 197–212. doi:10.1177/1063426609341645
Webster-Stratton, C. H., & Reid, M. J. (2010). The Incredible Years parents, teachers, and
children training series: A multifaceted treatment approach for young children with
conduct disorders. In J. R. Weisz & A. E. Kazdin (Eds.), Evidence-based psychotherapies
for children and adolescents (2nd ed., pp. 194–210). New York, NY: Guilford Press.
Webster-Stratton, C. H., Reid, M. J., & Beauchaine, T. (2011). Combining parent and
child training for young children with ADHD. Journal of Clinical Child and Adolescent
Wells, K. C., Chi, T. C., Hinshaw, S. P., Epstein, J. N., Pfiffner, L., Nebel-Schwalm, M., …
Wigal, T. (2006). Treatment-related changes in objectively measured parenting behav-
iors in the multimodal treatment study of children with attention-deficit/hyperactivity
disorder. Journal of Consulting and Clinical Psychology, 74, 649–657. doi:10.1037/0022-
006x.74.4.649
Wells, K. C., Pelham, W. E., Kotkin, R. A., Hoza, B., Abikoff, H. B., Abramowitz, A.,
… Schiller, E. (2000). Psychosocial treatment strategies in the MTA study: Rationale,
methods, and critical issues in design and implementation. Journal of Abnormal Child
Psychology, 28, 483–505. doi:10.1023/a:1005174913412
Willcutt, E. G., Doyle, A. E., Nigg, J. T., Faraone, S. V., & Pennington, B. F. (2005). Validity of
the executive function theory of attention-deficit/hyperactivity disorder: A meta-analytic
review. Biological Psychiatry, 57 , 1336–1346. doi:10.1016/j.biopsych.2005.02.006
Zisser, A., & Eyberg, S. M. (2010). Parent–child interaction therapy and the treatment of
disruptive behavior disorders. In J. R. Weisz (Ed.), Evidence-based psychotherapies for
children and adolescents (2nd ed., pp. 79–193). New York, NY: Guilford Press.
34
Conduct Disorder and
Delinquency
Michael R. McCart, Cindy Schaeffer,
and Scott W. Henggeler
Medical University of South Carolina, United States
Introduction
This chapter reviews evidence-based treatments that incorporate cognitive behavioral

interventions to target serious overt (e.g., physical aggression, property destruc-
tion, serious rule violations) and covert (e.g., stealing) behavior problems among
youth. Professional disciplines use different terms to categorize these behaviors.
For example, in the mental health field, such behaviors are subsumed within the
diagnostic category of conduct disorder (American Psychiatric Association, 2000).
Juvenile justice professionals, however, refer to these behaviors as forms of juve-
nile delinquency. Regardless of the labels applied, research indicates that youth
with serious behavior problems are at risk for a range of negative outcomes,
including poor educational attainment, family disruption, unwanted pregnancy,
and increased rates of injury and mortality (see McMahon & Kotler, 2006, for
a review). Fortunately, several evidence-based treatments have been developed
and validated for conduct disordered and delinquent youth (Eyberg, Nelson, &
Boggs, 2008). The current chapter summarizes those evidence-based protocols
that specifically utilize cognitive behavioral intervention strategies. In addition to
discussing the theoretical and clinical bases of these treatments, their evidence
base is summarized. To place these treatments in context, however, we begin
with an overview of the epidemiology and etiology of conduct disorder and
delinquency.

DOI: 10.1002/9781118528563.wbcbt34
Epidemiology of Conduct Disorder and Delinquency
Prevalence
Data from a nationally representative sample of adolescents reveal a lifetime prevalence
of 6.8% for conduct disorder (Merikangas et al., 2010). Regarding delinquency, a U.S.
Department of Justice report indicates that 1.9 million youth, or about 4% of the child
and adolescent population (aged 5–18 years), were arrested for delinquent offenses
in 2009 (Puzzanchera & Adams, 2011). It should be noted, however, that most
youth who engage in delinquent behavior never come to the attention of authorities.
More accurate prevalence estimates come from studies that gather self-report data
on youths’ participation in delinquent acts (Thornberry & Krohn, 2000). Between
2005 and 2007, the International Self-Report Delinquency Study-2 (Junger-Tas
et al., 2010) surveyed random samples of youth in several nations regarding their
involvement in delinquent behavior. In the U.S. sample, almost 30% of participants
reported committing at least one delinquent offense during the past year. The most
commonly reported offenses included participation in group fights (9.7%), shoplifting
(9.2%), and vandalism (8.7%). These prevalence data demonstrate the high rates of
conduct disorder and delinquency among youth in the United States.
Demographic Trends
Prevalence rates for conduct disorder and delinquency vary with age, gender, and
race. Youth antisocial behavior tends to peak in later adolescence (Junger-Tas,
Marshall, & Ribeaud, 2003; Merikangas et al., 2010), with most youth desisting
during emerging adulthood. Youth who develop serious behavior problems at a
young age (i.e., prior to the age of 14), however, are more likely to continue
offending into adulthood (Chen, Matruglio, Weatherburn, & Hua, 2005; Loeber &
Farrington, 2000). Regarding gender, conduct disorder and delinquency are
significantly more prevalent among boys than girls (Loeber, Burke, Lahey, Winters,
& Zera, 2000; Stahl, Finnegan, & Kang, 2007). In terms of race, discrepant trends
have been identified. For example, studies have reported no race differences in
rates of conduct disorder (Merikangas et al., 2010) and relatively small magnitudes
of race differences in rates of self-reported delinquency—with African American
youth tending to report more offenses than their white counterparts (Hawkins,
Laub, Lauritsen, & Cothern, 2000). Nevertheless, striking race differences in
rates of juvenile arrest have been observed. Indeed, in 2009, African American
youth were five times more likely than white youth to be arrested for a violent
crime (Puzzanchera & Adams, 2011). It has been suggested, however, that such
discrepancies might be the product of law enforcement and judicial practices as
opposed to actual differences in the rates of offending behavior by race (Snyder &
Sickmund, 2006).
Conduct Disorder and Delinquency 799
Etiology of Conduct Disorder and Delinquency
Decades of cross-sectional and longitudinal research have shed light on the

determinants of conduct disorder and delinquency among youth (Deater-Deckard,
Dodge, Bates, & Pettit, 1998; Elliott, 1994; Loeber, Farrington, Stouthamer-Loeber,
& Van Kammen, 1998; Thornberry & Krohn, 2003). Cognitive factors, specifically
social information processing deficits, represent one such determinant that has
received considerable support in the empirical literature. However, evidence also
clearly and consistently denotes a range of additional determinants that are present
across multiple individual and environmental contexts.
Social Information Processing

From a cognitive behavioral perspective, deficits at various levels of social information
processing (SIP) have been identified as proximal causes of conduct disorder and
delinquency. Several influential SIP models have guided research efforts in this area
(Crick & Dodge, 1994; Fontaine & Dodge, 2006; Huesmann, 1988), and a large
empirical literature supports many model components, especially for elementary
school-aged children (for reviews, see Fontaine, 2006; Gifford-Smith & Rabiner,
2004; Mize & Pettit, 2007). In social situations, conduct disordered and delinquent
youth tend to show aggressive biases both in their encoding of social cues (e.g.,
noticing a clenched fist but not a smile) and in their interpretation of such cues
(e.g., assuming that others have hostile intent). They also tend to have more
aggressive goals for social interactions (e.g., to win or defeat the other person), to
generate more antisocial and fewer prosocial ways of responding to social stimuli,
and to select and enact aggressive responses more often (e.g., hitting, shoving). Once
enacted, aggressive responses are reinforced by their effectiveness in meeting the
individual’s social goals. These positive experiences with aggression are encoded in
memory and over time develop into social scripts or schemas, templates that make
aggressive responding more cognitively accessible in future interactions (Huesmann,
1988).
An example illustrates how problems at each level of SIP can, according to
conceptual models, increase the odds of problem behavior. A peer knocks a youth
onto the ground during a pick-up basketball game. The youth encodes some cues
from the event (e.g., the peer had an angry look on his face, the youth’s own high
arousal level) but not others (e.g., the peer’s shoe was untied and he was stumbling).
The youth misinterprets the event as intentional (i.e., makes a hostile attribution).
Drawing from a memory store that includes being ridiculed by peers several times in
the past while playing sports, the youth sets a social goal to avoid appearing weak.
The youth generates two possible responses to the “provocation” (e.g., say a curse
word, push the peer) and judges that shoving the peer will have a more successful
outcome (i.e., he will look powerful). After shoving the peer, a supervising teacher
ends the game and sends the youth to the principal’s office. The youth feels satisfied
that he met his goal to not appear weak (i.e., a positive experience with aggression is
encoded in memory).
Recent research has focused on the most proximal (i.e., real time) step of this pro-
cess, the selection of the behavioral response (i.e., response decision making; Fontaine
& Dodge, 2006). Response decisions are comprised of multiple components, includ-
ing appraising the response along dimensions important to the individual (e.g., desire
to be friendly or to appear tough; response evaluation), anticipating the consequences
of various courses of action (i.e., outcome expectation), and evaluating his or her own
efficacy in enacting the response (i.e., self-efficacy evaluation). At the bivariate level,
deficits within each component of response decision making have been associated with
aggressive behavior in samples of adolescents and collectively, to account for signifi-
cant variance (Fontaine, 2006; Fontaine & Dodge, 2006). Response decisions may be
particularly important for understanding antisocial behavior among adolescents who
have the cognitive maturity to engage in complex mental representations of possible
behaviors and their outcomes (see Fontaine, Yang, Dodge, Bates, & Pettit, 2008).
Consistent with this view, adolescents’ response decision making appears to be more
consistent, differentiated, and predictive of antisocial behavior than that of elementary
school-aged children (Fontaine, Yang, Dodge, Pettit, & Bates, 2009; Lansford et al.,
2006).
Other Established Determinants

As noted previously, SIP deficits represent just one determinant for conduct disorder
and delinquency among youth. Indeed, research has shed light on several additional
domains of risk, some of which account for more variance in multivariate models of
antisocial behavior than do SIP deficits. These include biological factors, parenting
practices, peer relationships, school factors, and community factors.
Biological factors. Certain biological factors are distally associated with the devel-
opment of conduct disorder and delinquency through their influence on youth
temperament. For example, the presence of toxins (e.g., alcohol, nicotine) in the
prenatal environment negatively impacts neurological functioning and can lead
to temperamental difficulties in infancy characterized by emotional reactivity and
impulsivity (Lemola, Stadlmayr, & Grob, 2009; Wakschlag & Hans, 2002). These
temperamental difficulties increase the likelihood that youth will develop serious
behavior problems in later childhood (Caspi, Henry, McGee, & Moffitt, 1995; Frick
& Morris, 2004). It is of note that such biological variables tend to exert their
strongest influence at an early age, whereas environmental variables become stronger
predictors of behavior problems as youth progress through middle childhood and
adolescence (Moffitt, 1993).
Parenting practices. As noted in several comprehensive literature reviews (Biglan,

Brennan, Foster, & Holder, 2004; Hoge, Guerra, & Boxer, 2008; Patterson, 2002),
a strong link between maladaptive parenting practices (e.g., poor monitoring and
supervision; inconsistent, harsh, or lax discipline) and serious antisocial behavior
among youth has been established. Coercion theory, developed by Patterson (1982),
provides a compelling framework for understanding the association between ineffec-
tive parenting and behavior problem outcomes. According to this theory, a coercive
sequence begins when a parent makes a request for child compliance, one that often
is inadequate in some way (e.g., vague or insensitive to contextual factors such as
child fatigue). The child protests, but the parent’s request intensifies. This sequence
repeats several times, escalating to emotional displays of anger and frustration by both
the parent and child. The interaction typically ends in one of two ways. The parent
might discipline the youth either physically or by removing some privilege, although
implementation of the consequence is often too delayed to have an impact on the
youth’s future behavior. A more common outcome involves the parent “giving in”
and thus negatively reinforcing the youth’s defiance. The parent also is negatively
reinforced for backing down (i.e., the unpleasant exchange with the child ends).
Thus, through the coercive cycle, the youth learns over time that oppositional and
aggressive behaviors are effective ways to avoid undesired activities (e.g., going to
bed, doing chores), and parents become increasingly disengaged from attempting to
control the child’s behavior.
Several other aspects of family relations have been linked with antisocial behavior. By
middle childhood and adolescence, the families of youth with conduct problems and
delinquency tend to be characterized by an overall lack of warmth and involvement
among family members, high rates of family conflict, inept discipline, and poor parental
monitoring of youth whereabouts and behaviors (Dishion, Bullock, & Granic, 2002).
These problems set the stage for youth difficulties in peer and school contexts.
Peer relationships. Association with deviant peers (i.e., delinquent and/or substance
using friends) represents a powerful and proximal risk factor for adolescent behavior
problems (Dodge, Dishion, & Lansford, 2006). Numerous cross-sectional and longi-
tudinal studies have established positive relations between deviant peer affiliation and
youths’ own involvement in delinquent behavior (e.g., Andrews, Tildesley, Hops, &
Li, 2002; Liberman, 2008; Patterson, Dishion, & Yoerger, 2000). Further evidence
for the negative effects of deviant peer association comes from randomized prevention
trials demonstrating that the aggregation of high-risk youth in group-based inter-
ventions can yield iatrogenic effects (Dishion & Andrews, 1995; Metropolitan Area
Child Study Research Group, 2002). Consistent with these findings, results from
mediation studies of evidence-based interventions have supported the important role
of decreased association with deviant peers in reducing serious behavior problems
among juvenile offenders (Eddy & Chamberlain, 2000; Huey, Henggeler, Brondino,
& Pickrel, 2000).
School factors. Low academic achievement is associated with conduct problems during
adolescence, and poor school performance predicts elevated rates of conduct problems
in young adulthood (Loeber et al., 2005). Low bonding to school, a high number
of school transitions, high truancy, and dropping out of school are also associated
with conduct problems and delinquency (Janosz, Le Blanc, Boulerice, & Tremblay,
1997; Maguin & Loeber, 1996). In addition, studies indicate that when youth attend
schools characterized by a high student–teacher ratio, poor academic quality, and a
lack of perceived fairness and clarity of school rules, they are more likely to engage
in delinquent behavior (Gottfredson, Gottfredson, Payne, & Gottfredson, 2005;
Hellman & Beaton, 1986).
Community factors. Aspects of a youth’s community increase the likelihood of the

development of serious conduct problems. Key community-level risk factors include
social disorganization (i.e., a lack of support and cohesion among neighbors), poverty,
unemployment, and substandard housing (Attar, Guerra, & Tolan, 1994; Sampson,
Raudenbush, & Earls, 1997). Neighborhood violence is also associated with ado-
lescent problem behavior. For example, in a nationally representative sample of
urban adolescent boys, exposure to neighborhood violence predicted elevated rates
of delinquency, even after controlling for the effects of family violence (i.e., famil-
ial sexual assault, witnessed domestic violence), age, and ethnicity (McCart et al.,
2007).
Evidence-Based Treatments
In an exhaustive literature review, Eyberg et al. (2008) identified several evidence-

based treatments for serious youth behavior problems using the criteria established by
the American Psychological Association Task Force on the Promotion and Dissem-
ination of Psychological Procedures (Chambless et al., 1996). Briefly, these criteria
require treatments to have demonstrated efficacy in at least one randomized con-
trolled trial or in a series of controlled single-case studies. For the current chapter,
we reviewed those cited by Eyberg et al. (2008) and selected the evidence-based
treatments that utilize at least some cognitive behavioral intervention strategies. The
selected treatments fit into two categories. The first includes cognitive behavioral ther-
apy (CBT) programs that focus primarily on youths’ SIP deficits. The second includes
family-based treatments that incorporate CBT components as part of a broader array
of interventions that aim to change family and other systemic contributors to anti-
social behavior. Before these treatment approaches are described, it is important to
note that the CBT and family-based models typically target different populations of
youth. For example, the CBT programs have been designed primarily for school-aged
children (aged 5–12 years) who are beginning to display serious disruptive behavior
in home and school settings. In contrast, the family-based models target adolescents
(aged 12–17 years) who have graduated to more severe antisocial acts and are often
involved with the juvenile justice system.
In addition to using the well-accepted criteria for empirical support adopted by
the American Psychological Association, it is also important to make a distinction
between treatment outcomes that have been achieved in efficacy contexts versus those
achieved in real-world contexts, as these have important implications for the transport
of evidence-based treatments (Weisz & Kazdin, 2010) to community-based settings.
Efficacy studies typically aim to optimize the probability of observing treatment effects
by, for example, including highly motivated therapists (e.g., graduate students) with
intensive training, supervision, and fidelity monitoring from the treatment developer
and removing organizational barriers to treatment implementation (e.g., embedding
services within a university clinic). On the other hand, in effectiveness research ther-
apists are typically employed by community-based provider organizations, caseloads
can have greater heterogeneity and co-occurrence of problems, clinical supervision
is often minimal or nonexistent, and therapists have organizational demands that
often have little to do with achieving favorable outcomes for youth (e.g., meeting
billing requirements). Treatments that have proven successful in effectiveness research,
therefore, are more likely to be transported effectively to real-world settings.
Cognitive Behavioral Therapy Programs

Three CBT programs have been designated as meeting evidence-based practice
criteria.
Anger Coping and Coping Power Programs. The Anger Coping Program (Larson
& Lochman, 2002) is a group-based intervention for elementary school-aged youth
with disruptive behavior. Group sessions target cognitive processes that have been
empirically linked with behavior problem outcomes, including perspective taking,
affect awareness and management, and social problem-solving skills. The Coping
Power Program (Lochman, Wells, & Lenhart, 2008) was designed as an extension
of the Anger Coping Program and incorporates a parent training component as well
as additional group sessions for youth. Several research trials have supported the
effectiveness of these two interventions.
Theoretical bases. The Anger Coping and Coping Power Programs are both
influenced by the SIP model proposed by Crick and Dodge (1994). According to
this model, individuals process information in six sequential steps when responding
to social situations. The sequence is (a) encoding of information, (b) interpretation
of information, (c) specification of an interaction goal, (d) generation of potential
responses, (e) selection of an optimal response, and (f) enactment of that response.
Youth with behavior problems generally display deficits at each of these steps. For
example, they search for fewer social cues, are more likely to attribute hostile intent
to ambiguous situations, and have difficulty generating multiple potential solutions
to social problems (Lochman & Dodge, 1994). In addition, such youth display more
confidence in their ability to use aggression as a problem-solving strategy and have
higher expectations that aggression will lead to positive outcomes (Guerra, Huesmann,
& Spindler, 2003; Perry, Perry, & Rasmussen, 1986). The Anger Coping and Coping
Power Programs aim to improve youths’ behavioral outcomes by specifically targeting
each of these SIP deficits.
Model of service delivery. The Anger Coping and Coping Power Programs are
both typically delivered in a group-based format. The Anger Coping Program includes
18 child sessions that are 60 to 90 minutes in length. The Coping Power Program
consists of 34 child sessions and a 16-session parenting training group. The child
groups are co-led by two clinicians so that one can monitor the youths’ behavior
while the other leads the group activities. The Anger Coping and Coping Power
Programs are most commonly implemented in school settings, although they can also
be implemented in outpatient clinics.
Clinical overview. The procedures for implementing the Anger Coping Program
are specified in a treatment manual (Larson & Lochman, 2002). Across all 18 sessions,
youth earn points for good behavior and for progress made in meeting individualized
goals. Points can be cashed in to purchase prizes from a prize chest. During Session 1,
the group facilitators outline the group rules, and the youth participate in a cohesion-
building exercise. Then, to increase self-awareness, youth record their thoughts about
an ambiguous situation and listen to the recordings as a group. In Session 2, the
youth generate personal goals regarding self-control. Sessions 3 through 9 involve
a series of structured activities designed to improve the youths’ problem-solving
skills. For example, the youth are taught strategies for identifying and managing
anger (e.g., through self-talk, distraction, and/or relaxation methods). The youth
practice perspective taking and learn strategies for brainstorming multiple solutions
to problems. They also learn how to evaluate the consequences of different response
options. Finally, the youth are taught a problem-solving model that includes the
following key questions: (a) What is the problem?, (b) What are my feelings?, (c)
What are my choices?, (d) What will happen?, and (e) What will I do? During Sessions
10–17, group members create videos demonstrating how the problem-solving model
can be applied to real-life situations. The final session includes review of skills learned
and a graduation ceremony.
Procedures for implementing the Coping Power Program are described by Lochman
et al. (2008). The first 18 group sessions are similar to those described for the
Anger Coping Program. However, 16 extra group sessions focus on enhancing
youths’ emotional awareness and social skills. Periodic individual sessions are also
conducted with youth to help facilitate skill generalization. During the 16-session
parent group, caregivers are taught how to generate developmentally appropriate
rules for their youth, how to give effective commands, and how to implement rewards
and consequences based on their youth’s behavior. Parents also practice applying
the aforementioned problem-solving model to situations within the family. Finally,
caregivers are taught stress management techniques.
Empirical support. The Anger Coping Program has been evaluated in two ran-
domized hybrid efficacy and effectiveness trials with aggressive school-aged boys
(Lochman, Burch, Curry, & Lampron, 1984; Lochman, Lampron, Gemmer, Harris,
& Wyckoff, 1989). In both trials, youth receiving the Anger Coping Program demon-
strated significantly greater reductions in aggressive and disruptive behavior relative
to youth in the control condition. Moreover, a 3-year follow-up of the Lochman
et al. (1984) sample revealed continued treatment effects on several key outcomes
(Lochman, 1992). Youth in the Anger Coping Program group demonstrated bet-
ter problem-solving skills and lower levels of drug and alcohol use compared to
counterparts in the control group. Interestingly, moderator analyses suggested that
the Anger Coping Program was most beneficial for youth who had less advanced
problem-solving skills, higher levels of peer rejection, and more comorbid internalizing
symptoms (Lochman, Lampron, Burch, & Curry, 1985).
The Coping Power Program also has been evaluated in several studies. One
randomized efficacy trial tested the intervention with elementary school-aged boys
rated by parents and teachers as high on physical aggression (Lochman & Wells,
2004). Participants were randomly assigned to one of three conditions: child group-
based treatment only, child plus parent group-based treatment, or a no treatment
control. At a 1-year follow-up, youth in both treatment conditions exhibited lower

levels of delinquent behavior, disruptive school behavior, and substance use relative
to youth in the control condition. Further, the combined child and parent treatment
condition outperformed the child only treatment condition. The Coping Power
Program yielded similar positive effects when tested in the context of a randomized
effectiveness trial involving aggressive youth from 17 elementary schools (Lochman
& Wells, 2003). Additional studies indicate that the intervention can yield positive
outcomes when implemented in an abbreviated form (Lochman, Boxmeyer, Powell,
Roth, & Windle, 2006) and to clinic-based youth with disruptive behavior disorders
(van de Wiel et al., 2007). Importantly from a theoretical standpoint, mediation
research has supported the hypothesized mechanisms of change of the Coping Power
Program, as favorable outcomes were partially mediated by changes in youths’ SIP
patterns and improved parenting practices (Lochman & Wells, 2002). In conclusion,
the Anger Coping and Coping Power Programs both have strong empirical support.
Problem-solving skills training (PSST). PSST (Kazdin, 2010) is an individually admin-

istered intervention for elementary school-aged youth with conduct disorder. Like
the Anger Coping and Coping Power Programs, sessions focus primarily on targeting
youths’ SIP deficits through structured therapeutic exercises. PSST is sometimes com-
bined with a parent management training (PMT) program, which runs concurrent
with PSST and covers important behavioral principles for modifying youth behavior
(e.g., positive reinforcement, removal of privileges). The effectiveness of PSST has
been established in several research trials.
Theoretical bases. The theoretical foundation for PSST is almost identical to that
of the Anger Coping and Coping Power Programs. That is, PSST assumes that
impaired SIP patterns are key drivers for youth behavior problems. The intervention
aims to improve behavioral outcomes by helping youth learn more adaptive ways
of interpreting and responding to social cues. PSST draws heavily from learning-
based procedures to help youth develop new problem-solving skills. These procedures
include prompting, shaping, positive reinforcement, behavioral rehearsal, and response
cost.
Model of service delivery. PSST is an individually administered intervention con-

sisting of 12 core sessions that are 30 to 50 minutes in length and conducted weekly.
More sessions can be added as is clinically necessary. PSST is most commonly delivered
in an outpatient clinic setting by a trained clinician. When PSST is combined with
the aforementioned PMT program, the youth and his or her caregivers are seen by
separate clinicians during the same clinic visit.
Clinical overview. A treatment manual for PSST has not been published, although
a clinical description of the intervention is provided in Kazdin (2010). PSST strives
to enhance problem-solving skills by teaching youth to apply a five-step model to
difficult social situations. In step 1, the youth learns to recognize that problems can
be solved prosocially. In steps 2 and 3, the youth learns how to identify different
response options and to evaluate their potential consequences. In step 4, the youth
selects a response with the highest perceived benefits and the fewest perceived costs.
In step 5, the youth evaluates whether the chosen response effectively resolved the
problem.
The five problem-solving steps are introduced to the youth in Session 1. During
Sessions 2 and 3, the steps are applied to simple problems in a board game. During
these and all subsequent sessions, the youth also receives homework assignments to
practice the skills in real-life settings. Assignments start small and become increasingly
complex over the course of treatment. In Session 4, the youth and therapist practice
applying the steps in structured role plays. During Session 5, the youth models the
problem-solving steps for his or her caregiver. In addition, caregivers are taught to
provide verbal praise whenever they observe the youth implementing the model.
Sessions 6–11 involve continued application of the steps to real-life situations. Each
session focuses on different types of interpersonal problems and situations (e.g.,
conflict with peers, parents, siblings, and teachers). In Session 12, the skills acquired
during treatment are reviewed, and a role reversal exercise is conducted during which
the youth plays the part of the therapist and explains how to use each of the problem-
solving steps. To enhance motivation, youth receive tokens at the beginning of each
session that can be exchanged for prizes, and they can lose those tokens for failing to
use the problem-solving steps.
Empirical support. PSST has been evaluated in three randomized hybrid efficacy
and effectiveness trials with conduct disordered youth presenting to university-based
clinics (Kazdin, Bass, Siegel, & Thomas, 1989; Kazdin, Esveldt-Dawson, French,
& Unis, 1987; Kazdin, Siegel, & Bass, 1992). Across studies, PSST was more
effective than the comparison conditions at reducing youths’ externalizing behavior
and increasing their prosocial behavior. One of the trials showed that the addition of in
vivo homework assignments augmented PSST treatment effects (Kazdin et al., 1989),
and another demonstrated that the combined PSST plus PMT protocol was superior to
either individual treatment component alone (Kazdin et al., 1992). Several additional
studies have examined predictors of PSST and PMT outcomes. Variables positively
associated with treatment response include higher youth intellectual functioning,
higher levels of parent psychopathology, a more positive therapeutic alliance, and
lower caregiver-reported barriers to treatment participation (see Kazdin, 2010).
Together, these findings indicate that PSST and PMT both have strong empirical
support, but more work is needed to establish their effectiveness in community-based
settings.
Family-Based Treatments Incorporating Cognitive Behavioral Therapy

Components
As proximal antecedents of behavior problems, SIP deficits represent an appealing
target for intervention. However, the multidetermined nature of antisocial behavior
suggests that a broader approach might be needed, especially for adolescents engaged
in serious delinquent offending. Emerging research regarding the role of contextual
factors in maintaining or even causing SIP deficits also highlight the importance
of multifaceted interventions. For example, maladaptive parenting has been linked

to hostile attribution biases among youth (Nelson & Coyne, 2009). Peer factors,
such as rejection from mainstream peers (Lansford, Malone, Dodge, Pettit, & Bates,
2010) and association with deviant peers (Werner & Hill, 2010) contribute to and
are exacerbated by SIP deficits. In fact, two experimental studies have demonstrated
that hostile attributions and positive attitudes toward aggression can be caused by
peer endorsement of such beliefs (Cohen & Prinstein, 2006; Freeman, Hadwin,
& Halligan, 2011). Broader contextual factors, such as school monitoring and
consequences (Farrell et al., 2010) and community violence exposure (McMahon,
Felix, Halpert, & Petropoulos, 2009), also make both SIP deficits and antisocial
behavior more likely.
In light of this research, CBT programs that focus primarily on SIP deficits might
be insufficient to ameliorate serious behavior problems among adolescents. Without
changing the contextual factors that instill and reinforce maladaptive social decision
making, as well as factors that provide opportunities for continued conduct problems
(e.g., time with peers who are themselves delinquent, school expulsion), delinquent
behavior is likely to persist. Consistent with this view, the interventions with the
most empirical support in addressing serious adolescent behavior problems include
family-based treatments that target multiple risk factors simultaneously. The three
leading family-based treatments are described next.
Multisystemic therapy. Multisystemic therapy (MST) is a comprehensive family- and

community-based treatment for youth with serious delinquent behavior problems
who are at risk for out-of-home placement. MST is the most extensively validated
and widely transported of the empirically supported interventions for delinquency,
with multiple published outcome studies and delivery to more than 20,000 youth
and families annually (Henggeler & Sheidow, 2012). MST is specified in a clinical
volume (Henggeler, Schoenwald, Borduin, Rowland, & Cunningham, 2009), and
includes an intensive quality assurance system to sustain treatment fidelity and clinical
outcomes in real-world settings (see Schoenwald, 2008).
Theoretical bases. MST is based on Bronfenbrenner’s (1979) theory of social ecol-

ogy, which posits that youth behavior is largely determined by the functioning of the
multiple systems (i.e., family, school, peer, and neighborhood) in which the youth is
embedded and the reciprocal interplay between these systems (e.g., contacts between
caregivers and teachers). Thus, consistent with research on the development of seri-
ous antisocial behavior, conduct problems are viewed as multidetermined, requiring
interventions at the individual (e.g., addressing cognitive biases), family (e.g., chang-
ing parenting practices), peer (e.g., promoting associations with prosocial peers),
school (e.g., improving academic performance), and community (e.g., advocating for
increased police presence) levels.
MST uses a home-based model of service delivery that emphasizes ecological
validity in the assessment of behavior and delivery of interventions. Assessments are
considered ecologically valid when they integrate information from multiple sources
(e.g., caregivers, extended family, teachers) and gauge the youth’s functioning in
a variety of real-world settings. Similarly, MST interventions are provided where
problems occur (homes, schools, community locations) and, whenever possible, are
delivered to the youth by key members of the ecology.
A central assumption of MST is that caregivers are the key to achieving and sustain-
ing positive long-term outcomes. Thus, interventions focus intensely on empowering
caregivers to obtain the resources and skills needed to parent and manage their chil-
dren more effectively. As caregiver competencies (e.g., ability to provide consistent
monitoring and supervision) increase, the therapist guides caregiver efforts to address
other factors that might be contributing to a youth’s problem behavior, such as
associations with deviant peers and poor school performance. The ultimate goal is
to create a context that supports adaptive youth behavior (e.g., relationships with
prosocial peers, effective parenting), rather than a context that encourages antisocial
behavior. Importantly, the central emphases of MST on improved parenting and
decreased youth association with deviant peers as central vehicles for change have
been supported in mediation studies (e.g., Henggeler, Letourneau, et al., 2009; Huey
et al., 2000).
Model of service delivery. MST teams consist of two to four full-time master’s-
level therapists, an advanced master’s-level or doctoral-level supervisor who devotes
at least 50% of his or her professional time to the team, and administrative support.
Therapists carry caseloads of four to six families each. Therapists provide 24-hour-
a-day and 7-day-a-week availability, which allows them to work at times the family
finds convenient and to respond to clinical crises. Treatment duration is relatively
brief, ranging from 3 to 5 months. However, the intervention process is intensive
and often involves a total of 60 or more hours of direct contact with the family
and other ecology members. The strong emphasis on the delivery of MST services
in home and community settings enhances the ecological validity of assessments
and interventions, helps overcome barriers to service access, and facilitates family
engagement in treatment.
Clinical overview. Because of its highly individualized nature, MST does not follow
a rigid manualized plan for treatment. Rather, nine treatment principles provide the
underlying structure and framework upon which therapists build their interventions.
In addition to principles that stem from the social ecological model, interventions are
designed to be intensive (i.e., daily or weekly effort by family members), developmen-
tally appropriate, present-focused, and action-oriented. Interventions also encourage
responsible behavior by all parties, and are designed to promote the generalization
and long-term maintenance of therapeutic gains. Importantly, the nine treatment
principles are applied using an analytical decision-making process that structures the
treatment plan, its implementation, and the evaluation of its effectiveness.
Early in the treatment process, the problem behaviors to be targeted (i.e., treat-
ment goals) are specified clearly from the perspectives of key stakeholders (e.g.,
family members, teachers, juvenile justice authorities), and ecological strengths are
identified. Then, based on multiple perspectives, the ecological factors that seem to
be driving each problem are organized into a coherent conceptual framework (e.g.,
the youth’s vandalism is associated with a lack of caregiver monitoring, association
with delinquent peers, and poor school performance). Next, the MST therapist, with
support from other team members (i.e., other therapists, supervisor, consultant),
designs specific intervention strategies to target those “drivers.” Strategies incorpo-
rate interventions from empirically supported, pragmatic, problem-focused treatments
such as structural/strategic and behavioral family therapies (e.g., to address family
conflict), behavioral parent training, CBT, and psychopharmacology. Most relevant
to the present chapter, the primary MST text (Henggeler, Schoenwald, et al., 2009)
specifies evidence-based CBT interventions for a range of clinical issues (e.g., youth
and parent depression, substance use, difficulties with self-control and problem solv-
ing). Importantly, these empirically supported interventions are highly integrated and
are delivered in conjunction with interventions that address other pertinent ecolog-
ical drivers of the identified problems (e.g., advocating for more appropriate school
services, connecting caregivers with the parents of the youth’s peers).
Empirical support. The effectiveness of MST has been demonstrated in 22 pub-

lished clinical trials (Henggeler & Sheidow, 2012), 18 of which were conducted with
youths presenting serious antisocial behavior. For example, three randomized efficacy
and effectiveness trials with violent and chronic juvenile offenders were published in
the 1990s (Borduin et al., 1995; Henggeler, Melton, Brondino, Scherer, & Hanley,
1997; Henggeler, Melton, & Smith, 1992), with one producing sustained outcomes
at 14 and 21 years posttreatment (Sawyer & Borduin, 2011; Schaeffer & Borduin,
2005). Other randomized efficacy and effectiveness trials have been conducted with
substance-abusing offenders (e.g., Henggeler et al., 2006) and juvenile sexual offend-
ers (e.g., Letourneau et al., 2009). Importantly, independent effectiveness trials have
also been published in the United States (e.g., Timmons-Mitchell, Bender, Kishna, &
Mitchell, 2006) and Europe (Butler, Baruch, Hickley, & Fonagy, 2011; Ogden
& Hagen, 2006). Findings across these studies consistently have favored MST in
comparison with control conditions. For example, across studies, MST has achieved
a median reduction in recidivism of 39% and a median reduction in out-of-home
placement of 54%. Further, the fact that many of these studies were completed in field
settings demonstrates the ability of MST to be transported effectively to real-world
community contexts.
Functional Family Therapy. The efficacy and effectiveness of functional family therapy
(FFT) has been supported in six research trials (four randomized and two quasi-
experimental) with various samples of youth, including status offenders, serious
juvenile offenders, and substance-abusing adolescents. FFT is one of the most widely
transported evidence-based family therapies, with 270 programs worldwide treating
12,000 youth and their families annually. A clinical description of FFT is provided by
Alexander et al. (1998).
Theoretical bases. FFT has a strong relational focus, with youth conduct problems
viewed as a symptom of dysfunctional family relations. Interventions, therefore, aim
to establish and maintain new patterns of family behavior to replace dysfunctional
ones. In addition, FFT integrates behavioral (e.g., communication training) and
cognitive behavioral interventions (e.g., assertiveness training, anger management)
into treatment protocols while maintaining a relational focus.
Model of service delivery. FFT interventions tend to be less intensive than MST,
lasting for an average of 12 sessions spanning a 3- to 4-month duration. Services are
delivered primarily in clinic and home settings, supplemented by sessions in schools,
probation offices, or other community settings as needed. FFT programs typically
consist of teams of three to eight therapists each carrying caseloads of 12 to 15
families.
Clinical overview. FFT protocols call for a phase-based approach to interventions.

In the first phase, engagement and motivation, therapists engender hope and instill
positive expectations among family members, using a nonconfrontational and non-
blaming approach. During this phase, therapists actively direct family members away
from discussing the youth’s presenting problems, focusing instead on interrupting
aversive family interactions and reframing conflicts as relational attempts. In the sec-
ond phase, behavior change, the relational aspects of the problem behavior identified
in phase one are targeted so that new patterns of family interaction that are more
adaptive can be established. Interventions during this stage are drawn from evidence-
based behavioral and cognitive behavioral approaches. For example, a therapist might
use communication skills training to address family conflict, cognitive behavioral
techniques to alleviate maternal depression, and problem-solving skills training to
improve youth social skills. In the final stage, generalization, the therapist’s goal is to
extend changes made by the family to the broader environment and to sustain the
changes over time. The therapist may link with members of the broader environment
(e.g., school personnel, juvenile justice authorities) to support the family and create
plans with the family for how to address future problems.
Empirical support. FFT has been evaluated in one randomized efficacy trial with
male and female status offenders (Alexander & Parsons, 1973), a randomized effi-
cacy trial with substance-abusing adolescents (Waldron, Slesnick, Brody, Turner, &
Peterson, 2001), and in quasi-experimental studies that included youth charged with
serious delinquent offenses (Barton, Alexander, Waldron, Turner, & Warburton,
1985; Gordon, Arbuthnot, Gustafson, & McGreen, 1988). Across studies, FFT has
been shown to significantly reduce rates of delinquency recidivism and substance use
relative to control conditions. Treatment effects have also been maintained as long
as 5 years posttreatment (Gordon, Graves, & Arbuthnot, 1995). A recent large-scale
randomized effectiveness trial with juvenile offenders conducted by an independent
research group found positive outcomes for FFT on criminal recidivism 12 months
posttreatment, but only when therapist adherence to the model was high (Sexton &
Turner, 2010).
Multidimensional treatment foster care. Multidimensional treatment foster care

(MTFC) places offenders with specially trained foster parents in lieu of residential
placement, with the ultimate goal of eventually transitioning the youth back
to his or her biological family. Five research trials (three randomized and two
quasi-experimental) have evaluated MTFC, and the intervention has been transported
to more than 50 sites in the United States and internationally. Procedures for
implementing MTFC are described by Chamberlain (2003).
Theoretical bases. MTFC is based on the principles of social learning theory, which
include behavioral principles (i.e., learning through overt reward and punishment)
and the impact of the social context (i.e., learning through imitation and observa-
tion). As with MST, many of the specific intervention techniques used in MTFC are
derived from behavior therapy (e.g., development of behavior management plans) and
cognitive behavioral approaches (e.g., problem-solving skills training). These inter-
ventions also are implemented within a social ecological framework that emphasizes
the critical role of foster parent monitoring in engaging the youth in prosocial peer
activities, disengaging him or her from deviant peers, and promoting positive school
functioning.
Model of service delivery. MTFC includes multiple interrelated services provided

by several team members. The full-time master’s-level MTFC program supervisor
monitors and coordinates all interventions provided for the youth, including support-
ing foster parents through daily contact and crisis management. Each foster family has
only one MTFC youth whose placement with the family typically lasts 6 to 9 months.
Foster parents receive extensive training and ongoing guidance from the program
supervisor on how to closely supervise the youth, implement a highly structured
point-and-level behavior management plan, and provide frequent reinforcement of
the youth’s positive behavior. Foster parents also participate in weekly support groups
led by the program supervisor. A foster family recruiter/trainer assesses youth progress
daily and provides this information to the program supervisor, who uses it to refine
treatment plans.
An MTFC master’s-level therapist provides individual therapy to the youth, pri-
marily consisting of cognitive behavioral interventions targeting problem solving,
emotion management, social skill development, and educational/vocational plan-
ning. The therapist is on-call to the youth for support between sessions and works
closely with the program supervisor. A part-time bachelor’s-level skills trainer serves
as a coach to the youth, meeting with him or her one to two times each week in the
community to model and teach appropriate behaviors, based on needs identified by
the MTFC team. A family therapist works with the biological (or aftercare) family
to prepare for the youth’s return home. Initially, the family therapist meets alone
with the parents to provide PMT. After a few sessions, the family therapist begins
meeting with the parents and youth together. After rules are established, home visits
are initiated, with on-call support from the family therapist. All of these services are
coordinated through the program supervisor and weekly clinical meetings involving
all team members.
Clinical overview. The behavior management plan is the centerpiece of the MTFC
intervention. The purposes of this plan are to surround the youth with positive,
encouraging adults who provide a highly structured and supervised context, reduce
or eliminate exposure to other antisocial peers who encourage negative behaviors,
increase exposure to prosocial contacts, support and enhance school performance,
and set clear rules with frequent reinforcement of positive behaviors and consistent
consequences for negative behaviors. Plans are very specific, outlining a core set
of behavioral expectations (e.g., getting up on time, attending school, completing
chores) that are rewarded with points that can be exchanged for activities and
privileges. In addition, all MTFC team members use specific, verbal praise for positive
behaviors.
Empirical support. MTFC has been evaluated in one randomized, hybrid efficacy
and effectiveness trial with serious and chronic male juvenile offenders (Chamber-
lain & Reid, 1998) and in one quasi-experimental study (Chamberlain, 1990) with
delinquent boys. More recently, this family-based intervention was also evaluated
in a randomized, hybrid efficacy and effectiveness trial with delinquent girls (Leve,
Chamberlain, & Reid, 2005). In all three studies, youth receiving MTFC were less
likely to run away and more likely to complete treatment compared to youth placed in
community residential treatment settings. Youth who received MTFC also engaged in
fewer offenses at posttreatment, as measured by official arrest records and self-report
of delinquent behavior. Moreover, outcomes have been maintained for up to 2 years
following completion of treatment (Chamberlain, Leve, & DeGarmo, 2007; Eddy,
Whaley, & Chamberlain, 2004). Recently, an independent research group has demon-
strated favorable outcomes for MTFC in a randomized effectiveness trial (Westermark,
Hansson, & Olsson, 2011) and a quasi-experimental study (Westermark, Hansson,
& Vinnerljung, 2008) involving Swedish youth with conduct disorder.
Conclusions
Cognitive behavioral interventions have proven to be important components of

the leading evidence-based treatments of children and adolescents presenting serious
antisocial behavior. In light of the central role played by parenting and family relations
in the development and maintenance of conduct disorder and delinquency among
youth, it is not surprising that the close involvement of parents has significantly
augmented the positive effects of CBT models with school-aged children. For
adolescents, who are increasingly peer oriented, family-based approaches that address
a comprehensive array of risk factors, including peer relations, have been most
effective in attenuating serious antisocial behavior. Significantly, each of these family-
based treatments explicitly integrates cognitive behavioral interventions within their
comprehensive set of change strategies.
References
Alexander, J. F., Barton, C., Gordon, D., Grotpeter, J., Hansson, K., Harrison, R., …
Sexton, T. (1998). Blueprints for violence prevention: Functional family therapy. Boulder,
CO: Venture.
Alexander, J. F., & Parsons, B. V. (1973). Short-term behavioral intervention with delinquent
families: Impact on family process and recidivism. Journal of Abnormal Psychology, 81,
219–225.
Andrews, J. A., Tildesley, E., Hops, H., & Li, F. (2002). The influence of peers on young
adult substance use. Health Psychology, 21, 349–357.
Attar, B. K., Guerra, N. G., & Tolan, P. H. (1994). Neighborhood disadvantage, stressful life
events, and adjustment in urban elementary-school children. Journal of Clinical Child
Barton, C., Alexander, J. F., Waldron, H., Turner, C. W., & Warburton, J. (1985). Generalizing
treatment effects of functional family therapy: Three replications. American Journal of
Family Therapy, 13, 16–26.
Biglan, A., Brennan, P. A., Foster, S. L., & Holder, H. D. (2004). Helping adolescents at risk:
Prevention of multiple problem behaviors. New York, NY: Guilford Press.
Borduin, C. M., Mann, B. J., Cone, L. T., Henggeler, S. W., Fucci, B. R., Blaske, D. M., &
Williams, R. A. (1995). Multisystemic treatment of serious juvenile offenders: Long-term
prevention of criminality and violence. Journal of Consulting and Clinical Psychology, 63,
569–578.
Bronfenbrenner, U. (1979). The ecology of human development: Experiments by design and
nature. Cambridge, MA: Harvard University Press.
Butler, S., Baruch, G., Hickley, N., & Fonagy, P. (2011). A randomized controlled trial of
MST and a statutory therapeutic intervention for young offenders. Journal of the American
Academy of Child & Adolescent Psychiatry, 12, 1220–1235.
Caspi, A., Henry, B., McGee, R. O., & Moffitt, T. E. (1995). Temperamental origins of child
and adolescent behavior problems: From age three to fifteen. Child Development, 66,
55–68.
Chamberlain, P. (1990). Comparative evaluation of Specialized Foster Care for seriously
delinquent youths: A first step. Community Alternatives: International Journal of Family
Care, 2, 21–36.
Chamberlain, P. (2003). Treating chronic juvenile offenders: Advances made through the Oregon
multidimensional treatment foster care model. Washington, DC: American Psychological
Association.
Chamberlain, P., Leve, L. D., & DeGarmo, D. S. (2007). Multidimensional Treatment Foster
Care for girls in the juvenile justice system: 2-year follow-up of a randomized clinical trial.
Chamberlain, P., & Reid, J. (1998). Comparison of two community alternatives to incarceration
for chronic juvenile offenders. Journal of Consulting and Clinical Psychology, 6, 624–633.
Chambless, D. L., Sanderson, W. C., Shoham, V., Bennet Johnson, S., Pope, K. S.,
Crits-Cristoph, P., … McCurry, S. (1996). An update on empirically validated therapies.
Clinical Psychologist, 49, 5–18.
Chen, S., Matruglio, T., Weatherburn, D., & Hua, J. (2005). The transition from juvenile to
adult criminal careers. Crime and Justice Bulletin: Contemporary issues in crime and justice,
no. 86. Sydney, Australia: New South Wales Bureau of Crime Statistics and Research.
Cohen, G. L., & Prinstein, M. J. (2006). Peer contagion of aggression and health risk behavior
among adolescent males: An experimental investigation of effects on public conduct and
private attitudes. Child Development, 77 , 967–983.
Crick, N. R., & Dodge, K. A. (1994). A review and reformulation of social information-
processing mechanisms in children’s social adjustment. Psychological Bulletin, 115,
74–101.
Deater-Deckard, K., Dodge, K. A., Bates, J. E., & Pettit, G. S. (1998). Multiple risk factors
in the development of externalizing behavior problems: Group and individual differences.
Development and Psychopathology, 10, 469–493.
Dishion, T. J., & Andrews, D. W. (1995). Preventing escalation in problem behaviors with
high-risk adolescents: Immediate and 1-year outcomes. Journal of Consulting and Clinical
Dishion, T. J., Bullock, B. M., & Granic, I. (2002). Pragmatism in modeling peer influ-
ence: Dynamics, outcomes and change processes. Development and Psychopathology, 14,
969–981.
Dodge, K. A., Dishion, T. J., & Lansford, J. E. (Eds.). (2006). Deviant peer influence in
programs for youth: Problems and solutions. New York, NY: Guilford Press.
Eddy, J. M., & Chamberlain, P. (2000). Family management and deviant peer association as
mediators of the impact of treatment condition on youth antisocial behavior. Journal of
Eddy, J. M., Whaley, R., & Chamberlain, P. (2004). The prevention of violent behavior by
chronic and serious male juvenile offenders: A 2-year follow-up of a randomized clinical
trial. Journal of Family Psychology, 12, 2–8.
Elliott, D. S. (1994). Serious violent offenders: Onset, developmental course, and termination.
The American Society of Criminology 1993 presidential address. Criminology, 32, 1–21.
Eyberg, S. M., Nelson, M. M., & Boggs, S. R. (2008). Evidence-based psychosocial treatments
for children and adolescents with disruptive behavior. Journal of Clinical Child and
Adolescent Psychology, 37 , 215–237.
Farrell, A. D., Mays, S., Bettencourt, A., Erwin, E. H., Vulin-Reynolds, M., & Allison,
K. W. (2010). Environmental influences on fighting versus nonviolent behavior in peer
situations: A qualitative study with urban African American adolescents. American Journal
of Community Psychology, 46, 19–35.
Fontaine, R. G. (2006). Evaluative behavioral judgments and instrumental antisocial behaviors
in children and adolescents. Clinical Psychology Review, 26, 956–967.
Fontaine, R. G., & Dodge, K. A. (2006). Real-time decision making and aggressive behavior in
youth: A heuristic model of response evaluation and decision (RED). Aggressive Behavior,
32, 604–624.
Fontaine, R. G., Yang, C., Dodge, K. A., Bates, J. E., & Pettit, G. S. (2008). Testing
an individual systems model of response evaluation and decision (RED) and antisocial
behavior across adolescence. Child Development, 79, 462–475.
Fontaine, R. G., Yang, C., Dodge, K. A., Pettit, G. S., & Bates, J. E. (2009). Development
of response evaluation and decision (RED) and antisocial behavior in childhood and
adolescence. Developmental Psychology, 45, 447–459.
Freeman, K., Hadwin, J. A., & Halligan, S. L. (2011). An experimental investigation of peer
influences on adolescent hostile attributions. Journal of Clinical Child and Adolescent
Frick, P. J., & Morris, A. S. (2004). Temperament and developmental pathways to conduct
problems. Journal of Clinical Child and Adolescent Psychology, 33, 54–68.
Gifford-Smith, M. E., & Rabiner, D. L. (2004). Social information processing and children’s
social adjustment. In J. B. Kupersmidt & K. A. Dodge (Eds.), Children’s peer relations:
From development to intervention (pp. 61–79). Washington, DC: American Psychological
Association.
Gordon, D. A., Arbuthnot, J., Gustafson, K. E., & McGreen, P. (1988). Home-based
behavioral-systems family therapy with disadvantaged juvenile delinquents. American
Journal of Family Therapy, 16, 243–255.
Gordon, D. A., Graves, K., & Arbuthnot, J. (1995). The effect of functional family therapy for
delinquents on adult criminal behavior. Criminal Justice and Behavior, 22, 60–73.
Gottfredson, G. D., Gottfredson, D. C., Payne, A., & Gottfredson, N. C. (2005). School
climate predictors of school disorder: Results from a national study of delinquency
prevention in schools. Journal of Research in Crime and Delinquency, 42, 412–444.
Guerra, N. G., Huesmann, L. R., & Spindler, A. (2003). Community violence exposure, social
cognition, and aggression among urban elementary school children. Child Development,
74, 1561–1576.
Hawkins, D. F., Laub, J. H., Lauritsen, J. L., & Cothern, L. (2000). Race, ethnicity, and serious
and violent juvenile offending. Washington, DC: U.S. Department of Justice, Office of
Justice Programs, Office of Juvenile Justice and Delinquency Prevention.
Hellman, D. A., & Beaton, S. (1986). The pattern of violence in urban public schools: The
influence of school and community. Journal of Research in Crime and Delinquency, 23,
102–127.
Henggeler, S. W., Halliday-Boykins, C. A., Cunningham, P. B., Randall, J., Shapiro, S. B.,
& Chapman, J. E. (2006). Juvenile drug court: Enhancing outcomes by integrating
evidence-based treatments. Journal of Consulting and Clinical Psychology, 74, 42–54.
Henggeler, S. W., Letourneau, E. J., Chapman, J. E., Borduin, C. M., Schewe, P. A., &
McCart, M. R. (2009). Mediators of change for multisystemic therapy with juvenile sex
offenders. Journal of Consulting and Clinical Psychology, 77 , 451–462.
Henggeler, S. W., Melton, G. B., Brondino, M. J., Scherer, D. G., & Hanley, J. H. (1997).
Multisystemic therapy with violent and chronic juvenile offenders and their families: The
role of treatment fidelity in successful dissemination. Journal of Consulting and Clinical
Henggeler, S. W., Melton, G. B., & Smith, L. A. (1992). Family preservation using multisys-
temic therapy: An effective alternative to incarcerating serious juvenile offenders. Journal
Henggeler, S. W., Schoenwald, S. K., Borduin, C. M., Rowland, M. D., & Cunningham, P. B.
(2009). Multisystemic therapy for antisocial behavior in children and adolescents (2nd ed.).
Henggeler, S. W., & Sheidow, A. J. (2012). Empirically-supported family-based treatments for
conduct disorder and delinquency in adolescents. Journal of Marital and Family Therapy,
38, 30–58.
Hoge, R. D., Guerra, N. G., & Boxer, P. (Eds.). (2008). Treating the juvenile offender. New
Huesmann, L. R. (1988). An information processing model for the development of aggression.
Aggressive Behavior, 14, 13–24.
Huey, S. J., Henggeler, S. W., Brondino, M. J., & Pickrel, S. G. (2000). Mechanisms of change
in multisystemic therapy: Reducing delinquent behavior through therapist adherence and
improved family and peer functioning. Journal of Consulting and Clinical Psychology, 68,
451–467.
Janosz, M., LeBlanc, M., Boulerice, B., & Tremblay, R. E. (1997). Disentangling the weight
of school dropout predictors: A test on two longitudinal samples. Journal of Youth and
Adolescence, 26, 733–762.
Junger-Tas, J., Marshall, I. H., Enzmann, D., Killias, M., Steketee, M., & Gruszczynska, B.
(Eds.). (2010). Juvenile delinquency in Europe and beyond: Results of the second interna-
tional self-report delinquency study. Berlin, Germany: Springer.
Junger-Tas, J., Marshall, I. H., & Ribeaud, D. (2003). Delinquency in an international
perspective: The international self-reported delinquency study. Monsey, NY: Criminal Justice
Press.
Kazdin, A. E. (2010). Problem-solving skills training and parent management training for
oppositional defiant disorder and conduct disorder. In J. R. Weisz & A. E. Kazdin (Eds.),
Evidence-based psychotherapies for children and adolescents (pp. 211–226). New York, NY:
Guilford Press.
Kazdin, A. E., Bass, D., Siegel, T., & Thomas, C. (1989). Cognitive-behavioral treatment and
relationship therapy in the treatment of children referred for antisocial behavior. Journal
of Consulting and Clinical Psychology, 57 , 522–535.
Kazdin, A. E., Esveldt-Dawson, K., French, N. H., & Unis, A. S. (1987). Problem-solving
skills training and relationship therapy in the treatment of antisocial behavior. Journal of
Kazdin, A. E., Siegel, T., & Bass, D. (1992). Cognitive problem-solving skills training and
parent management training in the treatment of antisocial behavior in children. Journal
Lansford, J. E., Malone, P. S., Dodge, K. A., Crozier, J. C., Pettit, G. S., & Bates, J. E. (2006).
A 12-year prospective study of patterns of social information processing problems and
externalizing behaviors. Journal of Abnormal Child Psychology, 34, 715–724.
Lansford, J. E., Malone, P. S., Dodge, K. A., Pettit, G. S., & Bates, J. E. (2010). Developmental
cascades of peer rejection, social information processing biases, and aggression during
middle childhood. Development and Psychopathology, 22, 593–602.
Larson, J., & Lochman, J. E. (2002). Helping school children cope with anger: A cognitive-
behavioral intervention. New York, NY: Guilford Press.
Lemola, S., Stadlmayr, W., & Grob, A. (2009). Infant irritability: The impact of fetal alcohol
exposure, maternal depressive symptoms, and low emotional support from the husband.
Infant Mental Health Journal, 30, 57–81.
Letourneau, E. J., Henggeler, S. W., Borduin, C. M., Schewe, P. A., McCart, M. R., Chapman,
J. E., & Saldana, L. (2009). Multisystemic therapy for juvenile sexual offenders: 1-
year results from a randomized effectiveness trial. Journal of Family Psychology, 23,
89–102.
Leve, L. D., Chamberlain, P., & Reid, J. B. (2005). Intervention outcomes for girls referred
from juvenile justice: Effects on delinquency. Journal of Consulting and Clinical Psychology,
73, 1181–1185.
Liberman, A. M. (Ed.). (2008). The long view of crime: A synthesis of longitudinal research. New
York, NY: Springer.
Lochman, J. E. (1992). Cognitive-behavioral interventions with aggressive boys: Three-year
follow-up and preventive effects. Journal of Consulting and Clinical Psychology, 60,
426–432.
Lochman, J. E., Boxmeyer, C. L., Powell, N. P., Roth, D., & Windle, M. (2006). Masked
intervention effects: Analytic methods for addressing low dosage of intervention. New
Directions for Evaluation, 110, 19–32.
Lochman, J. E., Burch, P. P., Curry, J. F., & Lampron, L. B. (1984). Treatment and
generalization effects of cognitive-behavioral and goal setting interventions with aggressive
boys. Journal of Consulting and Clinical Psychology, 52, 915–916.
Lochman, J. E., & Dodge, K. A. (1994). Social cognitive processes of severely violent, mod-
erately aggressive, and nonaggressive boys. Journal of Consulting and Clinical Psychology,
62, 366–374.
Lochman, J. E., Lampron, L. B., Burch, P. R., & Curry, J. E. (1985). Client characteristics
associated with behavior change for treated and untreated boys. Journal of Abnormal
Child Psychology, 13, 527–538.
Lochman, J. E., Lampron, L. B., Gemmer, T. C., Harris, S. R., & Wyckoff, G. M. (1989).
Teacher consultation and cognitive-behavioral interventions with aggressive boys. Psychol-
ogy in the Schools, 26, 179–188.
Lochman, J. E., & Wells, K. C. (2002). Contextual social-cognitive mediators and child
outcome: A test of the theoretical model in the Coping Power Program. Development and
Psychopathology, 14, 971–993.
Lochman, J. E., & Wells, K. C. (2003). Effectiveness study of Coping Power and class-
room intervention with aggressive children: Outcomes at a one-year follow-up. Behavior
Therapy, 34, 493–515.
Lochman, J. E., & Wells, K. C. (2004). The Coping Power Program for preadolescent
aggressive boys and their parents: Outcome effects at the one-year follow-up. Journal of
Lochman, J. E., Wells, K. C., & Lenhart, L. (2008). Coping power: Child group facilitators’
guide. New York, NY: Oxford University Press.
Loeber, R., Burke, J. D., Lahey, B. B., Winters, A., & Zera, M. (2000). Oppositional defiant
and conduct disorder: A review of the past 10 years, part I. Journal of the American
Loeber, R., & Farrington, D. P. (2000). Young children who commit crime: Epidemiol-
ogy, developmental origins, risk factors, early interventions, and policy implications.
Development and Psychopathology, 12, 737–762.
Loeber, R., Farrington, D. P., Stouthamer-Loeber, M., & Van Kammen, W. B. (1998).
Antisocial behavior and mental health problems: Explanatory factors in childhood and
adolescence. Mahwah, NJ: Erlbaum.
Loeber, R., Pardini, D., Homish, D. L., Wei, E. H., Crawford, A. M., Farrington, D. P., …
Rosenfeld, R. (2005). The prediction of violence and homicide in young men. Journal of
Maguin, E., & Loeber, R. (1996). Academic performance and delinquency. In M. Tonry
(Ed.), Crime and justice: A review of the research (Vol. 20, pp. 145–264). Chicago, IL:
University of Chicago Press.
McCart, M. R., Smith, D. W., Saunders, B. E., Kilpatrick, D. G., Resnick, H., & Ruggiero, K. J.
(2007). Do urban adolescents become desensitized to community violence? Data from a
national survey. American Journal of Orthopsychiatry, 77 , 434–442.
McMahon, R. J., & Kotler, J. S. (2006). Conduct problems. In D. A. Wolfe & E. J. Mash
(Eds.), Behavioral and emotional disorders in adolescents: Nature, assessment, and treatment
McMahon, S. D., Felix, E. D., Halpert, J. A., & Petropoulos, L. A. N. (2009). Community
violence exposure and aggression among urban adolescents: Testing a cognitive mediator
model. Journal of Community Psychology, 37 , 895–910.
Merikangas, K. R., He, J., Burstein, M., Swanson, S. A., Avenevoli, S., Cui, L., … Swendsen, J.
(2010). Lifetime prevalence of mental disorders in U.S. adolescents: Results from the
National Comorbidity Survey Replication-Adolescent Supplement (NCS-A). Journal of
the American Academy of Child and Adolescent Psychiatry, 49, 980–989.
Metropolitan Area Child Study Research Group. (2002). A cognitive-ecological approach to
preventing aggression in urban settings: Initial outcomes for high-risk children. Journal
Mize, J., & Pettit, G. S. (2007). Social information processing and the development of conduct
problems in children and adolescents: Looking beneath the surface. In D. J. Flannery, A.
T. Vazsonyi, & I. D. Waldman (Eds.), Social cognition and developmental psychopathology
(pp. 141–174). New York, NY: Oxford University Press.
Moffitt, T. E. (1993). Adolescence-limited and life-course persistent antisocial behavior: A
developmental taxonomy. Psychological Review, 100, 674–701.
Nelson, D. A., & Coyne, S. M. (2009). Children’s intent attributions and feelings of distress:
Associations with maternal and paternal parenting practices. Journal of Abnormal Child
Psychology, 37 , 223–237.
Ogden, T., & Hagen, K. A. (2006). Multisystemic therapy of serious behaviour problems in
youth: Sustainability of therapy effectiveness two years after intake. Journal of Child and
Adolescent Mental Health, 11, 142–149.
Patterson, G. R. (1982). Coercive family process. Eugene, OR: Castalia.
Patterson, G. R. (2002). The early development of coercive family process. In J. B. Reid,
G. R. Patterson, & J. Snyder (Eds.), Antisocial behavior in children and adolescents:
A developmental analysis and model for intervention (pp. 25–44). Washington, DC:
American Psychological Association.
Patterson, G. R., Dishion, T. J., & Yoerger, K. (2000). Adolescent growth in new forms of
problem behavior: Macro- and micro-peer dynamics. Prevention Science, 1, 3–13.
Perry, D. G., Perry, L. C., & Rasmussen, P. (1986). Cognitive social learning mediators of
aggression. Child Development, 57 , 700–711.
Puzzanchera, C., & Adams, B. (2011). Juvenile arrests 2009. Washington, DC: U.S. Depart-
ment of Justice, Office of Justice Programs, Office of Juvenile Justice and Delinquency
Prevention.
Sampson, R. J., Raudenbush, S. W., & Earls, F. (1997). Neighborhoods and violent crime: A
multilevel study of collective efficacy. Science, 277 , 918–924.
Sawyer, A. M., & Borduin, C. M. (2011). Effects of multisystemic therapy through midlife:
A 21.9-year follow-up to a randomized clinical trial with serious and violent juvenile
offenders. Journal of Consulting and Clinical Psychology, 79, 643–652.
Schaeffer, C. M., & Borduin, C. M. (2005). Long-term follow-up to a randomized clinical
trial of multisystemic therapy with serious juvenile offenders. Journal of Consulting and
Schoenwald, S. K. (2008). Toward evidence-based transport of evidence-based treatments:
MST as an example. Journal of Child and Adolescent Substance Abuse, 17 , 69–91.
Sexton, T., & Turner, C. W. (2010). The effectiveness of functional family therapy for youth
with behavioral problems in a community practice setting. Journal of Family Psychology,
24, 339–348.
Snyder, H. N., & Sickmund, M. (2006). Juvenile offenders and victims: 2006 national report.
Washington, DC: U.S. Department of Justice, Office of Justice Programs, Office of
Juvenile Justice and Delinquency Prevention.
Stahl, A., Finnegan, T., & Kang, W. (2007). Easy access to juvenile court statistics: 1985–2004.
Retrieved from http://ojjdp.ncjrs.gov/ojstatbb/ezajcs/
Thornberry, T. P., & Krohn, M. D. (2000). The self-report method for measuring delinquency
and crime. In D. Duffee, R. D. Crutchfield, S. Mastrofski, L. Mazerolle, D. McDowall,
& B. Ostrom (Eds.), CJ 2000: Innovations in measurement and analysis (pp. 33–83).
Washington, DC: National Institute of Justice.
Thornberry, T. P, & Krohn, M. D. (Eds.). (2003). Taking stock of delinquency: An overview of
findings from contemporary longitudinal studies. New York, NY: Kluwer/Plenum.
Timmons-Mitchell, J., Bender, M. B., Kishna, M. A., & Mitchell, C. C. (2006). An independent
effectiveness trial of multisystemic therapy with juvenile justice youth. Journal of Clinical
Child and Adolescent Psychology, 35, 227–236.
van de Wiel, N. M. H., Matthys, W., Cohen-Kettenis, P. T., Maassen, G. H., Lochman, J. E.,
& van Engeland, H. (2007). The effectiveness of an experimental treatment when
compared with care as usual depends on the type of care as usual. Behavior Modification,
31, 298–312.
Wakschlag, L. S., & Hans, S. L. (2002). Maternal smoking during pregnancy and conduct prob-
lems in high-risk youth: A developmental framework. Development and Psychopathology,
14, 351–369.
Waldron, H. B., Slesnick, N., Brody, J. L., Turner, C. W., & Peterson, T. R. (2001).
Treatment outcomes for adolescent substance abuse at 4- and 7-month assessments.
Weisz, J. R., & Kazdin, A. E. (Eds.). (2010). Evidence-based psychotherapies for children and
adolescents (2nd ed.). New York, NY: Guilford Press.
Werner, N. E., & Hill, L. G. (2010). Individual and peer group normative beliefs about
relational aggression. Child Development, 81, 826–836.
Westermark, P. K., Hansson, K., & Olsson, M. (2011). Multidimensional treatment foster care
(MTFC): Results from an independent replication. Journal of Family Therapy, 33, 20–41.
Westermark, P. K., Hansson, K., & Vinnerljung, B. (2008). Does Multidimensional Treatment
Foster Care (MTFC) reduce placement breakdown in foster care? International Journal
of Child & Family Welfare, 4, 155–171.
35
Depression, Bipolar Disorder,
and Suicidal Behavior in
Children
Rachel D. Freed, Priscilla T. Chan,
David A. Langer, and Martha C. Tompson
Mood disorders represent the third most common psychiatric disorder among ado-
lescents (Merikangas et al., 2010), with 14.3% of youth aged 13–18 diagnosed with
a depressive disorder (major depressive disorder or dysthymic disorder) or bipolar
disorder (bipolar I or II). Mood disorders are relatively rare prior to adolescence
but increase markedly as children reach puberty, particularly among females, with a
nearly twofold increase from early to late adolescence (Costello, Mustillo, Erkanli,
Keeler, & Angold, 2003; Merikangas et al., 2010). For children under 13, estimates
suggest that 2.8% are affected by depressive disorders (Costello, Erkanli, & Angold,
2006). A recent meta-analysis of epidemiologic studies conducted in the United
States and internationally estimates a mean prevalence rate of 1.8% for bipolar I
and II in individuals aged 7–21, with studies that used broader criteria to diagnose
bipolar disorder (e.g., bipolar disorder not otherwise specified) showing rates as
high as 6.7% (Van Meter, Moreira, & Youngstrom, 2011). Retrospective reports of
adults with bipolar disorder suggest that 40% experience initial onset between the
ages of 13 to 18, and 30% experience onset prior to the age of 13 (Perlis et al.,
2004).
Among the negative sequelae of youth mood disorders is the fact that they
increase risk for suicide (Shaffer et al., 1996). In one study, more than 25%
of prepubertal children and 50% of adolescents with major depression endorsed
at least one suicide attempt when followed up over 10–15 years (Weissman,
Wolk, Goldstein, et al., 1999; Weissman, Wolk, Wickramaratne, et al., 1999).
Goldstein et al. (2005) found that almost one-third of children and adolescents
aged 7–17 years with bipolar disorder had attempted suicide at least once. Sui-
cide is a leading cause of death among 10- to 24-year-olds in the United States

DOI: 10.1002/9781118528563.wbcbt35
(Centers for Disease Control and Prevention [CDC], National Center for Injury
Prevention and Control, 2009), and approximately 14% of high school students
in the United States report having seriously considered suicide (CDC, 2010).
Although suicide attempts in younger children are rare (Dervic, Brent, & Oquendo,
2008; Goldstein et al., 2005), suicidal ideation may occur as often in children
with mood disorders as it does in adolescents (Lewinsohn, Rohde, & Seeley,
1996).
Cognitive behavioral therapy (CBT) has strong empirical support as an effec-
tive treatment for child and adolescent depressive disorders (David-Ferdon &
Kaslow, 2008) and is developing efficacy as an adjunct to psychopharmacologi-
cal treatment for youth with bipolar disorder (Lofthouse & Fristad, 2004) and
as a treatment for youth suicide attempters (Spirito, Esposito-Smythers, Wolff,
& Uhl, 2011). Although the focus of this chapter is on cognitive behavioral
interventions for mood disorders, research also supports the efficacy of psychophar-
macological treatment of mood disorders in youth, particularly for bipolar disor-
der (Kowatch et al., 2005). Combining medication and CBT may be especially
efficacious in the treatment of mood disorders in adolescents and may offer
additional protection against suicidality (Birmaher et al., 2007; Treatment for
Adolescents with Depression Study [TADS] Team, 2004). However, medication
use is often less acceptable to youth and families, especially for younger chil-
dren (Jaycox et al., 2006; Stevens et al., 2009). This may be particularly the
case given recent evidence suggesting that increased suicidal ideation may be a
side effect of antidepressant medication use in young people. Two meta-analytic
studies examining randomized clinical trials of antidepressant medications in youth
have found small but significant increases in suicide risk in antidepressant-treated
groups (Bridge et al., 2007; Hammad, Laughren, & Racoosin, 2006). These
findings underscore the utility of combined medication–psychotherapy interven-
tions, where suicidality can be carefully monitored and addressed. In addition,
medication and medication adherence can be particularly challenging for individ-
uals, especially youth, with bipolar disorders (Case, 2011; Colom, Vieta, Tac-
chi, Sanchez-Moreno & Scott, 2005), further warranting adjunctive psychosocial
intervention.
In this chapter we have six goals: (a) to describe mood disorders in youth,
(b) to outline existing evidence for the efficacy and effectiveness of CBT for
youth mood disorders and suicidality, (c) to describe specific CBT interventions
among youth with mood disorders and suicidality, (d) to introduce some essential
treatment considerations in youth populations, (e) to outline the specific com-
ponents included in some of the most prominent CBT protocols, and (f) to
discuss future directions. We use the term mood disorders to describe the pres-
ence of symptoms that meet DSM-IV criteria for a depressive disorder (major
depressive disorder, dysthymic disorder, depressive disorder not otherwise speci-
fied) or bipolar disorder (bipolar I disorder, bipolar II disorder, bipolar disorder
not otherwise specified). In addition, we use the term youth to describe individu-
als under the age of 18, children and pre-adolescents to describe individuals under
the age of 13, and adolescents to describe individuals between the ages of 13
and 18.
Depression, Bipolar Disorder, and Suicidal Behavior in Children 823
Clinical Characteristics and Course of Mood Disorders

in Youth
Depression in youth is diagnosed using the same DSM-IV criteria (American

Psychiatric Association, 1994) as depression in adults; however, there may be
some distinctions between child, adolescent, and adult onset. For example, pre-
adolescent children tend to present with more somatic complaints (e.g., stomach
aches, headaches, and muscle aches), psychomotor agitation, and anxiety compared
to adolescents and adults, whereas weight loss, psychomotor retardation, fatigue,
and hypersomnia are less common in pre-adolescents (Campo & Fritsch, 1994;
Kovacs, 1996; Ryan, Puig-Antich, Ambrosini, & Rabinovich, 1987; Yorbik, Birma-
her, Axelson, Williamson, & Ryan, 2007). Adolescents with depression are more likely
to endorse hopelessness and suicidality than children with depression (Ryan et al.,
1987; Yorbik et al., 2007).
Bipolar disorder with initial onset in mid-to-late adolescence is generally considered
to resemble adult disorders (Birmaher et al., 2009). The exact clinical presentation of
bipolar disorder that occurs in pre- and early adolescence is the subject of considerable
debate among researchers and clinicians (see Carlson & Glovinsky, 2009). However,
there are a number of features that are consistently found in children with bipolar
disorder (Pavuluri, Birmaher, & Naylor, 2005). In contrast to adults and older
adolescents, pre- and early adolescents with bipolar disorder rarely experience distinct
episodes of mania or major depression; rather, longitudinal studies suggest that
pediatric bipolar disorder is more often characterized by chronic or long episodes or
by rapid or continuous cycling (Biederman et al., 2005; Craney & Geller, 2003).
In addition, irritable and mixed episodes (i.e., symptoms for both a manic and
depressive episode are met) are more common in pediatric bipolar disorder than is
euphoria (Biederman et al., 2005). Many of these children have persistent difficulties
with emotion regulation, which often leads to explosive and/or aggressive outbursts
(Wozniak, Biederman, Kiely, & Ablon, 1995).
The overlap in symptoms and associated features of youth bipolar disorder and
attention-deficit/hyperactivity disorder (ADHD) (e.g., hyperactivity, distractibility,
impulsivity, talkativeness, increased involvement in and shifting of activities) can
make differential diagnosis a challenge (Carlson & Glovinsky, 2009; Leibenluft &
Rich, 2008). This may be especially true when ADHD co-occurs with oppositional
defiant disorder or conduct disorder (e.g., volatile and irritable behavior; Carlson &
Glovinsky, 2009). For this reason, Leibenluft and Rich (2008) suggest that a diagnosis
of bipolar disorder should be assigned if the symptoms represent a distinct change
from the child’s usual level of function and if symptoms occur solely during a mood
episode, or if they worsen during the mood episode. Alternately, if the symptoms are
chronic and longstanding, they would be more consistent with a diagnosis of ADHD.
Further, the presence of other bipolar symptoms (e.g., racing thoughts, euphoria,
grandiosity) can aid in diagnosing a youth with bipolar disorder over ADHD and/or
another psychiatric disorder.
Compared to adult-onset mood disorders, when depression and bipolar disorder
onset prior to adulthood they tend to be more chronic and severe (Birmaher et al.,
2009; Craney & Geller, 2003) and are associated with significant morbidity and
persistent psychosocial dysfunction, including poor academic and work performance,
and impaired interpersonal and social functioning (Goldstein et al., 2009; Jaycox
et al., 2009). In addition, more often than not, youth with mood disorders will also
have one or more comorbid conditions (Angold, Costello, & Erkanli, 1999; Pavuluri
et al., 2005; TADS Team, 2004).
As mentioned previously, mood disorders put youth at risk for suicidal ideation
and behavior, particularly as youth enter adolescence. However, there are certain
characteristics that increase the risk for suicidality in youth with mood disorders
(see Spirito & Esposito-Smythers, 2006, for a review). Severity and chronicity of
mood disorder, history of a previous suicide attempt, emotional lability, hopelessness,
withdrawal, psychiatric comorbidity (particularly anxiety, externalizing, or substance
use disorders), poor problem-solving skills, impulsive aggression, anger, and lack
of ability to sustain positive feelings may all increase risk for suicidal ideation and
behavior. These risk factors in the child may be particularly associated with suicidality
in the face of stressful life events (Asarnow et al., 2008). Although the majority of
youth who contemplate or attempt suicide suffer from mood disorders (Asarnow
et al., 2008), other factors also contribute to suicidality. For example, bullying/peer
victimization, aggression, early involvement in substance use, risky sexual behavior,
and health problems may increase risk for suicidal ideation and behaviors (Epstein
& Spirito, 2009). Given that there may be factors other than or in addition to
depression that impact suicidality, interventions are needed specifically to address
suicidal thoughts and behaviors.
Evidence for Efficacy and Effectiveness of Cognitive

Behavioral Therapy
Depression
CBT has been investigated more than any other psychosocial approach for treat-
ing youth depression (David-Ferdon & Kaslow, 2008) and is considered the best
supported treatment for youth depression in boys and girls across multiple ethnici-
ties with an average treatment effect size of 0.87 (Chorpita et al., 2011). CBT for
depression is “highly trainable” and effective with various levels of clinician training
(Chorpita et al., 2011). Results from large multisite randomized controlled trials
(RCTs) and smaller singlesite trials document the efficacy and effectiveness of CBT
and combined treatments (i.e., CBT plus medication) for youth depression in both
reducing symptoms and enhancing psychosocial functioning (see David-Ferdon &
Kaslow, 2008). In addition, the benefits of CBT for youth depression have been
shown to generalize to usual care settings (Asarnow et al., 2005; Clarke et al., 2005).
Most of the research has focused on CBT for depression in adolescents, but CBT has
also proved effective for children with elevated depressive symptoms (e.g., Asarnow,
Scott, & Mintz, 2002; Weisz, Thurber, Sweeney, Proffitt, & LeGagnoux, 1997). No
published RCTs have evaluated CBT for children with a depressive disorder, although
there have been some treatment development studies with diagnosed children (e.g.,
Stark et al., 2005; Tompson et al., 2007).
Bipolar Disorder
Psychosocial interventions for treating bipolar disorder in children and adolescents
have been developed and tested only recently, within the past 15 years (Young &
Fristad, 2007). Such interventions generally consist of cognitive behavioral com-
ponents and are designed to be adjunctive to psychopharmacological treatment
(Lofthouse & Fristad, 2004). The RCTs that have been conducted to evaluate psy-
chosocial interventions for youth with bipolar disorder demonstrated that youth and
families who participated in treatment reported more improvement in mood symp-
tom severity and recovered faster from mood episodes than comparison groups and
improvements appeared to increase over time (Fristad, Verducci, Walters, & Young,
2009; Miklowitz et al., 2008). However, for one study, treatment benefits affected
depressive symptoms only and did not extend to manic symptoms (Miklowitz et al.,
2008). A small number of additional psychosocial treatments with cognitive behav-
ioral elements are in development (e.g., Feeny, Danielson, Schwartz, Youngstrom,
& Findling, 2006; Pavuluri et al., 2004; West et al., 2009). Open trials of these
interventions show promise in improving symptoms and psychosocial functioning
and suggest that they are feasible and acceptable to youth and families, though their
effectiveness remains unclear.
Suicidality
Most studies of CBT for depression in youth have been shown to reduce suicidal
ideation and behavior (Spirito et al., 2011). A handful of investigations have tested
CBT interventions developed specifically for use with suicidal adolescents. These
interventions generally help adolescents to strengthen their coping, problem-solving,
and emotion regulation skills to prevent future suicidal behavior. The treatment
outcome literature is limited, partly because of concerns inherent in conducting
clinical trials with such high-risk patients (Spirito & Esposito-Smythers, 2006);
however, the studies that have been conducted show promise for CBT in reducing
depression and suicidality in this population (see Spirito et al., 2011, for a review).
To our knowledge, no treatments exist for pre-adolescents with suicidal ideation or
behavior, perhaps due to the low base rates of suicidality in younger children (Dervic
et al., 2008).
Cognitive Behavioral Techniques for Mood Disorders

in Youth
CBT for youth mood disorders is based on the cognitive behavioral model of depres-
sion, which posits that negative thought patterns and interpretations put youth at
risk for and maintain depressed mood, and certain behaviors (e.g., social withdrawal,
inactivity, or maladaptive social behaviors) further exacerbate low mood and vulner-
ability to depression. Deficits in coping, problem-solving, and social skills may make
it even more challenging for youth to handle stressors when they occur. Indeed,
children and adolescents with mood disorders tend to show negative attributional
styles and cognitive distortions (Garber & Hilsman, 1992) and have poorer social,
problem-solving, and coping skills than nondepressed youth (Becker-Weidman et al.,
2010; Spirito, Hart, Overholser, & Halverson, 1990). CBT interventions are generally
designed to help youth develop more positive, adaptive patterns of thinking, increase
positive behavioral patterns, and boost coping, mood regulation, and problem-solving
skills (Lewinsohn, Clarke, Rohde, Hops, & Seeley, 1996). In addition, given find-
ings that hostility, criticism, and negative communication among family members
may contribute to stress within the family environment and, subsequently, poorer
prognosis in youth with mood disorders (Asarnow, Goldstein, Tompson, & Guthrie,
1993), some interventions aim to improve family communication and functioning
(e.g., Fristad, Gavazzi, & Soldano, 1998; Miklowitz et al., 2004; Tompson et al.,
2007). Interventions for bipolar disorder in youth generally include strategies for
maintaining medication adherence (e.g., Feeny et al., 2006; Fristad et al., 1998;
Miklowitz et al., 2004; West, Henry, & Pavuluri, 2007).
Interventions for suicidal youth also include family members in some or all of the
sessions, and contain modules aimed at strengthening and stabilizing the family system
(e.g., Asarnow, Berk, & Baraff, 2009; Rotheram-Borus, Piacentini, Cantwell, Belin,
& Song, 2000; Stanley et al., 2009). Another common element in CBT interventions
for suicidal youth is the development of a safety plan that includes a specific set of
coping strategies and sources of support that families can use during a suicidal crisis.
Some treatments also aim to increase hopefulness by helping youth create tangible
reminders of positive things in their lives. For example, a “hope box” or “emergency
kit,” with reminders of reasons to live and cues/facilitators of the safety plan, can
serve as a memory aid in times of crisis (Asarnow et al., 2009; Stanley et al., 2009).
Like other CBT treatments, CBT for mood disorders and suicidality in youth is
present-oriented and skills-based. Throughout treatment, the clinician adopts the
role of “coach” or “instructor,” with the youth (and, sometimes, family) actively
involved as “students.” Youth/families are encouraged to practice skills within and
between sessions. Some treatments are designed to be used with small groups of youth
and/or parents, whereas others are intended for use with individual youth, with or
without their parents/families. CBT programs also vary in the number of sessions,
emphasis on cognitive versus behavioral skills, and specific techniques employed.
Given the differences in symptom presentation in youth at different developmental
stages (outlined earlier), treatment strategies are generally tailored to the specific
needs and cognitive capacities of the client. In this section, we describe a selection of
CBT techniques that address youth mood disorders and suicidality, focusing only on
the most common techniques due to space limitations.
Psychoeducation
CBT interventions for mood disorders in youth generally include a psychoeducation
component, usually at the start of treatment, to educate the youth and/or family
about the disorder, including the symptoms, etiology, course, comorbidity, treatment,
impact of the disorder on family and youth functioning, and role of risk and protective
factors. Handouts or videos (e.g., Miklowitz et al., 2004) can be used to present or
accompany this information. The CBT model of treatment should also be explained
early on, along with expectations of treatment, including session number, length, and
structure. Psychoeducation is important for debunking myths about mood disorders,
distinguishing normative child or adolescent behavior from symptoms, normalizing
occasional feelings of sadness, decreasing blame, identifying triggers of mood episodes,
and enhancing motivation.
When explaining mood disorders to younger children, it is important to use
developmentally appropriate language. For example, low mood and irritability can
be described as feeling “sad,” “bummed,” “like crying,” or “cranky.” Instead of
“manic,” youth may prefer “wired” or “hyper” (Miklowitz et al., 2004). In describing
anhedonia, it is usually helpful to use the word “boredom.” Using a child’s own labels
for emotions may also help the child feel understood. Finally, when explaining mood
disorders and the cognitive behavioral model, it is important to adapt descriptions
to the particular child’s experience. Here is one way to introduce to children the
relationship between thoughts, feelings, and behaviors:
When kids have a lot of stress they have all kinds of thoughts and feelings. They sometimes
have trouble sleeping, feel really down and grouchy, believe things just aren’t going to get
better, and feel like they are not good people. It seems like after your grandmother died,
the whole family went through a hard time and you started feeling pretty bad, stopped
doing the fun things you enjoy and things just got worse. Does this sound like what was
happening? (Tompson et al., 2010, p. 12)
In addition to teaching about the youth’s mood disorder, psychoeducation involves

discussion of the cognitive and behavioral factors that maintain the disorder and how
treatment will address each of these factors (i.e., the CBT model). The clinician should
first discuss the links between emotions, thoughts, and behaviors, using relevant
examples from the youth’s or family members’ particular experiences. Specifically, the
clinician should explain that depression is a disorder that, in addition to influencing
mood, affects a person’s thoughts and behaviors—and that each of these parts works
with and affects the other two. For example, a youth who does poorly on a math
test might tell himself, “I’m a failure” (thought), become frustrated or discouraged
(emotion), and go home and withdraw to his room, rather than going to his friend’s
house or studying for his next test (behavior). The clinician might next point out
that this pattern would be likely to maintain the youth’s depression because he would
be more likely to fail his next exam, further depleting his confidence, and he would
be less likely to engage in positive activities to lift his mood, like spending time
with friends—leading to what is known as a “downward spiral.” The clinician should
emphasize that it is hard simply to change the way we feel; rather, we can change our
mood by changing our negative thoughts or behavior. For example, if the youth in
our example tells himself, “I did poorly on this test, but I will do better next time if I
work a bit harder” and goes home and studies for the next test or spends time with
his friend after school, his mood would be more positive—leading to an “upward
spiral.” Lastly, the clinician should explain that CBT is designed to help individuals
learn to recognize these connections and learn ways to change their thoughts and
behaviors, thereby changing their mood.
Behavioral Activation
Behavioral activation—encouraging the youth to engage in behaviors that result
in positive changes in mood—is often one of the first skills taught in CBT for
youth mood disorders. Commonly referred to as “fun activities scheduling,” its
straightforward practice assignments may have a quicker impact on a youth’s mood
than more complex cognitive techniques. It is suitable for youth of all ages since the
cognitive demands are low (even children who do not understand the concept of
behavioral activation can have their moods lifted by engaging in fun activities), and,
if done correctly, it enables the clinician to build rapport with the youth while doing
fun things during in-session practice. The primary objectives of a behavioral activation
module is to help youth (a) understand the connection that their actions have with
their thoughts and feelings, (b) generate a diverse, realistic set of fun activities, (c)
develop and implement a plan to incorporate fun activities into daily life, and (d)
review the effects of following the plan and refine the plan so that it will continue to
be helpful in the future.
Behavioral activation often begins by reviewing the cognitive behavioral model, with
a focus on activities. Older youth may more readily recognize the connections between
actions and feelings, but may not recognize that the connection between feelings
and actions is bidirectional (i.e., they may recognize that they isolate themselves
when sad, but not recognize that isolating themselves may lead to them feeling more
sad). Younger children may respond to simpler examples, such as direct comparisons
of their mood in a desired activity compared to a disliked activity. To highlight
the relevance of this module, it is often helpful to ask the youth to think about
the day when he or she was happiest the previous week, and the day when he or
she was saddest. Then, the clinician might ask about what the youth was doing on
each of those days. Most likely, a clear link between activities and feelings will be
apparent.
Next, the clinician will work with the youth to generate a list of potentially fun
activities. Some youth may already engage in some fun activities, and the focus can
be on increasing their frequency. Others may have engaged in fun activities in the
past and the focus can be on reinitiating those activities. Clinicians should encourage
the youth to identify a diverse set of fun activities, ranging from easy-to-do (e.g.,
coloring, playing cards) to requiring planning (e.g., going to the park, going out to
dinner), and ranging from individual activities to activities with friends or family. The
goal is that there will always be a fun activity available when needed, whether it is
on a weeknight with limited time or during a vacation when there is more time and
more resources are available. Clinicians may find it handy to have a pre-existing list of
potentially fun activities that they can bring in to session to help with the generation
of ideas, though youth may benefit most when they generate their lists with minimal
clinician guidance.
If there is sufficient time available, in-session practice is a great way to illustrate the
benefits of fun activity scheduling most clearly. First, the clinician will take a mood
rating, then play a game with the youth, then take another mood rating. Typically,
the mood rating will go up after playing a game, providing evidence that this strategy
works. One variant of this activity is to conduct a brief mood induction first, asking
the child to think about something slightly sad. This will lower the starting mood
rating, leaving more room for an increase after doing the fun activity. As with most
skills, out-of-session practice is necessary. Practice typically consists of planning a
specific number of fun activities over the following week. Having the parent join the
session to discuss the practice assignment may help ensure the availability of the time
(and any materials) needed for the activities.
In the cognitive model of depression (Beck, Rush, Shaw, & Emery, 1979), depres-
sive symptoms are viewed as consequences of negative thought patterns, schemas,
and cognitive errors that serve to maintain negative beliefs despite the presence of
contradictory evidence. Depressed youth may fall prey to the same negative pat-
terns, schemas, and errors as adults, though helping youth identify and correct
these unhelpful thinking styles requires adapting standard cognitive restructuring
techniques to youth who are earlier in their cognitive development and often still
developing metacognition (the awareness that they have thoughts; Kuhn, 2000). As
mentioned above, depressed youth who are also suicidal have shown elevated levels
of cognitive errors (Brent, Kolko, Allan, & Brown, 1990). The goals of cognitive
restructuring in the treatment of youth mood disorders and suicidality are to help
the youth (a) discriminate between “helpful” and “unhelpful” thoughts, and (b)
develop strategies for generating more helpful thoughts in the context of his or her
life.
The first step in cognitive restructuring is identifying and labeling negative thoughts
as such. Children may need additional help in noticing that they have thoughts, and
exercises such as handouts of cartoon characters engaging in an activity with thought
bubbles may be useful (e.g., “What might this boy sitting alone with a frown be think-
ing?”). Often, this work of identifying thoughts may occur earlier in the treatment,
during the psychoeducation phase. Ideally, the clinician will work with the youth to
identify his or her common positive and negative thoughts by asking about specific
or recurrent situations. While many youth may not be ready at first to challenge
negative thoughts they believe are true, the clinician could at least point out that the
thoughts are negative and that they are connected to negative feelings and behaviors
(e.g., if a youth asked a friend to spend time with her after school and the friend
said she was a busy, a thought like “she doesn’t like me” would lead to a lower
mood and may discourage her from asking her friend in the future). The clinician
can teach the common thought distortions (e.g., “all or nothing” thinking, catas-
trophizing) and practice labeling negative thoughts with what type of distortion the
youth is exhibiting. Youth-oriented CBT programs use youth-friendly terms for types
of cognitive distortions, such as “blaming myself” and “unhappy guessing.” There
are also many games that may help keep youth engaged in the session. For example,
the clinician could bring a list of negative thoughts and the youth could cross them
out with a different color marker for each distortion, or the negative thoughts could
be written on index cards and the youth could sort them into piles by distortion
type.
Once the youth is able to identify thought distortions, even if only at a basic level,
the remainder of the work will focus on restructuring the negative thoughts into more
realistic or positive thoughts. An example dialogue of this process is presented in
Box 35.1. Clinicians are not responsible for generating a positive counter-thought for
every negative thought or distortion; in fact, it is preferable that clinicians present a
Box 35.1 Cognitive restructuring vignette

CLINICIAN: Joey, you’ve done a really great job finding all the different
types of negative thoughts on this sheet. It could help you to realize that
negative thoughts aren’t always true, but sometimes just labeling them
isn’t enough.
JOEY: Yeah, even when I know that I’m focusing on the bad parts of
something, I still feel crappy.
CLINICIAN: Right, so we need to go one step further—we need to think of
what we’ll call a “positive counter-thought.” This is a more realistic
thought that may also help us feel better. Let’s say one of your friends told
you that he got a bad grade on his math test and that now he knows he’s a
moron. What kind of thought would that be?
JOEY: Well, it would be a [distortion term].
CLINICIAN: Right. Now, what might you tell your friend to help him feel
better?
JOEY: Maybe that it was a really hard test and a lot of people got bad
grades.
CLINICIAN: Good positive counter-thought! And how do you think your
friend would feel having that thought instead?
JOEY: Probably a lot better. I guess I could also tell him that he’s got really
good grades on all the other math tests this year, so he’s definitely not a
moron.
CLINICIAN: You’re really getting this, Joey! Yes, there are a lot of more
positive ways to think about this.
JOEY: But what if he really is bad at math?
CLINICIAN: Good question. What do you think?
JOEY: Well, I guess he could be bad at math but good at other things, so
he’s still not a moron.
CLINICIAN: Good point—coming up with a positive counter-thought
doesn’t mean that there can’t be anything wrong, like needing extra help
in math, but it could help us realize that things may not be as bad as they
seem at first. Now let’s think about an example that you brought up in the
beginning of our session, about when you got into a fight with your sister
over the weekend and thought “she’s going to hate me for the rest of my
life.”
negative thought (fictional at first) for the youth to label and counter. In this way the
youth assumes the role of the “person with the positive counter-thoughts,” which not
only builds the youth’s cognitive restructuring skills, but also his or her self-efficacy
to counter negative thoughts. As always, practice is an important component of
mastering the skills. Practice worksheets may include a table in which there is a row
for each day and the columns are: youth-identified negative thoughts, mood ratings
associated with the negative thoughts, labels of the thought distortions, positive
counter-thoughts, and mood ratings associated with the positive thoughts.
Problem-Solving Skills Training

Providing youth with problem-solving skills can help them play a more active role
in identifying and addressing problems that lead to stress and low moods. The
problem-solving steps are: stating the problem, brainstorming possible solutions,
evaluating each solution, choosing a solution, trying out the solution, and, finally,
evaluating how well the solution worked. The clinician encourages the youth to
choose a problem that is concrete, “doable,” and current, versus one that may be
more complex or abstract or that has happened in the past. For example, a youth
who chooses “my parents are divorced” would be encouraged to revise the problem
to something more realistic such as “I miss my dad.” A general guideline to follow
is that the problem should be stated in a clear and straightforward manner. Once
the problem has been defined, the clinician guides the youth to brainstorm (without
evaluation) all possible solutions, including unrealistic or even silly solutions. During
the evaluation phase, the youth determines the pros and cons of each solution. Once
all the solutions have been evaluated, the youth picks a solution to try out for weekly
practice, detailing the plan to implement the solution. Lastly, the youth evaluates
whether the solution worked to determine whether to continue using that solution or
to try another solution. These problem-solving skills can also be applied in situations
when youth are feeling suicidal to help them seek alternative and safer responses to
their negative emotions, as discussed in more detail later in this chapter. When family
members are involved in therapy, the problem-solving component may be conducted
as a group effort, and may be especially effective in identifying and managing problems
impacting the family as a whole, while enhancing communication and relationships.
Communication Enhancement and Social Skills Training

Mood disorders can have a particularly negative impact on interpersonal functioning.
Even among youth who have recovered from mood disorders, interpersonal function-
ing may continue to be impaired (Puig-Antich, 1985). Disruptions in interpersonal
functioning may also contribute to the onset and maintenance of mood episodes
(Miklowitz et al., 2004). Thus, strategies for enhancing communication and social
skills may be essential in reducing symptoms, restoring functioning, and reducing
relapse risk. Improving these skills is likely to decrease depressive withdrawal and
enhance effective coping in interpersonal situations. Components focused on improv-
ing interpersonal functioning have been shown to be particularly effective in treating
depression in youth (Kennard et al., 2009).
Communication enhancement training skills include giving positive feedback, active

listening, giving negative feedback, and requesting behavior change. When learning
these skills, role playing is crucial, as is active family participation when possible. These
sessions allow each member to role play the part of both the speaker and the listener
and provide an opportunity to allow youth and their family members to engage in new
and gratifying ways. Focusing initially on positive communication often allows family
members to gain comfort with role playing and establishes a positive environment. By
providing family members with handouts outlining the steps of each communication
skill, the clinician sets up expectations and allows family members to monitor each
other’s use of the skills. The clinician should model the skills first, and family members
should then take turns with each skill. The clinician should also make liberal use of
praise to shape the communicative behavior. In Box 35.2, the clinician works with
a depressed 10-year-old girl and her father on giving positive feedback and active
listening.
Box 35.2 Communication enhancement vignette

CLINICIAN: So, Anna, we are going to work with you and your father on
giving positive feedback. Here are the steps [presenting an instructional
handout]: look at him, tell him exactly what he did that you liked, and tell
him how it made you feel. Mr. Jones, I’d like you to do the active
listening [also providing an instructional handout]—look at her, listen
carefully, nod to let her know you are with her, ask any questions, and
summarize what you’ve heard.
ANNA: OK, Dad, I really like it when you are so nice to me when I get
home from school. It really makes me feel good.
CLINICIAN: That was great! I loved how you said how it made you feel.
[To father] So did she do all the steps?
FATHER: [Looking at the instruction handout] Well, she looked at me and
she did say how it made her feel, but I’m not sure I know exactly what it
was I did that she liked.
CLINICIAN: Hmm, what exactly was it, Anna?
ANNA: I liked that he cut up some fruit and we had snacks together!
CLINICIAN: That is very specific and clear! Giving positive feedback does
two things. It makes the other person feel good, and it also gives them
information about how to please us. So, Anna, would you try it again,
being specific?
ANNA: Sure. Dad, I liked it when you shared snacks with me after school.
It made me feel like you really care about me.
FATHER: So you liked having a snack with me after school. It made you
feel cared about. I’m glad. I liked it too.
CLINICIAN: Anna, I thought that was perfect! And Mr Jones, you get an
“A” for active listening.
In families with mood disorders, emotions may be strong and affect may be volatile.
Thus, the clinician must take an active role in structuring role plays, modeling
behavior, and setting limits. Making “rules” at the outset can be helpful, including:
no name calling, no blaming, keep it short and specific, and only speak for yourself. In
highly affectively-charged families, these structured interventions can allow members
to begin to create an emotionally safer environment.
Social skills training can range from micro-level skills (e.g., appropriate smiling, eye
contact, posture), to general conversation skills (e.g., introductions, asking questions,
listening, showing interest), to more complex skills for making friends (e.g., expressing
empathy, sharing, inviting others, and giving compliments) and being assertive. Skills
are taught and reinforced using modeling, role playing, and in vivo social practice.
Some interventions also include built-in social/recreational activities to allow for
practice in a naturalistic environment (Clarke, Lewinsohn, & Hops, 1990; Fristad
et al., 1998) or assign social tasks for homework (e.g., social initiating, group
activity; Danielson, Feeny, Findling, & Youngstrom, 2004). Social skills can also be
incorporated into other modules. For example, youth can practice problem solving
or cognitive restructuring in the context of social situations, and behavioral activation
can include planning social activities with peers.
Relaxation Training
Relaxation training may be particularly helpful for youth who experience heightened
physiological arousal, such as muscle tension, difficulty falling asleep, or concentration
difficulties, especially when using coping skills is too challenging. The primary
objective of this module is to help youth (a) understand the relationship between
their somatic feelings and depressive feelings, (b) learn that their somatic feelings of
depression may be related to muscle tension, and (c) practice an additional coping
strategy to deal with stress. The first step is helping youth become more aware of how
their bodies feel when tensed versus relaxed by guiding youth through progressive
muscle relaxation (PMR), which is the tensing and releasing of specific muscle groups.
For younger children, it can be helpful to describe the tensing and releasing of muscles
more concretely, such as describing tension in the lower arms as “squeezing lemons”
or tensing and releasing the shoulder muscles as “shrugging your shoulders up
and down.” Another aspect of relaxation training is teaching youth diaphragmatic
breathing in which they take a few minutes to breathe deeply in and out through their
belly, rather than their chests, in a calm manner. Assigning out-of-session homework
can be helpful to facilitate practice of these relaxation skills during times of low stress,
so that youth are able more easily to access and engage in these strategies during
times of high stress.
Safety Planning
Recent research has shown that using cognitive behavioral principles to address youth
suicidality is feasible (Stanley et al., 2009) and may protect against future suicidality
relative to medication alone (TADS Team, 2004). While there are entire CBT-based
protocols devoted to treating youth suicidality (e.g., Brent et al., 2009; Stanley et al.,
2009; Tompson, Boger, & Asarnow, 2012), two techniques, among others, are
common to many of the protocols—chain analysis and safety planning.
Chain analysis (or “cognitive behavioral fit analysis”) is closely related to basic
CBT psychoeducation in which youth work to understand the relationships among
thoughts, feelings, and behaviors. When the focus is on a suicidal event, the clinician
works with the youth to identify the antecedents of the suicidal thoughts or behaviors
(i.e., stressful events, other thoughts, feelings or behaviors). A step-by-step, detailed
analysis of these antecedents will assist in safety planning, will help the youth
view suicidal thoughts and behaviors in a CBT framework, and will send the implicit
message that suicidal thoughts and behaviors do not occur without warning. Clinicians
may choose to include the parent(s) in this process if they can help in providing
additional detail and use the information to help the youth stay safe.
The main point of safety planning is to develop a list of clear, personalized coping
strategies that a youth could use when he or she is feeling at risk for uncontrolled,
dangerous, or suicidal behavior. The list should include strategies that are behavioral
(e.g., listening to comforting music, relaxation, distraction, seeking support from
parents or other responsible adults) and cognitive (e.g., “coping” thoughts, which
can come from the cognitive restructuring module, or temporary coping thoughts
could be developed if safety planning occurs at the beginning of treatment). If those
behavioral and cognitive strategies are not sufficient, the list should include contact
information of available emergency psychiatric services (e.g., 911). The clinician and
youth should write the list clearly and each sign the list as if it were a contract. If
possible, parents will be invited in toward the end of the session to review the list,
offer any suggestions, and also agree to support the youth in the ways detailed in the
list. Some protocols include the parents for the majority of safety planning, which
may be preferable depending on the youth’s and family’s needs. The list may be
updated throughout treatment, and may also include restriction of dangerous items
(e.g., firearms) from the home (Spirito, Esposito-Smythers, Weismoore, & Miller,
2012; Stanley et al., 2009).
Medication Management
Medication is an essential component of a comprehensive treatment approach for
bipolar disorders (McClellan, Kowatch, & Findling, 2007), and, as noted earlier,
combining medication and CBT has been shown to be particularly efficacious in the
treatment of depression in adolescents (Birmaher et al., 2007; TADS Team, 2004).
However, studies focusing on youth suggest medication adherence is often dismal
(Case, 2011). The intent of this module is to describe strategies used within a CBT
model to address medication adherence.
The first step in addressing medication nonadherence is to understand what is
driving it. Numerous factors underlie medication nonadherence, including, but not
limited to, simple forgetting, a poor understanding of the disorder, side effects, lack
of financial resources, concerns regarding blood tests, stigma, and negative feelings
about having one’s mood controlled (Colom et al., 2005). These concerns are likely
to evolve across development with more concrete concerns in school-aged children
(swallowing pills, getting blood tests, teasing by peers) and more concerns about
social stigma, autonomy, and the meaning of medications for the self in adolescents.
The clinician should choose an intervention strategy to directly address the cause
of nonadherence. The second step is to determine who is involved in medication
adherence. Medications have the potential to be a “battleground” for adolescents to
act out their struggles for autonomy, contributing to problems with nonadherence.
Thus, even for older adolescents, involving parents or other family members in
some treatment sessions may be essential for maximizing adherence. Additionally,
in cases where the CBT clinician is not the prescribing physician, it is essential that
there be ongoing communication between treatment providers and, in service of the
therapeutic alliance, that the youth be apprised of these communications.
Third, the clinician selects specific CBT strategies to enhance medication adherence.
Where nonadherence results from a poor understanding of the disorder or rationale for
medication treatment, psychoeducation about the disorder, its symptoms, causes, and
treatment is essential. More concrete problems (side effects, concerns about blood
tests, forgetting, inability to obtain) are often addressed through problem-solving
interventions. Cognitive restructuring can be particularly useful in addressing under-
lying thoughts and assumptions that fuel nonadherence, including such thoughts as
“If I stop taking medication I can prove I’m my own boss,” “Taking medication means
I’m under the control of my parents,” and “If I take medication, my emotions aren’t
‘real’.” Parents often need to be engaged in problem-solving discussions regarding
medication to balance the adolescent’s desire to make his or her own decisions with
the parents’ need to ensure that the youth is receiving appropriate care.
Other Challenges and Considerations in Applying Cognitive

Behavioral Therapy with Youth with Mood Disorders
Developmental Phase
Several important developmental factors have strong implications for treatment deliv-
ery. First, each developmental phase is associated with new cognitive skills. The more
limited cognitive abilities of children, as opposed to adolescents, have implications
for both risk models and treatment. Children may not have developed the requi-
site cognitive abilities for the formation of cognitive vulnerabilities for depression,
such as internal, global, and stable explanatory styles for negative events (Turner &
Cole, 1994), and, as noted previously, their limited metacognitive abilities may make
techniques such as cognitive restructuring challenging. Younger children may prefer
behavioral to cognitive components of CBT (Asarnow et al., 2002). Second, develop-
mental tasks and challenges change as youth mature. During adolescence, the focus
shifts from the family to the peer group, and youth begin to attend increasingly to
peer feedback, leading to increased peer-related stress (Rudolph & Hammen, 1999;
Wagner & Compas, 1990). This changed focus, combined with adolescents’ increas-
ing cognitive perspective-taking abilities, enables them to engage more frequently in
social comparison in evaluating their self-worth (Stark et al., 2006). These factors
contribute to the enhanced risk for mood disorders in adolescence as compared to
childhood. Pre-adolescents are often more strongly embedded in their family context
and are more dependent on parents for guidance, feedback, and support in negoti-
ating the outside world. Effective CBT treatment means tailoring interventions for
developmental level, with attention to cognitive capacity, development challenges,
and family involvement.
Comorbidity
As mentioned earlier, youth mood disorders are often comorbid with other psychi-
atric conditions, including anxiety disorders and attention deficit disorder, and, in
adolescence, substance abuse (Angold et al., 1999; Goldstein et al., 2008; Pavuluri
et al., 2005; TADS Team, 2004). Recent studies underscore the enhanced risk for
depression among individuals with autism spectrum disorders (Matson & Nebel-
Schwalm, 2007). Among youth with bipolar disorders, comorbidity with disruptive
behavior disorders during euthymic periods may be normative (Findling et al., 2001),
and comorbid conduct disorder and substance use has been associated with more
restrictive care settings (Rizzo et al., 2007). When comorbidity complicates treatment,
clinicians need carefully to consider working with a team of providers, using a modular
format, and sequencing treatment according to levels of impairment and likelihood
of success. Attention to specific comorbid symptoms—for example, the rigidity and
limited perspective-taking abilities of youth with autism spectrum disorders—may be
important in implementing specific cognitive interventions.
Parental Psychopathology
Children of parents with mood disorders are at significantly enhanced risk for
the development of these disorders themselves (Beardslee & Martin, 2010). Mood
disorders in parents may impact their ability to provide effective care for their children,
limit their ability to collaborate in their child’s treatment, and increase family stress.
In implementing CBT with youth with mood disorders, clinicians may need to refer
parents to their own treatment, include parents in sessions, and work with youth
on coping with parental psychopathology. During conjoint sessions, clinicians can
work with youth and parents on reducing family tension through implementing
communication enhancement and problem-solving exercises. In addition, helping
parents to find ways to talk to their offspring about their own mood disorders can
help reduce stigma and self-blame, enhance children’s feeling of security, and improve
the parent–child relationship.
Stress Context
Stress is one of the predominant pathways to the development of and manifestation
of youth mood disorders (Stark et al., 2005; Stark et al., 2006). Depressed youth
and their families report more negative life events and chronic stress (Compas, 1987;
Garber & Robinson, 1997; Hammen, 2002). Among youth with bipolar disorder,
affective dysregulation may diminish interpersonal function and increase interpersonal
stress, and life stress appears to negatively impact the course of the disorder (Keenan-
Miller & Miklowitz, 2011). Knowledge of the stress context is therefore crucial
in designing and implementing effective treatments. For example, in cases where

peer conflicts and/or bullying contribute to mood symptoms, engaging with school
personnel may be essential in reducing these stressors. Alternatively, where academic
stressors predominate, using problem solving to enhance resources (such as locating
tutoring) may be particularly helpful.
Ethnic Background
Different ethnic/cultural groups demonstrate differences in their level of mental
health service utilization. For example, although African American youth may
show higher depressive symptoms, they may be less likely than European American
youth to receive outpatient treatment for any disorder and be more likely to drop
out of treatment early (Cuffe, Waller, Cuccaro, & Pumariega, 1995). Findings
from current clinical trials may not generalize to ethnic/racial minorities (Bernal,
Bonilla, & Bellido, 1995; Bernal & Scharron-Del-Rio, 2001). Beliefs and values
about psychopathology and treatment are influenced by cultural background (Weisz,
Doss, & Hawley, 2005), and a sensitive understanding of these beliefs/values is
essential to accurate assessment and effective treatment planning.
Programs in Action
Table 35.1 provides information about a selection of existing CBT programs for
depression, bipolar disorder, and suicidality in children and adolescents and indicates
which CBT components described above are included in each. For information about
efficacy and effectiveness of particular programs, readers are advised to read the numer-
ous review articles on the topic (e.g., Asarnow, Jaycox, & Tompson, 2001; David-
Ferdon & Kaslow, 2008; Spirito et al., 2011; Young & Fristad, 2007). It is important
to note that some of the programs on our list guided the development of other
treatment protocols on our list. For example, the CBT treatment administered in the
TADS study was based on other treatment manuals, including the Adolescent Coping
with Depression Course (Lewinsohn, Clarke, Hops, & Andrews, 1990) and Treating
Depressed and Suicidal Adolescents: A Clinician’s Guide (Brent, Poling, & Goldstein,
2011). As Table 35.1 shows, there is substantial overlap in CBT components across
treatments. We also note that some treatments are applied flexibly and contain some of
the CBT elements in required modules and others in optional modules (e.g., TADS).
Discussion and Future Directions
Mood disorders in youth represent a clear public health burden, with long-term and
far-reaching consequences for youth and families. Fortunately, CBT has established
efficacy for reducing symptoms and improving quality of life in youth and families.
A number of CBT interventions have been developed for treating youth with mood
disorders and suicidality. Although these programs vary considerably in terms of
Table 35.1 Information about and Components of a Sample of Cognitive Behavioral Therapy Protocols for Youth Mood Disorders
Treatment components
Therapy Disorders targeted Age range Number of Format
sessions
Psychoeducation
Problem solving
Cognitive restructuring
Communication enhancement
Medication management
Activities scheduling
Social skills
Relaxation
Safety planning
Family Focused Treatment for MDD, DD, 8–15 years 15 Family X X X X

Depressed Children (FFT-CD) DDNOS
(Tompson, Boger, & Asarnow,
2012)
Penn Prevention Program/Penn High depressive 10–14 years 12 Group X X X X X
Resiliency Program (Gillham, symptoms
Brunwasser, & Freres, 2008)
Stress-Busters (Asarnow, Scott, & High depressive Grades 4–6 10 Group, with 1 family X X X X X
Mintz, 2002) symptoms group session
Primary and Secondary Control High depressive 8–15 years 18 Individual with 1 X X X X X
Enhancement Therapy symptoms parent session and
(PASCET) (Bearman & Weisz, optional home and
2009) school visits
Coping with Depression Course MDD, DD, high 14–18 years 16; plus booster Separate parent and X X X X X X X
(CWD-A) (Clarke & DeBar, depressive sessions child groups
2010) symptoms
Taking ACTION (Stark & MDD, DD, high 9–13 years 30 Individual and group X X X X X
Kendall, 1996) depressive components with
symptoms separate parent
training
The Pittsburgh MDD 13–18 years 12–16; plus 2–4 Individual X X X X X
Cognitive-Behavioral Therapy booster sessions
Program (Brent, Poling, &
Goldstein, 2011)
Treatment of Resistant MDD 12–18 years 12; plus 6+ booster Individual with some X X X X X
Depression in Adolescents sessions family sessions
(TORDIA) (Brent et al., 2008)
Treatment for Adolescents With MDD 12–17 years 15; plus 3–6 Individual with some X X X X X X X
Depression Study (TADS) maintenance family/parent
(Curry et al., 2005) sessions; plus sessions
booster sessions
Family-Focused Therapy for BP-I, BP-II, 12–17 years 21 Family X X X X
Adolescents (FFT-A) BP-NOS
(Miklowitz et al., 2004)
Multifamily Psychoeducation BP, MDD, DD 8–11 years 8 Separate parent and X X X X
Group (MFPG) (Fristad, child groups
Gavazzi, & Soldano, 1998)
Child and Family Focused BP 5–17 years 12 Individual, parent, X X X X
Cognitive Behavioral Therapy and family sessions
(CFF-CBT) (Pavuluri et al.,
2004)
Treatment components
Therapy Disorders targeted Age range Number of Format
sessions
Psychoeducation
Problem solving
Cognitive restructuring
Communication enhancement
Medication management
Activities scheduling
Social skills
Relaxation
Safety planning
Adjunctive CBT for Pediatric BP 10–17 years 12; plus 6–10 session Individual with X X X X X X
Bipolar Disorder (Danielson, maintenance phase flexible parental
Feeny, Findling, & involvement
Youngstrom, 2004)
Successful Negotiation Acting Suicide attempt 12–18 years 1 specialized ER care Family X X X
Positively (SNAP) session; plus 6
(Rotheram-Borus et al., 1994) outpatient sessions
Cognitive-Behavioral Therapy for Suicide attempt 13–19 years 12–16; plus 6-session Mostly individual X X X X X X
Suicide Prevention (CBT-SP) continuation phase with some family
(Stanley et al., 2009) sessions
Skills-based treatment for Suicide attempt 12–17 years 7; plus 3-session Individual with 1 X X X X X X
adolescent suicide attempters maintenance phase family session
(Donaldson, Spirito, &
Esposito-Smythers, 2005)
Notes. *Some treatments are applied flexibly and contain some of these elements in optional modules; MDD = major depressive disorder, DD = dysthymic disorder,
DDNOS = depressive disorder, not otherwise specified, ER = emergency room, BP = bipolar disorder, BP-NOS = bipolar disorder not otherwise specified.
session length, modality (e.g., group vs. individual), extent of parent involvement, and
specific components included, they are each generally designed to help youth develop
more positive or adaptive patterns of thinking, increase positive behavioral patterns,
and boost coping, mood regulation, and problem-solving skills. Some interventions
also focus on improving family communication and functioning and include strategies
for medication management and planning for emergency situations. Regardless of
format, the quality of the therapeutic alliance is an important predictor of treatment
outcome with youth (Shirk, Karver, & Brown, 2011) and building rapport and trust
with youth and family is a critical first step. In addition, clinicians must adapt cognitive
behavioral approaches to the individual needs of youth and families.
Given the overlap in treatment components across interventions, little is known
about which components are most effective in treating youth mood disorders. Future
research is needed to identify the relative contributions of specific CBT components
to symptom reduction and long-term improvement in functioning. Further, studies
with diverse patient populations are needed to evaluate generalizability of available
interventions. New and innovative methods have emerged in recent years to increase
the transportability of delivering CBT to youth, including computerized CBT, school-
based CBT, camp-based CBT, and CBT delivered in primary care settings (Elkins
et al., 2011). These various modalities have shown promise in the dissemination
and implementation of CBT programs for children and adolescents with mood
disorders (Elkins et al., 2011). Such new developments and continued testing will
help us continue to refine cognitive behavioral treatments and demonstrate even
better outcomes for youth and families.
References
Angold, A., Costello, E. J., & Erkanli, A. (1999). Comorbidity. Journal of Child Psychology and
Asarnow, J. R., Baraff, L. J., Berk, M., Grob, C., Devich-Navarro, M., Suddath, R., … Tang, L.
(2008). Pediatric emergency department suicidal patients: Two-site evaluation of suicide
ideators, single attempters, and repeat attempters. Journal of the American Academy of
Child and Adolescent Psychiatry, 47 , 958–966.
Asarnow, J. R., Berk, M. S., & Baraff, L. J. (2009). Family Intervention for Suicide Prevention: A
specialized emergency department intervention for suicidal youths. Professional Psychology:
Research and Practice, 40, 118–125.
Asarnow, J. R., Goldstein, M. J., Tompson, M. C., & Guthrie, D. (1993). One-year outcomes
of depressive disorders in child psychiatric in-patients: Evaluation of the prognostic power
of a brief measure of expressed emotion. Journal of Child Psychology and Psychiatry, 34,
129–137.
Asarnow, J. R., Jaycox, L. H., Duan, N., LaBorde, A. P., Rea, M. M., Murray, P., … Wells,
K. B. (2005). Effectiveness of a quality improvement intervention for adolescent depression
in primary care clinics: A randomized controlled trial. JAMA, 293, 311–319.
Asarnow, J., Jaycox, L. H., & Tompson, M. C. (2001). Depression in youth: Psychoso-
cial interventions. Journal of Clinical Child Psychology, 30, 33–47. doi:10.1207/
S15374424JCCP3001_5
Asarnow, J. R., Scott, C. V., & Mintz, J. (2002). A combined cognitive-behavioral family edu-
cation intervention for depression in children: A treatment development study. Cognitive
Therapy and Research, 26, 221–229.
Beardslee, W. R., & Martin, J. L. (2010). Children of parents with psychiatric and substance
abuse disorders. In M. K. Dulcan (Ed.), Dulcan’s textbook of child and adolescent psychiatry
(pp. 623–635). Arlington, VA: American Psychiatric Publishing.
Bearman, S. K., & Weisz, J. R. (2009). Primary and Secondary Control Enhancement Training
(PASCET): Applying the deployment-focused model of treatment development and
testing. In C. A. Essau (Ed.), Treatments for adolescent depression: Theory and practice (pp.
97–122). Oxford, England: Oxford University Press.
Becker-Weidman, E. G., Jacobs, R. H., Reinecke, M. A., Silva, S. G., & March, J. S. (2010).
Social problem-solving among adolescents treated for depression. Behaviour Research and
Therapy, 48, 11–18.
Bernal, G., Bonilla, J., & Bellido, C. (1995). Ecological validity and cultural sensitivity for
outcome research: Issues for the cultural adaptation and development of psychosocial
treatments with Hispanics. Journal of Abnormal Child Psychology, 23, 67–82.
Bernal, G., & Scharron-Del-Rio, M. R. (2001). Are empirically supported treatments valid
for ethnic minorities? Toward an alternative approach for treatment research. Cultural
Diversity and Ethnic Minority Psychology, 7 , 328–342.
Biederman, J., Faraone, S. V., Wozniak, J., Mick, E., Kwon, A., Cayton, G. A., & Clark, S. V.
(2005). Clinical correlates of bipolar disorder in a large, referred sample of children and
adolescents. Journal of Psychiatric Research, 39, 611–622.
Birmaher, B., Axelson, D., Strober, M., Gill, M. K., Yang, M., Ryan, N., … Leonard, H.
(2009). Comparison of manic and depressive symptoms between children and adolescents
with bipolar spectrum disorders. Bipolar Disorders, 11, 52–62.
Birmaher, B., Brent, D., Bernet, W., Bukstein, O., Walter, H., Benson, R. S., … Medicus, J.
(2007). Practice parameter for the assessment and treatment of children and adolescents
with depressive disorders. Journal of the American Academy of Child and Adolescent
Psychiatry, 46, 1503–1526.
Brent, D., Emslie, G., Clarke, G., Wagner, K. D., Asarnow, J. R., Keller, M., … Zelazny J.
(2008). Switching to another SSRI or to venlafaxine with or without cognitive behav-
ioral therapy for adolescents with SSRI-resistant depression: The TORDIA randomized
controlled trial. JAMA, 299, 901–913.
Brent, D. A., Greenhill, L. L., Compton, S., Emslie, G., Wells, K., Walkup, J. T., …
Turner, J. B. (2009). The Treatment of Adolescent Suicide Attempters Study (TASA):
Predictors of suicidal events in an open treatment trial. Journal of the American Academy
of Child and Adolescent Psychiatry, 48, 987–996.
Brent, D. A., Kolko, D. J., Allan, M. J., & Brown, R. V. (1990). Suicidality in affectively
disordered adolescent inpatients. Journal of the American Academy of Child and Adolescent
Brent, D. A., Poling, K. D., & Goldstein, T. R. (2011). Treating depressed and suicidal
adolescents: A clinician’s guide. New York, NY: Guilford Press.
Bridge, J. A., Iyengar, S., Salary, C. B., Barbe, R., Birmaher, B., Pincus, H., …
Brent, D. A. (2007). Clinical response and risk for reported suicidal ideation and suicide
attempts in pediatric antidepressant treatment: A meta-analysis of randomized controlled
trials. JAMA, 297 , 1683–1696.
Campo, J. V., & Fritsch, S. L. (1994). Somatization in children and adolescents. Journal of the
Carlson, G. A., & Glovinsky, I. (2009). The concept of bipolar disorder in children: A history
of the bipolar controversy. Child and Adolescent Psychiatric Clinics of North America, 18,
257–271.
Case, B. (2011). Nonadherence: The silent majority. Journal of the American Academy of Child
and Adolescent Psychiatry, 50, 435–437.
Centers for Disease Control and Prevention. (2010). Youth Risk Behavior
Surveillance—United States, 2009, surveillance summaries. Morbidity and Mortality
Weekly Report, 59, 1–142.
Centers for Disease Control and Prevention, National Center for Injury Prevention and
Control. (2009). Web-based Injury Statistics Query and Reporting System (WISQARS).
Retrieved from http://www.cdc.gov/ncipc/wisqars
Chorpita, B. F., Daleiden, E. L., Ebesutani, C., Young, J., Becker, K. D., Nakamura, B. J., …
Starace, N. (2011). Evidence-based treatments for children and adolescents: An updated
review of indicators of efficacy and effectiveness. Clinical Psychology: Science and Practice,
18, 154–172.
Clarke, G., & DeBar, L. (2010). Group cognitive-behavioral treatment for adolescent depres-
sion. In J. R. Weisz & A. E. Kazdin (Eds.). Evidence-based psychotherapies for children and
adolescents (pp. 100–125). New York, NY: Guilford Press.
Clarke, G., Debar, L., Lynch, F., Powell, J., Gale, J., O’Connor, E., … Hertert, S. (2005). A
randomized effectiveness trial of brief cognitive-behavioral therapy for depressed adoles-
cents receiving antidepressant medication. Journal of the American Academy of Child and
Clarke, G., Lewinsohn, P., & Hops, H. (1990). Leader’s manual for adolescent groups;
Adolescent Coping with Depression Course. Retrieved from http://www.kpchr.org/
acwd/acwd.html
Colom, F., Vieta, E., Tacchi, M. J., Sanchez-Moreno, J., & Scott, J. (2005). Identifying and
improving non-adherence in bipolar disorders. Bipolar Disorders, 7 , 24–31.
Compas, B. E. (1987). Coping with stress during childhood and adolescence. Psychological
Bulletin, 101, 393–403.
Costello, E. J., Erkanli, A., & Angold, A. (2006). Is there an epidemic of child or adolescent
depression? Journal of Child Psychology and Psychiatry, 47 , 1263–1271.
Costello, E. J., Mustillo, S., Erkanli, A., Keeler, G., & Angold, A. (2003). Prevalence and
development of psychiatric disorders in childhood and adolescence. Archives of General
Craney, J. L., & Geller, B. (2003). A prepubertal and early adolescent bipolar disorder–I
phenotype: Review of phenomenology and longitudinal course. Bipolar Disorders, 5,
243–256.
Cuffe, S. P., Waller, J. L., Cuccaro, M. L., & Pumariega, A. J. (1995). Race and gender
differences in the treatment of psychiatric disorders in young adolescents. Journal of the
Curry, J. F., Wells, K. C., Brent, D. A., Clarke, G. N., Rohde, P., Albano, A. M., …
March, J. S. (2005). Treatment for Adolescents with Depression Study (TADS) cognitive
behavior therapy manual; Introduction, rationale, and adolescent sessions. Retrieved from
https://trialweb.dcri.duke.edu/tads/tad/manuals/TADS_CBT.pdf
Danielson, C. K., Feeny, N. C., Findling, R. L., & Youngstrom, E. A. (2004). Psychosocial treat-
ment of bipolar disorders in adolescents: A proposed cognitive-behavioral intervention.
Cognitive and Behavioral Practice, 11, 283–297.
David-Ferdon, C., & Kaslow, N. J. (2008). Evidence-based psychosocial treatments for child
and adolescent depression. Journal of Clinical Child and Adolescent Psychology, 37 ,
62–104.
Dervic, K., Brent, D. A., & Oquendo, M. A. (2008). Completed suicide in childhood.
Psychiatric Clinics of North America, 31, 271–291.
Donaldson, D., Spirito, A., & Esposito-Smythers, C. (2005). Treatment for adolescents
following a suicide attempt: Results of a pilot trial. Journal of the American Academy of
Child and Adolescent Psychiatry, 44, 113–120.
Elkins, R., McHugh, R., Santucci, L. C., & Barlow, D. H. (2011). Improving the transporta-
bility of CBT for internalizing disorders in children. Clinical Child and Family Psychology
Review, 14, 161–173.
Epstein, J. A. & Spirito, A. (2009). Risk factors for suicidality among a nationally representative
sample of high school students. Suicide and Life-Threatening Behavior, 39, 241–251.
Feeny, N. C., Danielson, C. K., Schwartz, L., Youngstrom, E. A., & Findling, R. L. (2006).
Cognitive-behavioral therapy for bipolar disorders in adolescents: A pilot study. Bipolar
Findling, R. L., Gracious, B. L., McNamara, N. K., Youngstrom, E. A., Demeter, C. A.,
Branicky, L. A., & Calabrese, J. R. (2001). Rapid, continuous cycling and psychiatric
co-morbidity in pediatric bipolar I disorder. Bipolar Disorders, 3, 202–210.
Fristad, M. A., Gavazzi, S. M., & Soldano, K. W. (1998). Multi-family psychoeducation
groups for childhood mood disorders: A program description and preliminary efficacy
data. Contemporary Family Therapy, 20, 385–402.
Fristad, M. A., Verducci, J. S., Walters, K., & Young, M. E. (2009). Impact of multifamily
psychoeducational psychotherapy in treating children aged 8 to 12 years with mood
disorders. Archives of General Psychiatry, 66, 1013–1020.
Garber, J., & Hilsman, R. (1992). Cognitions, stress, and depression in children and adoles-
cents. Child and Adolescent Psychiatric Clinics of North America, 1, 129–167.
Garber, J., & Robinson, N. S. (1997). Cognitive vulnerability in children at risk for depression.
Cognition and Emotion, 11, 619–635.
Gillham, J. E., Brunwasser, S. M., & Freres, D. R. (2008). Preventing depression in early
adolescence: The Penn Resiliency Program. In J. Z. Abela & B. L. Hankin (Eds.),
Handbook of depression in children and adolescents (pp. 309–332). New York, NY:
Guilford Press.
Goldstein, B. I., Strober, M. A., Birmaher, B., Axelson, D. A., Esposito-Smythers, C., Goldstein,
T. R., … Keller, M. B. (2008). Substance use disorders among adolescents with bipolar
spectrum disorders. Bipolar Disorders, 10, 469–478.
Goldstein, T. R., Birmaher, B., Axelson, D., Goldstein, B. I., Gill, M. K.,
Esposito-Smythers, C., … Keller, M. (2009). Psychosocial functioning among bipolar
youth. Journal of Affective Disorders, 114, 174–183.
Goldstein, T. R., Birmaher, B., Axelson, D., Ryan, N. D., Strober, M. A., Gill, M. K., …
Keller, M. (2005). History of suicide attempts in pediatric bipolar disorder: Factors
associated with increased risk. Bipolar Disorders, 7 , 525–535.
Hammad, T. A., Laughren, T., & Racoosin, J. (2006). Suicidality in pediatric patients treated
with antidepressant drugs. Archives of General Psychiatry, 63, 332–339.
Hammen, C. (2002). Context of stress in families of children with depressed parents. In
S. H. Goodman & I. H. Gotlib (Eds.), Children of depressed parents: Mechanisms of risk
and implications for treatment (pp. 175–199). Washington, DC: American Psychological
Association.
Jaycox, L. H., Asarnow, J. R., Sherbourne, C. D., Rea, M. M., LaBorde, A. P., & Wells,
K. B. (2006). Adolescent primary care patients’ preferences for depression treatment.
Administration and Policy in Mental Health and Mental Health Services Research, 33,
198–207.
Jaycox, L. H., Stein, B. D., Paddock, S., Miles, J. N. V., Chandra, A., Meredith, L. S., …
Burnam, M. A. (2009). Impact of teen depression on academic, social, and physical
functioning. Pediatrics, 124, e596–e605.
Keenan-Miller, D., & Miklowitz, D. J. (2011). Interpersonal functioning in pediatric bipolar
disorder. Clinical Psychology: Science and Practice, 18, 342–356.
Kennard, B. D., Clarke, G. N., Weersing, V. R., Asarnow, J. R., Shamseddeen, W., Porta, G., …
Brent, D. A. (2009). Effective components of TORDIA cognitive-behavioral therapy for
adolescent depression: Preliminary findings. Journal of Consulting and Clinical Psychology,
77 , 1033–1041.
Kovacs, M. (1996). Presentation and course of major depressive disorder during childhood
and later years of the life span. Journal of the American Academy of Child and Adolescent
Kowatch, R. A., Fristad, M., Birmaher, B., Wagner, K. D., Findling, R. L., & Hellander, M.
(2005). Treatment guidelines for children and adolescents with bipolar disorder. Journal
of the American Academy of Child and Adolescent Psychiatry, 44, 213–235.
Kuhn, D. (2000). Metacognitive development. Current Directions in Psychological Science, 9,
178–181.
Leibenluft, E., & Rich, B. A. (2008). Pediatric bipolar disorder. Annual Review of Clinical
Lewinsohn, P. M., Clarke, G. N., Hops, H., & Andrews, J. A. (1990). Cognitive-behavioral
treatment for depressed adolescents. Behavior Therapy, 21, 385–401.
Lewinsohn, P. M., Clarke, G. N., Rohde, P., Hops, H., & Seeley, J. R. (1996). A course
in coping: A cognitive-behavioral approach to the treatment of adolescent depression.
In E. D. Hibbs & P. S. Jensen (Eds.), Psychosocial treatments for child and adolescent
disorders: Empirically based strategies for clinical practice (pp. 109–135). Washington,
DC: American Psychological Association.
Lewinsohn, P. M., Rohde, P., & Seeley, J. R. (1996). Adolescent suicidal ideation and attempts:
Prevalence, risk factors, and clinical implications. Clinical Psychology: Science and Practice,
3, 25–46.
Lofthouse, N., & Fristad, M. A. (2004). Psychosocial interventions for children with early-onset
bipolar spectrum disorder. Clinical Child and Family Psychology Review, 7 , 71–88.
Matson, J. L., & Nebel-Schwalm, M. S. (2007). Comorbid psychopathology with autism
spectrum disorder in children: An overview. Research in Developmental Disabilities, 28,
341–352.
McClellan, J., Kowatch, R., & Findling, R. L. (2007). Practice parameter for the assessment
and treatment of children and adolescents with bipolar disorder. JAMA, 46, 107–125.
Merikangas, K. R., He, J. P., Burstein, M., Swanson, S. A., Avenevoli, S., Cui, L., …
Swendsen, J. (2010). Lifetime prevalence of mental disorders in U.S. adolescents: Results
from the National Comorbidity Survey Replication-Adolescent Supplement (NCS-A).
Journal of the American Academy of Child and Adolescent Psychiatry, 49, 980–989.
Miklowitz, D. J., Axelson, D. A., Birmaher, B., George, E. L., Taylor, D. O., Schneck, C. D.,
… Brent, D. A. (2008). Family-focused treatment for adolescents with bipolar disorder:
Results of a 2-year randomized trial. Archives of General Psychiatry, 65, 1053–1061.
Miklowitz, D. J., George, E. L., Axelson, D. A., Kim, E. Y., Birmaher, B., Schneck, C., …
Brent, D. A. (2004). Family-focused treatment for adolescents with bipolar disorder.
Journal of Affective Disorders, 82, S113–S128.
Pavuluri, M. N., Birmaher, B., & Naylor, M. W. (2005). Pediatric bipolar disorder: A review
of the past 10 years. Journal of the American Academy of Child and Adolescent Psychiatry,
44, 846–871.
Pavuluri, M. N., Graczyk, P. A., Henry, D. B., Carbray, J. A., Heidenreich, J., & Miklowitz,
D. J. (2004). Child- and family-focused cognitive-behavioral therapy for pediatric bipolar
disorder: Development and preliminary results. Journal of the American Academy of Child
and Adolescent Psychiatry, 43, 528–537.
Perlis, R. H., Miyahara, S., Marangell, L. B., Wisniewski, S. R., Ostacher, M., DelBello, M. P.,
& Nierenberg, A. A. (2004). Long-term implications of early onset in bipolar disorder:
Data from the first 1000 participants in the systematic treatment enhancement program
for bipolar disorder (STEP-BD). Biological Psychiatry, 55, 875–881.
Puig-Antich, J. (1985). Psychosocial functioning in prepubertal major depressive disorders:
II Interpersonal relationships after sustained recovery from affective episode. Archives of
Rizzo, C. J., Esposito-Smythers, C., Swenson, L., Birmaher, B., Ryan, N., Strober, M., …
Keller, M. (2007). Factors associated with mental health service utilization among bipolar
youth. Bipolar Disorders, 9, 839–850.
Rotheram-Borus, M. J., Piacentini, J., Cantwell, C., Belin, T. R., & Song, J. (2000). The
18-month impact of an emergency room intervention for adolescent female suicide
attempters. Journal of Consulting and Clinical Psychology, 68, 1081–1093.
Rotheram-Borus, M. J., Piacentini, J., Miller, S., Graae, F., & Castro-Blanco, D. (1994).
Brief cognitive-behavioral treatment for adolescent suicide attempters and their families.
Rudolph, K. D. & Hammen, C. (1999). Age and gender as determinants of stress exposure,
generation, and reactions in youngsters: A transactional perspective. Child Development,
70, 660–677.
Ryan, N. D., Puig-Antich, J., Ambrosini, P., & Rabinovich, H. (1987). The clinical picture of
major depression in children and adolescents. Archives of General Psychiatry, 44, 854–861.
Shaffer, D., Gould, M., Fisher, P., Trautman, P., Moreau, D., Kleinman, M., &
Flory, M. (1996). Psychiatric diagnosis in child and adolescent suicide. Archives of
Shirk, S. R., Karver, M. S., & Brown, R. (2011). The alliance in child and adolescent
psychotherapy. Psychotherapy, 48, 17–24.
Spirito, A., & Esposito-Smythers, C. (2006). Attempted and completed suicide in adolescence.
Annual Review of Clinical Psychology, 2, 237–266.
Spirito, A., Esposito-Smythers, C., Weismoore, J., & Miller, A. (2012). Adolescent suicidal
behavior. In P. C. Kendall (Ed.), Child and adolescent therapy: Cognitive-behavioral
procedures (4th ed., pp. 234–256). New York, NY: Guilford Press.
Spirito, A., Esposito-Smythers, C., Wolff, J., & Uhl, K. (2011). Cognitive-behavioral therapy
for adolescent depression and suicidality. Child and Adolescent Psychiatric Clinics of North
America, 20, 191–204.
Spirito, A., Hart, K., Overholser, J., & Halverson, J. (1990). Social skills and depression in
adolescent suicide attempters. Adolescence, 25, 543–552.
Stanley, B., Brown, G., Brent, D. A., Wells, K., Poling, K., Curry, J, … Hughes, J. (2009).
Cognitive-behavioral therapy for suicide prevention (CBT-SP): Treatment model, feasibil-
ity, and acceptability. Journal of the American Academy of Child and Adolescent Psychiatry,
48, 1005–1013.
Stark, K., & Kendall, P. C. (1996). Treating depressed children: Therapist manual for “Taking
ACTION”. Ardmore, PA: Workbook.
Stark, K. D., Hoke, J., Ballatore, M., Valdez, C., Scammaca, N., & Griffin, J. (2005).
Treatment of child and adolescent depressive disorders. In E. D. Hibbs & P. S. Jensen
(Eds.), Psychosocial treatments for child and adolescent disorders: Empirically based strategies
for clinical practice (2nd ed., pp. 239–265). Washington, DC: American Psychological
Association.
Stark, K. D., Sander, J., Hauser, M., Simpson, J., Schnoebelen, S., Glenn, R., & Molnar, J.
(2006). Depressive disorders during childhood and adolescence. In E. J. Mash & R. A.
Barkley (Eds.), Treatment of childhood disorders (3rd ed., pp. 336–410). New York, NY:
Guilford Press.
Stevens, J., Wang, W., Fan, L., Edwards, M. C., Campo, J. V., & Gardner, W. (2009). Parental
attitudes towards children’s use of antidepressants and psychotherapy. Journal of Child
and Adolescent Psychopharmacology, 19, 289–296.
Tompson, M. C., Asarnow, J. R., Pierre, C. B, Fogler, J. M., Haber, F. M., & Smetana,
C. (2010). Family-focused intervention for childhood-onset depression (Unpublished
manuscript). Boston University, MA.
Tompson, M. C., Boger, K. D., & Asarnow, J. R. (2012). Enhancing the developmental
appropriateness of treatment for depression in youth: Integrating the family in treatment.
Child and Adolescent Psychiatric Clinics of North America, 21, 345–384.
Tompson, M. C., Pierre, C. B., Haber, F. M., Fogler, J. M., Groff, A. R., & Asarnow, J. R.
(2007). Family-focused treatment for childhood-onset depressive disorders: Results of an
open trial. Clinical Child Psychology and Psychiatry, 12, 403–420.
Treatment for Adolescents with Depression Study Team. (2004). Fluoxetine, cognitive-
behavioral therapy, and their combination for adolescents with depression: Treatment for
Adolescents with Depression Study (TADS) randomized controlled trial. JAMA, 292,
807–820.
Turner, J. E., & Cole, D. A. (1994). Development differences in cognitive diatheses for child
depression. Journal of Abnormal Child Psychology, 22, 15–32.
Van Meter, A. R., Moreira, A. L., & Youngstrom, E. A. (2011). Meta-analysis of epidemiologic
studies of pediatric bipolar disorder. Journal of Clinical Psychiatry, 72, 1250–1256.
Wagner, B. M., & Compas, B. E. (1990). Gender, instrumentality, and expressivity: Moderators
of the relation between stress and psychological symptoms during adolescence. American
Journal of Community Psychology, 18, 383–406.
Weissman, M. M., Wolk, S., Goldstein, R. B., Moreau, D., Adams, P., Greenwald, S., …
Wickramaratne, P. (1999). Depressed adolescents grown up. JAMA, 281, 1707–1713.
Weissman, M. M., Wolk, S., Wickramaratne, P., Goldstein, R. B., Adams, P., Greenwald, S.,
… Steinberg, D. (1999). Children with prepubertal-onset major depressive disorder and
anxiety grown up. Archives of General Psychiatry, 56, 794–801.
Weisz, J. R., Doss, A. J., & Hawley, K. M. (2005). Youth psychotherapy outcome research: A
review and critique of the evidence base. Annual Review of Psychology, 56, 337–363.
Weisz, J. R., Thurber, C. A., Sweeney, L., Proffitt, V. D., & LeGagnoux, G. L. (1997). Brief
treatment of mild-to-moderate child depression using primary and secondary control
enhancement training. Journal of Consulting and Clinical Psychology, 65, 703–707.
West, A. E., Henry, D. B., & Pavuluri, M. N. (2007). Maintenance model of integrated
psychosocial treatment in pediatric bipolar disorder: A pilot feasibility study. Journal of
West, A. E., Jacobs, R. H., Westerholm, R., Lee, A., Carbray, J., Heidenreich, J., & Pavuluri,
M. N. (2009). Child and family-focused cognitive-behavioral therapy for pediatric bipolar
disorder: Pilot study of group treatment format. Journal of the Canadian Academy of
Wozniak, J., Biederman, J., Kiely, K., & Ablon, J. S. (1995). Mania-like symptoms suggestive
of childhood-onset bipolar disorder in clinically referred children. Journal of the American
Yorbik, O., Birmaher, B., Axelson, D., Williamson, D. E., & Ryan N. D. (2007). Clinical
characteristics of depressive symptoms in children and adolescents with major depressive
disorder. Journal of Clinical Psychiatry, 65, 1654–1659.
Young, M. E., & Fristad, M. A. (2007). Evidence based treatments for bipolar disorder in
children and adolescents. Journal of Contemporary Psychotherapy, 37 , 157–164.
36
Anxiety Disorders in Children
and Adolescents
Candice Chow and Donna B. Pincus
Introduction
In everyday conversation, “anxiety” is commonly used to describe the stressful

demands of daily life—the juggling of commitments at work and at home, the
anticipation of an upcoming job interview, or concerns about an ailing fam-
ily member, perhaps. The word does not automatically evoke images of a child
who refuses to speak out loud at school, a middle school student who spends
several hours washing his hands daily, or an adolescent who is concerned about
suffering a heart attack during strenuous physical activity. For many children, ado-
lescents, and their families, however, this is an all too familiar picture of anxiety.
An alarming percentage of youth—in the range of 5–20%—experience debilitating
symptoms of anxiety that are distressing and impairing on a daily basis (Costello
et al., 1996; Costello, Egger, & Angold, 2004; McCracken, Walkup, & Koplewicz,
2002).
Once thought of as an adult affliction primarily, research over the past several
decades has illuminated the fact that anxiety disorders affect individuals of all ages
and are one of the most common psychiatric conditions observed in children and
adolescents worldwide (Costello et al., 2004). Untreated, these conditions can
lead to significant impairment in academic, social, and family functioning (Strauss,
Frame, & Forehand, 1987). Anxiety disorders in youth are associated with increased
risk of educational underachievement and impairment in workplace performance in
adulthood (Greenberg et al., 1999; Woodward & Fergusson, 2001). Furthermore,
anxiety disorders in childhood frequently predict the development of other psychiatric
disorders in later adolescence and adulthood, including subsequent anxiety disorders,
conduct disorder, substance use disorders, and major depressive disorder (Bittner

DOI: 10.1002/9781118528563.wbcbt36
et al., 2007; Costello, Mustillo, Erkanli, Keeler, & Angold, 2003; Pine, Cohen,
Gurley, Brook, & Ma, 1998; Pollack et al., 1996).
In addition to the negative effects that anxiety disorders inflict on youth and their
families, these conditions bring with them serious societal implications. A cost-of-
illness study conducted in the Netherlands revealed that the societal costs (e.g., health
care costs, child absences from school, productivity loss due to parents’ work absences)
incurred by families with children with an anxiety disorder were approximately 21
times the cost incurred by families in the general population (Bodden, Dirksen,
& Bogels, 2008). In the United States, the annual cost of anxiety disorders for
individuals aged 15 and older is estimated to be over $40 billion, accounting
for one-third of the national psychiatric treatment costs overall (Greenberg et al.,
1999).
The far-reaching consequences of childhood anxiety disorders point to the need
for an understanding of the factors that lead to their development, and for effective
and accessible interventions that can quickly return children and adolescents to their
developmentally appropriate tasks and activities. Fortunately, we are at an exciting
point in our understanding of child and adolescent anxiety disorders. Etiological
investigations of anxiety disorders in youth have now led us to a much more
comprehensive working knowledge of the many factors that, in combination with
one another, can lead to the development and maintenance of anxiety disorders
(Barlow, 2002). Additionally, years of devising, honing, and testing psychosocial
interventions for anxious youth have yielded efficacious treatments for this population.
Cognitive behavioral therapy (CBT) has emerged as the front-runner in psychosocial
treatments for anxious youth. Although CBT for anxiety in children and adolescents
began as a downward extension of CBT for anxious adults, innovative treatment
adaptations have resulted in developmentally appropriate CBT interventions for
anxious youth.
Despite the proven efficacy of CBT for anxious children and adolescents, there
is a wide gap that exists between families who are in need of services, and acces-
sibility to trained practitioners who can effectively deliver empirically supported
treatments (Buckner & Bassuk, 1997; Kendall & Southam-Gerow, 1995; Merikangas
et al., 2011). The field as a whole is moving toward closing this service gap and
ensuring that CBT for anxiety disorders in youth is a transportable and accessible
treatment for individuals and families who need it the most. As such, much of the
current research in the area of child anxiety disorders is focused on novel ways to
deliver treatment to families that may not have immediate access to trained CBT
practitioners.
This chapter provides an overview of CBT for anxious youth and a discussion of
the current state of intervention research in this area. Specifically, the goals of this
chapter are (a) to review the clinical characteristics of anxiety disorders in children
and adolescents, (b) to discuss the current understanding of the etiology of anxiety
disorders in youth, (c) to examine research on the efficacy and effectiveness of CBT
for anxious youth, (d) to outline the main components of CBT for childhood anxiety
disorders, and (e) to introduce recent innovative adaptations of CBT for anxious
youth.
Anxiety Disorders in Children and Adolescents 851
Clinical Characteristics of Anxiety Disorders in Youth
Separation Anxiety Disorder

In young children, fear of separation from a major attachment figure can signal the
presence of a healthy, secure relationship (Ainsworth & Bowlby, 1991; Pianta, 1999;
Vasey & Dadds, 2001). Typically developing children begin to exhibit this behavior
(sometimes termed “stranger anxiety”) between 9 and 13 months; the anxiety then
begins to decrease naturally around 2 years of age (Williams, Reardon, Murray, &
Cole, 2005). For a subset of youth, however, anxiety around being separated from
a major attachment figure, typically a caregiver, continues into later childhood and
begins to interfere with school attendance and other developmentally appropriate
activities (Kearney, Sims, Pursell, & Tillotson, 2003).
Approximately 2.4–12% of youth experience persistent, distressing separation
anxiety when faced with the prospect of being away from an attachment figure
(Bowen, Offord, & Boyle, 1990; Costello & Angold, 1995; Silverman & Ginsburg,
1998). The primary feature of separation anxiety disorder (SAD) is the presence of
developmentally inappropriate and persistent anxiety with regard to being separated
from the home or from individuals to whom the individual is attached (American
Psychiatric Association [APA], 2000). Children with SAD frequently worry that
an untoward event (e.g., car accident, kidnapping, getting lost) will result in
permanent separation from a major attachment figure. As a result, children with
SAD are very reluctant to be alone or away from individuals to whom they are
attached; they may become tearful, exhibit temper tantrums, or display clinginess
at times when they are expected to separate. Somatic complaints (e.g., nausea,
stomachaches, headaches) are common in children with SAD and are typically expe-
rienced when faced with a situation in which separation from an attachment figure is
anticipated.
The current version of the Diagnostic and Statistical Manual of Mental
Disorders (5th ed.; DSM-V; APA, 2013) specifies that a diagnosis of SAD can be
assigned if the disturbance is present for at least 4 weeks. The average age of onset for
SAD is 7 years (Kessler et al., 2005); an early onset specifier can be assigned to individu-
als who develop symptoms of SAD prior to the age of 6. SAD demonstrates continuity
over time and has been linked to the development of panic disorder and depression
in adolescence and adulthood (Foley et al., 2008; Lewinsohn, Holm-Denoma,
Small, Seeley, & Joiner, 2008; Silove, Manicavasagar, Curtis, & Blaszczynski,
1996).
Generalized Anxiety Disorder

Children and adolescents with generalized anxiety disorder (GAD) are typically
described by their families as “worriers.” The main hallmark of GAD is persistent
and excessive worry about a number of areas of one’s life. Topics of concern for
youth with GAD can include schoolwork, performance on extracurricular activities,
health of self and others, world events (e.g., war, natural disasters), minor matters
(e.g., saying the wrong thing), novel situations, and perfectionism in carrying out
daily tasks. Youth with GAD often espouse dysfunctional cognitions and overestimate
the likelihood that a negative or catastrophic outcome will occur in a given situation
(Bogels & Zigterman, 2000). A diagnosis of GAD is considered when the worry
occurs on most days, is at least 6 months in duration, and is difficult to control (APA,
2000). In addition to experiencing persistent and distressing worries, youth with GAD
often report the presence of somatic symptoms, including muscle tension, abdominal
distress, and headaches (Masi, Favilla, Millepiedi, & Mucci, 2000). Other related
difficulties include irritability, problems with concentration, restlessness, fatigue, and
interruptions in sleep.
The prevalence of GAD in pre-adolescents is estimated to be between 2.9%
(Anderson, Williams, McGee, & Silva, 1987) and 3.6% (Bowen et al., 1990), with an
average age of onset typically around 8 years (Last, Perrin, Hersen, & Kazdin, 1992).
There is substantial comorbidity associated with GAD, with other anxiety disorders
and major depressive disorder being the most commonly co-occurring disorders in
youth with this disorder (Masi, Mucci, Favilla, Romano, & Poli, 1999).
Social Phobia
Social phobia (SP) is marked by excessive apprehension and anxiety in social situations
due to a fear of negative evaluation, rejection, or humiliation (APA, 2000). Children
and adolescents with SP are extremely fearful of social or performance situations,
typically because they worry that they will act in ways that will cause them to be
embarrassed. Due to this fear, youth with SP often avoid social or performance
situations such as musical and athletic performances, oral presentations, answering
questions in class, seeking help from teachers, spending time with friends, and
attending parties or school activity nights. Young children may withdraw, cry, freeze,
or exhibit temper tantrums when asked to enter social situations. Insight into the
excessive and unreasonable nature of these fears may be absent, particularly in young
children. The disturbance also needs to be present for at least 6 months before a
diagnosis of SP can be assigned.
Data from both community and clinical samples estimate that the onset of SP
occurs most frequently during middle adolescence, around the age of 16 (Last
et al., 1992). Prevalence rates of SP among youth are estimated to be a little
over 1% (Anderson et al., 1987; Essau, Conradt, & Petermann, 1999a). Over half
of youth with SP also meet diagnostic criteria for comorbid psychiatric disorders,
including depressive disorders, somatoform disorders, and substance use disorders;
however, few seek treatment for their difficulties (Essau et al., 1999a). Children and
adolescents with SP have been found to have high levels of general emotional over-
responsiveness, social inhibition, dysphoria, and loneliness, and often have poorer
social skills than their non-socially-phobic counterparts (Beidel, Turner, & Morris,
1999). In adolescent school samples, girls tend to report more symptoms of social
anxiety than boys; girls with high levels of social anxiety also report fewer friendships,
and less intimacy, companionship, and support in their close friendships (La Greca &
Lopez, 1998).
Panic Disorder and Agoraphobia

A panic attack is characterized by a discrete episode during which the onset of
uncomfortable physical symptoms occurs rapidly (APA, 2000). The symptoms develop
abruptly and reach a peak within the time span of 10 minutes. Among the list of
symptoms that individuals can experience during a panic attack, the most common
are heart palpitations, trembling and shaking, nausea or abdominal pain, and chills or
hot flashes (Essau, Conradt, & Petermann, 1999b).
Panic disorder (PD) is characterized by the presence of recurrent, unexpected panic
attacks, followed by at least one month of worry about having another panic attack,
or concern about the implications or consequences of the panic attacks (APA, 2000).
PD can also co-occur with agoraphobia, which is characterized by anxiety about
being in places or situations in which escape might be difficult in the event of an
unexpected panic attack (APA, 2000). Common settings that are avoided due to
panic disorder with agoraphobia include crowded places, large open spaces, enclosed
areas, and various modes of transportation. With children and adolescents, school may
also be avoided or endured with distress; in the event of a panic attack, youth with
PD worry that they will not be able to leave the classroom easily. It is estimated that
approximately half of youth with PD also meet criteria for a diagnosis of agoraphobia
(Doerfler, Connor, Volungis, & Toscano, 2007).
While panic attacks are common in youth with approximately 18% of adolescents
reporting a positive history of having had at least one panic attack, PD affects a
much smaller subset of youth at a prevalence rate of 0.6–1% (Essau et al., 1999b;
Von Korff, Eaton, & Keyl, 1985; Whitaker et al., 1990). Retrospective reports
provided by adults with PD reveal that panic symptoms typically begin in childhood
or adolescence and peak between 15 and 19 years of age (Von Korff et al., 1985).
There is evidence that PD is maintained by a misinterpretation of bodily symptoms
(Clark, 1986) and that youth who receive high scores on measures of anxiety sensitivity
(i.e., fear of and sensitivity to bodily sensations) are more likely to meet diagnostic
criteria for PD (Calamari et al., 2001; Lau, Calamari, & Waraczynski, 1996).
Obsessive-Compulsive Disorder
Obsessive-compulsive disorder (OCD) is characterized by the presence of obsessions
and compulsions. Obsessions are thoughts, images, or impulses that are persistent,
experienced as intrusive, and cause anxiety or distress (APA, 2000). Compulsions
are defined as behaviors or mental acts that are performed, typically in a repetitive
manner, to prevent or reduce anxiety experienced because of an obsession (APA,
2000). Compulsions can also be performed in an effort to prevent an untoward
outcome or event in a given situation.
Epidemiological research suggests that OCD affects approximately 2–3% of children
and adolescents (Zohar, 1999), with an average age of onset at 7 years (Flessner,
Berman, Garcia, Freeman, & Leonard, 2009). Frequently reported obsessions in
children and adolescents include intrusive thoughts around contamination, hurting
oneself or others, symmetry and exactness, superstitious and magical beliefs, and
thoughts that are religious in nature (Hanna, 1995). Common compulsions in youth
include checking, washing, repeating, ordering and arranging, touching, counting,

and hoarding behaviors (Hanna, 1995). In order to receive a diagnosis of OCD, an
individual must engage in compulsions for at least one hour per day (APA, 2000).
It is important to note that while superstitious and repetitive behaviors are common
among young children, a diagnosis of OCD is only assigned in the presence of marked
distress, time-consuming obsessions or compulsions, and significant interference in
the child’s daily tasks and activities.
Specific Phobia
While it is developmentally appropriate for young children to endorse a variety
of fears (see Gullone, 1999), approximately 5% of children and adolescents expe-
rience persistent fear and distress in the presence of various stimuli (Costello &
Angold, 1995). A diagnosis of specific phobia is characterized by excessive fear
in the presence of a particular object or situation (APA, 2000). Often, the anx-
ious response that is invariably invoked by the presence of the feared stimulus can
take the form of a situationally bound panic attack. The DSM-5 highlights five
different subtypes of specific phobia. These are animal (e.g., dogs, insects), nat-
ural environment (e.g., storms, water), blood-injection-injury (e.g., seeing blood,
getting shots), situational (e.g., elevators, enclosed places, flying in an airplane),
and other (e.g., vomiting, choking, contracting an illness, loud noises, costumed
characters). Children and adolescents with a specific phobia will exhibit extreme
distress in the presence of the feared stimulus, may display tearfulness or have
a temper tantrum, and will typically attempt to avoid the feared object or sit-
uation whenever possible. Specific phobias are commonly comorbid with other
anxiety disorders such as GAD, SP, SAD, and attention-deficit/hyperactivity disor-
der (ADHD) (Ollendick, Raishevich, Davis, Sirbu, & Ost, 2010). Because many
fears are present in normally developing children, a diagnosis of specific phobia is
only warranted if the distress and impairment associated with the fear is interfering
with daily functioning and is over and above what other children of the same age
experience.
Posttraumatic Stress Disorder

The primary feature of posttraumatic stress disorder (PTSD) is the onset of specific
symptoms following exposure to a traumatic event. To receive a diagnosis of
PTSD, the traumatic event has to involve actual or threatened death or serious
injury to oneself, witnessing of the threatened death or serious injury of another
individual, or learning of the unexpected or violent death, harm, or threat of
death or injury experienced by an individual to whom the child or adolescent is
close (APA, 2000). Symptoms experienced after the traumatic event fall into three
categories—reexperiencing (e.g., distressing recollections of the traumatic event,
feeling as if the traumatic event were occurring again, nightmares about the event),
avoidance (e.g., avoiding stimuli related to the event, decreased interest in activities,
blunted affect), and increased physiological arousal (e.g., sleep disturbance, irritability,
hypervigilance). The prevalence of PTSD among children and adolescents remains
unknown, though the rates appear to vary widely depending on the type of trauma
to which youth are exposed. For instance, traumatic events such as rape yield higher
rates of PTSD than do accidents and learning about traumatic events (see Yehuda,
2002).
Selective Mutism
Selective mutism (SM), an anxiety disorder with an average age of onset ranging
between 2.7 and 4.1 years (Cunningham, McHolm, Boyle, & Patel, 2004; Kristensen,
2000), is characterized by a failure to speak in certain settings where speech is expected,
despite normal speech in other settings (APA, 2000). Children and adolescents with
SM typically speak fluently in their home settings and with immediate family members,
but will not exhibit verbal speech in other settings (e.g., school). Youth with SM
will often have peers speak for them, or use nonverbal gestures to communicate their
needs. The disturbance interferes with developmentally appropriate tasks, such as
educational or occupational achievement. SM affects less than 1% of the population
and is more commonly observed in females than in males (Steinhausen & Juzi, 1996).
Seventy-four percent of youth diagnosed with SM are also assigned a comorbid
anxiety disorder, most commonly SP and SAD (Kristensen, 2000). Black and Uhde
(1992) posit that SM may be a more severe form of social phobia.
Etiology and Maintenance of Anxiety Disorders in Youth
A number of factors have been implicated in the pathogenesis and maintenance

of anxiety disorders in youth, including genetic factors, child-specific factors (e.g.,
temperament, cognitions, and behaviors), parenting behaviors, and environmental
influences. An understanding of the various factors that may cause and maintain
anxiety symptoms is critical for the development and successful implementation of
effective interventions for anxious youth and their families.
Genetic Factors
Evidence for the familial transmission of anxiety is robust. Offspring of adults with
anxiety disorders are far more likely than offspring of nonanxious individuals to
meet diagnostic criteria for an anxiety disorder (Turner, Beidel, & Costello, 1987;
Weissman, Leckman, Merikangas, Gammon, & Prusoff, 1984). Twin studies have
been utilized to tease apart the relative contributions of genetics and environmental
factors in the development of anxiety disorders. Findings from these studies have
shown a higher concordance of anxiety disorders in monozygotic than dizygotic
twins, suggesting that genetics are a stronger influence than shared environments on
the development of anxiety disorders (e.g., Thapar & McGuffin, 1995). PD, GAD,
specific phobias, and OCD all have significant familial aggregation that can likely be
explained by genetic influences (Hettema, Neale, & Kendler, 2001).
Amid mixed findings, there does appear to be some specificity in the heritability of
anxiety disorders; if an individual has a specific anxiety disorder diagnosis, there is a
higher likelihood that a first-degree relative will meet criteria for the same diagnosis
(Fyer, Mannuzza, Chapman, Martin, & Klein, 1995). Other findings suggest that
psychological characteristics, rather than specific disorders, are transmitted from one
generation to the next. For instance, anxiety sensitivity (Stein, Jang, & Livesley, 1999)
and introversion and neuroticism (Bienvenu, Hettema, Neale, Prescott, & Kendler,
2007) have been shown to predispose individuals to the development of a variety of
anxiety disorders. The overall heritability of anxiety disorders is estimated to be in
the range of 30–40% (Hettema et al., 2001). These estimates are significantly lower
than those observed in the familial transmission of schizophrenia or bipolar disorder,
suggesting that much of the variance can be explained by factors other than genetics.
Child Factors
Children and adolescents with anxiety disorders display some characteristic patterns in
temperament, attentional and interpretational biases, cognitive processes, and behav-
ior. Many of these factors can maintain symptoms of anxiety. Certain temperaments
have been shown to be more closely associated with the development of anxiety disor-
ders in youth. For instance, behavioral inhibition, a temperamental style characterized
by heightened responses to new stimuli and withdrawal from situations that are novel
or unfamiliar, has been shown to be predictive of the development of anxiety disorders
in children and adolescents (Fox & Pine, 2012; Kagan, Reznick, Clarke, Snidman, &
Garcia-Coll, 1984).
Much like anxious adults, youth with anxiety disorders tend to display characteristic
attentional and interpretational biases with regard to threatening information (Kindt,
Bierman, & Brosschot, 1997; Kindt, Brosschot, & Everaerd, 1997). These biases
lead to the overestimation of threat posed in ambiguous situations. In comparison
to their nonanxious counterparts, youth with anxiety disorders engage in increased
dysfunctional thinking around the danger involved in various situations (Bogels
& Zigterman, 2000). As a result of maladaptive cognitions, anxious children and
adolescents are less likely to approach situations in which a negative outcome is feared
to occur. Behavioral avoidance has been implicated in the maintenance of anxiety
symptomatology, as it decreases opportunities for anxious youth to challenge their
maladaptive cognitions.
Parental Factors
Parenting behaviors also play a role in the development and maintenance of anxiety
disorders in youth, though a recent meta-analysis concluded that only 4% of the
variance in childhood anxiety disorders is related to parenting behaviors (McLeod,
Wood, & Weisz, 2007). Parents can sometimes inadvertently convey anxious messages
to their children, through modeling of anxious behaviors, limiting opportunities for
approaching feared situations, exerting excessive control over children, or providing
verbal information about the threat involved in a given situation. For example, an
observational study of family processes, conducted by Barrett, Rapee, Dadds, and Ryan
(1996), revealed that anxious children are more likely to choose avoidant responses
to ambiguous situations after briefly speaking to their parent about how to cope
with those scenarios. Parents sometimes encouraged avoidance rather than approach
of presented situations. Parental intrusiveness has been shown to exacerbate anxiety
symptoms in children by decreasing autonomy and conveying negative messages about
their ability to cope in distressing situations. Mothers of anxious children tend to
exhibit increased levels of intrusiveness in the presence of child negative affect or dis-
tress, in comparison to mothers of nonanxious children (Hudson, Comer, & Kendall,
2008). In parent–child interactions, observed parental control has also been repeat-
edly linked to shyness and anxiety disorders in youth (McLeod et al., 2007; Wood,
McLeod, Sigman, Hwang, & Chu, 2003). Conclusions regarding the direction of the
effects linking parenting and child anxiety symptoms cannot be definitively made.
Early experiences can play a large role in the development of anxiety disorders.
Negative and stressful life events have been shown to increase the likelihood of
developing anxiety symptomatology in youth (Benjamin, Costello, & Warren, 1990).
Weems, Silverman, Rapee, and Pina (2003) found that perceived control over
anxiety-related situations was significantly negatively correlated with self-reported
anxiety symptomatology; children who reported low perceived control in anxiety-
provoking situations also reported higher levels of anxiety, supporting the notion that
anxious children may be more likely than nonanxious children to perceive events as
uncontrollable. Chorpita and Barlow (1998) and Barlow (2002) have posited that
repeated early experiences of diminished control may lead to processing of subsequent
events as out of one’s control and predispose youth to the development of anxiety
disorders.
Efficacy and Effectiveness of Cognitive Behavioral Therapy for

Anxious Youth
CBT is currently the most efficacious psychosocial treatment for anxiety disorders in
children and adolescents. The first randomized clinical trial examining the effectiveness
of CBT for childhood anxiety disorders was Kendall’s (1994) study of children aged
8–13 years, with a diagnosis of SAD, GAD, and SP. Children in the CBT condition,
who received Kendall and Hedtke’s (2006a, 2006b) manual-based “Coping Cat”
treatment over 16 sessions, exhibited significant improvements on self- and parent-
reported measures of distress and coping abilities. At posttreatment, 66% of the 47
participants no longer met criteria for their primary anxiety diagnosis.
A number of randomized controlled trials have reported on the efficacy of CBT for
anxious youth and have made comparisons between CBT and medication treatments
for this population. In the Child/Adolescent Anxiety Multimodal Study (CAMS),
a large-scale treatment study of anxiety disordered youth conducted by Walkup
et al. (2008), children between the ages of 7 and 17 were assigned to either 14
sessions of CBT, medication (sertraline), a combination of sertraline and CBT, or
a pill placebo. Both CBT and sertraline reduced the severity of anxiety symptoms
in youth. While CBT alone produced a 59.7% response rate, and sertraline alone
produced a 54.9% response rate, the combination of CBT and sertraline yielded the
highest response rate, with 80.7% of participants in this condition being rated as much
improved or very much improved on the Clinical Global Impression-Improvement
Scale. Despite the efficacy of both CBT and pharmacotherapy for the treatment
of anxiety disorders in youth, parents of anxious youth perceive CBT as a more
acceptable and effective treatment, regardless of their child’s treatment history (Brown,
Deacon, Abramowitz, Dammann, & Whiteside, 2007). While adults may readily seek
medication for their own psychiatric symptoms, parents are typically less eager to select
psychopharmacological interventions as a first response for their anxious children.
Various modalities of CBT have been tested in children and adolescents with anxiety
disorders. The relative merits of individual, group, and family-based CBT have been
well studied. It appears that in some cases, such as with children and adolescents
reporting high social anxiety and exhibiting a vulnerability to depression, youth may
respond preferentially to individual treatment (Manassis et al., 2002). However, the
majority of studies have found no significant differences in treatment outcome between
individual and group-based CBT for anxious youth (see In-Albon & Schneider, 2007;
Silverman, Pina, & Viswesvaran, 2008, for a review). Due to the negligible difference
between treatment outcomes in individual and group CBT, the choice to utilize one
or the other could depend on more practical considerations such as parent and child
preferences, therapeutic resources, and referral rates (Liber et al., 2008).
As discussed in the previous section, parenting behaviors may partially contribute
to the development and maintenance of anxiety disorders in children and adolescents.
It makes sense, then, that interventions for anxious youth might also include a
parent-focused component. A number of studies have compared treatment outcomes
in individual CBT without parental involvement, and individual CBT with parental
involvement. Again, we see that there may be certain subgroups for which a parenting
component may be most helpful. In a study comparing the relative efficacy of
individual CBT, CBT and family management, and a wait-list control condition,
both treatment conditions led to comparable decreases in anxiety symptomatology;
however, younger children responded better in the CBT and family management
condition (Barrett, Dadds, & Rapee, 1996). Family CBT, in comparison to individual
CBT, may be less beneficial when the child’s parents also meet diagnostic criteria for
one or more anxiety disorders (Bodden, Bogels, et al., 2008; Kendall, Hudson, Gosch,
Flannery-Schroeder, & Suveg, 2008). In an examination of therapist-delivered parent
training techniques, Khanna and Kendall (2009) found that transfer-of-control and
parental anxiety management techniques significantly predicted improvement on both
clinician and parent ratings of child global functioning, and contributed significantly
to treatment outcome.
Cognitive Behavioral Therapy Treatment Components
CBT for childhood anxiety disorders is typically delivered in a weekly, individual

format, over the course of approximately 12 to 20 weeks. The primary goal of
treatment is not to eliminate anxiety completely, but to provide the child and his
or her parents with coping skills they can utilize in the face of anxiety-provoking
situations. Homework is assigned between sessions to facilitate practice of learned

skills in the child’s home, school, and social environments. While the core treatment
components of CBT for anxious youth do not differ from the components utilized in
CBT for anxious adults, the presentation of these components is modified to match
the developmental level of the child or adolescent. As such, clinicians should be
flexible in their delivery of treatment. Although a child’s age can serve as one indicator
of developmental level, clinicians should synthesize other information about the child
in order to fully understand his or her cognitive, emotional, and social presentation
(Kingery, Roblek, Suveg, Grover, & Sherrill, 1996). This section discusses the core
components of CBT for anxiety disorders in youth and touches on some of the ways
in which these components may be tailored to children at various developmental
levels.
Psychoeducation and Rapport-Building

The first sessions of CBT for anxious youth are dedicated to rapport-building,
addressing questions and concerns that the child and his or her parent(s) may have
about treatment, and providing psychoeducation about emotions and the nature
of anxiety. Because the majority of children and adolescents are not self-referred,
it is important that they have a basic understanding of the structure and rationale
for treatment, and a good working alliance with the clinician. A strong therapeutic
alliance and child engagement early on in therapy can be critical to the success
of treatment. With younger children, therapeutic engagement can be established
through more playful, interactive activities. The use of storybooks, games, puppets,
props, online pictures and videos, creative activities, and pretend play can all be useful
tools that allow for increased engagement in therapy with young children. While play
therapy has not been shown to be an efficacious treatment for anxious youth, utilizing
play as a method of providing cognitive behavioral skills to young children can be
very beneficial (Pincus, Chase, Chow, Weiner, & Pian, 2011). Older children and
adolescents, who can be particularly difficult to engage in treatment, can sometimes
benefit from a more collaborative relationship with the therapist. Client contributions
to the session agenda, goal-setting, and homework assignments, for example, can
grant the child increased autonomy in sessions and lead to a more developmentally
appropriate delivery of treatment.
In early sessions, young children are asked to identify emotions (e.g., by look-
ing at facial expressions of characters in pictures, or listening to stories and
discussing characters’ feelings), to ensure that the child and the clinician have a
common language with which to label feelings. The clinician also provides infor-
mation about the nature of anxiety, explaining that the evolutionarily adaptive
experience of anxiety helps ready an individual for action in the face of danger.
It is in this initial psychoeducation portion of treatment that the child is intro-
duced to the three-component model of anxiety, which outlines the cyclical and
bidirectional relationship between cognitions, physical feelings, and behaviors in
anxiety-provoking situations. These three components lay the foundation for the
other interventions introduced in CBT for anxious youth; the components are
discussed in detail, and examples of each are elicited from the child. Through mon-
itoring thoughts, feelings, and behaviors over the course of several weeks, the child
will hopefully begin to understand the common patterns present in his own cycle of
anxiety.
As mentioned in the previous section on etiology and maintenance of anxiety
symptoms, maladaptive thoughts, primarily about the threat involved in a given
situation, can maintain anxiety symptoms in children and adolescents. Anxious
youth often espouse catastrophic thoughts and perceive the likelihood of a negative
outcome in a given situation as significantly higher than it really is. Through cognitive
restructuring, a strategy used to evaluate maladaptive cognitions, anxious youth are
taught to think more realistically about anxiety-provoking situations. They are first
asked to identify their anxious thought (e.g., “A robber is going to come into my
house tonight”). Then they are asked to evaluate the evidence both for and against
that thought (e.g., evidence for the thought: “Robbers do exist and sometimes break
into people’s houses”; evidence against the thought: “Nobody in my neighborhood
has ever been robbed,” and “When houses are robbed, it is usually during the day
when no one is at home”). The child is asked to evaluate the thought based on the
evidence he or she generated (i.e., “Knowing the evidence, how likely is it that a
robber will break into my house tonight?”). With events that are more likely to occur
(e.g., “I will stumble on my words and feel embarrassed during an oral presentation”),
the child is instructed to think about the consequences of the scenario (e.g., “If you
feel embarrassed, will that feeling last forever? Will you lose friends if you stumble
over your words during your oral presentation?”). Thinking more realistically not
only about the likelihood of a feared outcome, but also about the often time-limited
nature of the consequences in a situation, can help anxious individuals restructure
their maladaptive thoughts.
Relaxation Training
While relaxation training is not an essential component of CBT for every anxious
child or adolescent, it can be helpful in reducing physiological arousal, muscle tension,
and feelings of nervousness. Additionally, it can aid in increasing sleep quality and
concentration. Relaxation training can be particularly useful for individuals with
high baseline levels of physiological arousal. During relaxation training, children and
adolescents are first taught to recognize how their body feels in both a tense and
relaxed state; being able to identify how the body feels in the presence of anxiety
allows the child to be more aware of his or her symptoms and of the antecedents
that might precede feelings of tensions or anxiety. The clinician guides the child
through progressive muscle relaxation (PMR), during which the child is asked to
tense and relax isolated muscle groups. Younger children are asked to focus on just
a few muscle groups, while adolescents might be led through a more comprehensive
series of exercises.
It is important that anxious children and their parents only utilize relaxation outside
the context of in vivo exposures (see below), as relaxation during exposures can serve
as a distraction and ultimately an avoidance tactic in the face of a feared situation.
In Vivo Exposure
The most common behavior observed in anxious youth is an avoidance of feared
situations. The latter part of treatment is focused on helping the child approach,
rather than avoid, these situations. In vivo exposure, which involves gradual exposure
to a child’s feared situations, is one of the most effective components of CBT for
anxious youth. It is during in vivo exposures that children and adolescents begin
to challenge their maladaptive cognitions with regard to the threat involved in their
feared situations. The child, parents, and clinician collaborate on the generation of
a fear and avoidance hierarchy, or “bravery ladder” for younger children, which is a
list of feared situations ordered from least to most anxiety-provoking for the child.
In vivo exposures begin with tasks that are low on the hierarchy and progressively
increase in difficulty until the most anxiety-provoking situation is tackled. Beginning
with an exposure task that is at the bottom of the hierarchy, and advancing to the
next exposure only when the child is able to approach the previous one with relative
ease, ensures that the child experiences success and continues to stay motivated to
face his or her fears. Children and adolescents are praised and rewarded for their
exposure efforts, toward the goal of positively reinforcing their approach behaviors.
See Table 36.1 for a sample fear and avoidance hierarchy for a child diagnosed with
specific phobia, blood-injection-injury type.
In the presence of a feared stimulus, it is expected that the child’s initial anxiety
response will be high; however, over time and repeated exposure exercises, the child’s
anxiety and physiological arousal should dissipate. This process is termed habituation
and while there is evidence to suggest that habituation is not a necessary ingredient in
a successful exposure task, its repeated occurrence provides evidence to the child that
without engaging in any special behaviors, his or her anxiety can decrease over time.
Because it is important that anxious youth observe that they can cope independently in
a feared situation, they are encouraged during exposures to limit their safety behaviors,
which are behaviors that increase their perception of safety (e.g., carrying a lucky
charm, pill bottle, or cell phone; utilizing relaxation techniques; reading a book, etc.).
These behaviors serve to lessen anxiety in the short run, but ultimately feed into
cognitions that the situation was only safe because of the presence of a safe object or
behavior. This limits the child’s ability to conclude that the feared situation is truly
nonthreatening.
For younger children, in vivo exposures can occur in the context of games or
playful activities to increase engagement. A number of clinically useful games have
been developed and successfully implemented to help engage younger clients. Some
examples of these include “Bravery Bingo,” during which the child is asked to
complete one exposure task for every box on his Bingo card, “Scavenger Hunts”
(e.g., a child with a diagnosis of SAD may be asked to separate from parents to find
fun items around the clinic), and relay races (e.g., to bring on physical symptoms of
anxiety prior to an in vivo exposure) (see Pincus et al., 2011, for a full description).
Table 36.1 A Sample Fear and Avoidance Hierarchy for a Child with a Specific Phobia,
Blood-Injection-Injury Type
0 1 2 3 4 5 6 7 8
No fear A little fear Moderate fear A lot of fear Very much fear
Never avoid Rarely avoid Sometimes avoid Often avoid Always avoid
Description Fear Avoid

0–8 0–8
1. The worst Getting my blood drawn 8 8

situation
2. The 2nd worst Getting a vaccination 7 8
situation
3. The 3rd worst Watching someone get their blood 6 5
situation drawn
4. The 4th worst Watching someone get a shot 6 5
situation
5. The 5th worst Seeing a needle at the doctor’s office 6 5
situation
6. The 6th worst Watching when someone puts a ban- 4 4
situation dage on one of my cuts or scrapes
7. The 7th worst Being near someone who has a cut or 3 3
situation a scrape
8. The 8th worst Seeing a bloody scene on TV 2 3
situation
Interoceptive Exposure
For patients with PD in particular, interoceptive exposures can be helpful in reducing
the fear associated with the experience of uncomfortable physical sensations. Inte-
roceptive exposures involve exposure to physical sensations such as rapid heartbeat,
shortness of breath, sweating, dizziness, and nausea. Various exercises, such as run-
ning in place, spinning in a circle, staring at a light, sitting in a heated room, and
breathing through a narrow straw, are employed to expose anxious children to their
feared physical sensations. Just as with in vivo exposures, it is expected that the
physical feelings and associated anxiety will dissipate over time and demonstrate to
the child that the physiological experience of anxiety cannot last forever (a common
maladaptive cognition, particularly in PD). Interoceptive exposures can be paired with
in vivo exposures to increase the intensity of in vivo exposures and further mimic the
physiological arousal that occurs during an anxiety-provoking experience.
Relapse Prevention
By the end of treatment, the child or adolescent should have a solid understanding of
the skills that can be utilized to target maladaptive thoughts, uncomfortable physical
feelings, and avoidance behaviors. Parents should also feel competent in facilitating
use of these skills outside of therapy sessions. Depending on the child’s age and
developmental level, the clinician might work toward transferring leadership of in

vivo exposure to parents in later sessions. It is expected that the child will continue to
practice learned skills over the weeks and months following the end of treatment in
order to maintain gains. The clinician is expected to provide some education around
periods during which symptoms may resurface; times of stress, illness, or transition
are often periods during which anxiety symptoms return. In preparation for natural
spikes in anxiety symptoms at certain times, the child is asked to anticipate periods
during which anxiety symptoms may reemerge and generate ways in which learned
skills can be used to decrease those symptoms.
Trauma-Focused Cognitive Behavioral Therapy

A slight variation on traditional CBT is utilized for children and adolescents who have
experienced a traumatic event and meet diagnostic criteria for PTSD. Trauma-focused
CBT (TF-CBT) includes many of the same components as CBT for other anxiety
disorders, such as psychoeducation, relaxation training, and in vivo exposures, with
the additional inclusion of cognitive processing and reframing. Cognitive processing
and reframing involves challenging the child’s irrational or unhelpful thoughts related
to the trauma (e.g., “I am to blame,” or “I will never be safe again”). In the context
of gradual exposure, the child might be asked to create a trauma narrative, a story
recounting the traumatic event. The child might then be instructed to tell the story,
in increasing detail, repeatedly until thoughts around the traumatic event no longer
elicit feelings of intense anxiety and physiological arousal.
Recent Innovative Approaches to Treatment
As the beneficial effects of CBT for childhood and adolescent anxiety disorders have
been repeatedly observed in controlled research settings, recent investigations have
moved toward promoting the widespread dissemination of CBT for anxious youth;
however, there are a number of barriers to the dissemination of evidence-based
treatments. While there are highly trained clinicians delivering CBT in community
settings, training the majority of clinicians in both community and school settings
requires extensive resources. Even when high-quality CBT services are available, there
is no guarantee that anxious youth and their families will have the resources to be able
to access those services. The utilization of mental health services varies widely across
demographic and socioeconomic categories, such that racial and ethnic minorities
and uninsured families are less likely than Caucasian or insured families to receive
assistance (Kataoka, Zhang, & Wells, 2002; Merikangas et al., 2011). Additionally,
children with internalizing symptomatology, such as anxiety disorders, are less likely
to receive mental health services than those with externalizing difficulties (Wu et al.,
1999). Without easy access to CBT, anxious youth and their families will be far less
likely to receive the treatment they need. Because of these issues, the effectiveness and
generalizability of CBT is now being put to the test, with the intention of maximizing
the accessibility and feasibility of delivering CBT to a range of populations. The
following is a sampling of innovative adaptations of CBT for anxious youth that have
been developed and tested by researchers who are invested in ensuring that CBT is
effective and can be widely disseminated.
While a full course of CBT typically consists of 12 to 20 weekly sessions, not
everyone can access a provider on a weekly basis over the course of several months.
Brief, intensive treatments for anxiety disorders have emerged as a way to provide cost-
effective treatment to individuals for whom weekly treatment is not feasible. Intensive
treatments can allow for the delivery of CBT over the course of a short, defined
period of time (e.g., during a school vacation), decrease travel costs, and rapidly
return youth to developmentally appropriate activities that they might be avoiding
because of their anxiety. Comparisons of intensive and weekly treatments for a variety
of anxiety disorders have shown that the two treatments perform comparably. For the
treatment of OCD, Storch et al. (2008) compared the efficacy of a 14-session, weekly
treatment, to a 14-session, daily treatment (excluding weekends) for pediatric OCD
and found that the two treatments yielded similarly positive treatment outcomes, with
both providing significant reductions in global symptoms of anxiety and depression.
A shorter, 5-day intensive treatment for pediatric OCD has also been shown to be
efficacious (Whiteside & Jacobsen, 2010). Pincus et al. (2010) tested the efficacy
of an 8-day intensive treatment for adolescent panic disorder (with or without
agoraphobia). Results from this trial revealed that after just 6 days (approximately 20
hours) of in-clinic treatment involving psychoeducation, interoceptive exposures, and
in vivo exposures, and 2 days of independent in vivo exposure practice, adolescents
exhibited significant reductions in anxiety symptoms as rated by the adolescent, his
parent, and the treating clinician. Santucci, Ehrenreich, Trosper, Bennett, and Pincus
(2009) designed and evaluated an intensive program for school-age girls with a
diagnosis of SAD. An initial evaluation of the program yielded significant reductions
in SAD severity and avoidance of separation situations after one week of treatment.
The briefest intensive treatment for anxiety disorder in youth, a one-day intensive
treatment for specific phobias conducted by Ollendick and colleagues (2009), was
compared to an education support treatment and a wait-list condition. Individuals
in the intensive treatment condition outperformed individuals in the other two
conditions on clinician-rated and self-report measures of anxiety symptomatology.
In an effort to enhance the generalizability of evidence-based treatments for
anxiety disorders in youth, there has been a push toward conducting treatment in
settings that are accessible and relevant to the daily lives of anxious children and
their families. Training school-based personnel and transporting CBT into school-
based mental health programs is a solid next step in translating treatment gains
to the settings in which children spend most of their time (Ginsburg, Becker,
Kingery, & Nichols, 2008). Masia-Warner et al. (2005) demonstrated the efficacy of
a school-based intervention for adolescents with social anxiety disorder. In addition
to providing CBT to adolescents, the clinicians provided education to teachers on
anxiety symptomatology, treatment techniques, and school-based exposure tasks.
Adolescents in the intervention group, in comparison to the wait-list control group,
demonstrated significantly greater reductions in social anxiety and avoidance, and
improvements in overall functioning. A small pilot study conducted by Ginsburg
and Drake (2002) suggested the effectiveness of a school-based, group treatment
for anxious African American adolescents. Other studies have provided support for
school-based prevention programs targeting anxiety symptoms in the general school

population (e.g., Barrett & Turner, 2001).
Manual-based treatments for anxious youth, such as the Coping Cat (Kendall &
Hedtke, 2006a, 2006b), have allowed for the widespread dissemination of CBT
principles in clinical practice. However, strict adherence to treatment protocols
without regard to individual child, family, and therapist characteristics can lead to
a nonengaging and impersonal therapeutic delivery. Kendall et al. (2008) argue
for “flexibility within fidelity,” pointing to the need to adhere to the underlying
principles of CBT while providing treatment that can flexibly shift in response to
client characteristics and outcomes. Modular treatments have emerged as a way
to formally address this issue and enhance the clinical utility, applicability, and
effectiveness of evidence-based treatments. In modular treatments, an intervention is
guided by treatment components that are matched to a child’s individual presentation.
While some core treatment components are delivered to all clients, others are hand-
picked based on the child’s presentation and needs. Weisz et al. (2012) found that
in comparison to usual care and standard evidence-based treatments, an integrated,
modular treatment for depression, anxiety, and conduct problems performed better
on clinical outcome measures. In an evaluation of modular CBT for childhood anxiety
disorders conducted by Chorpita and colleagues (2004), all participants were provided
with core treatment components such as anxiety psychoeducation and the creation
of a fear and avoidance hierarchy, while selected participants were given additional
information about time out procedures, active ignoring, social skills training, and
cognitive restructuring based on their needs. Results showed preliminary support for
this type of intervention as an efficacious treatment for anxious youth.
Transdiagnostic treatments are also being developed as a way to enhance the parsi-
mony and dissemination of interventions for a range of disorders. Rather than having
to learn a different manual-based treatment for the treatment of every psychological
disorder, transdiagnostic treatments allow for clinicians to become proficient in one
treatment that can address multiple symptom presentations. Unified protocols have
been developed and tested successfully with adults with emotional disorders (e.g.,
Barlow et al., 2011; Wilamowska et al., 2010). Downward extensions of these pro-
tocols are now being tested with children and adolescents presenting with a range of
anxiety and depression symptoms, and initial findings in a small sample point to their
efficacy (Ehrenreich-May & Bilek, 2012).
The rapid development of technology is creating new and exciting opportunities
for the delivery of CBT for youth with anxiety disorders. Computer-assisted therapy,
which involves the use of computer programs to augment therapy, has been developed
and evaluated with anxious youth. Khanna and Kendall (2008) developed the Coping
Cat CD-ROM, entitled “Camp Cope-A-Lot,” a computer-assisted CBT for anxiety
disorders in youth. The program is designed to be used independently at the
beginning of treatment, and with the assistance of a therapist during in vivo exposure
practice. In a randomized controlled trial examining the relative efficacy of computer-
assisted CBT with Camp Cope-A-Lot, individual CBT, and a computer-assisted
education, support, and attention condition for anxious youth between the ages
of 7 and 13, both the individual and computer-assisted CBT yielded significantly
better treatment gains than the computer-assisted education, support, and attention
condition (Khanna & Kendall, 2010). Wuthrich et al. (2012) tested the efficacy
of a computerized program, entitled “Cool Teens,” targeted at adolescents with
anxiety disorders. After participating in this 12-week computerized CBT program
for anxiety management, adolescents exhibited significant reductions in parent- and
child-reported severity of their primary anxiety disorder in comparison to individuals
on a 12-week wait-list.
Internet-based treatments are also being evaluated. With barriers to treatment
being quite high for children and families who live in remote or rural areas where
treatment providers are lacking, Internet-delivered treatments can offer a viable
alternative. These treatments, while still relatively new to the field, are receiving
positive feedback from families. Spence, Holmes, March, and Lipp (2006) conducted
a study in which anxious youth were randomly assigned to clinic-based CBT, the
same treatment partially delivered via the Internet and partially delivered in the
clinic, or a wait-list control group. When surveyed about the combined Internet and
in-clinic treatment, participants reported high acceptability, consumer satisfaction,
and credibility. Another trial in 7- to 12-year-olds with anxiety disorders conducted
by March, Spence, and Donovan (2009) showed small but significantly greater
reductions in anxiety and increased functioning in participants in an Internet-based
CBT condition as compared to a wait-list condition. Also currently underway, Comer
and colleagues at Boston University and Brown University are conducting an efficacy
and feasibility study for Internet-delivered, family-based treatment of OCD (Comer
et al., in press). The clinician delivers 12 sessions of family-based CBT for OCD
(Freeman & Garcia, 2009) via Webcam. The feasibility and acceptability of this
modality of treatment will continue to be evaluated.
Conclusion
While CBT for anxiety in children and adolescents began as a downward extension of
CBT for anxious adults, it has evolved into a developmentally appropriate treatment
for youth. The efficacy of CBT for childhood and adolescent anxiety disorders has
been demonstrated repeatedly. However, a proportion of anxious youth do not exhibit
symptom remission after a full course of CBT. In an evaluation of individual and
group CBT for anxious youth, Flannery-Schroeder and Kendall (2000) found that
37% of youth in the individual CBT condition and 50% of youth in the group CBT
condition still met criteria for a primary anxiety disorder after 18 weeks of treatment.
Most trials evaluating the efficiency of CBT have been efficacy trials and therefore
have limited generalizability to community settings (Cartwright-Hatton, Roberts,
Chitsabesan, Fothergill, & Harrington, 2004), and there is some evidence to suggest
that CBT may not provide benefits above and beyond usual care in community clinics
(Pincus et al., 2011; Southam-Gerow et al., 2010).
The recent adaptations of CBT for anxious youth discussed in this chapter offer
innovative and exciting ways to begin to disseminate CBT widely and increase its reach
to children and families who may not otherwise have access to mental health services.
Additionally, the continued examination of mediators and moderators of treatment
outcome—why and for whom treatments work—will be a critical tool in determining
how best to tailor and adapt treatments to a child’s or adolescent’s individual needs.
These continued efforts will help to ensure that anxious children and adolescents and
their families are receiving the best possible care for their difficulties.
References
Ainsworth, M. D., & Bowlby, J. (1991). An ethological approach to personality development.
American Psychologist, 46, 333–341.
Anderson, J. C., Williams, S., McGee, R., & Silva, P. A. (1987). DSM-III disorders in
preadolescent children: Prevalence in a large sample from the general population. Archives
Anstendig, K. D. (1999). Is selective mutism an anxiety disorder? Rethinking its DSM-IV
classification. Journal of Anxiety Disorders, 13, 417–434.
Barlow, D. H. (2002). Anxiety and its disorders: The nature and treatment of anxiety and panic
Barlow, D. H., Farchione, T. J., Fairholme, C. P., Ellard, K. K., Boisseau, C. L., Allen, L. B.,
& Ehrenreich-May, J. (2011). Unified protocol for transdiagnostic treatment of emotional
disorders: Therapist guide. New York, NY: Oxford University Press.
Barrett, P. M., Dadds, M. R., & Rapee, R. M. (1996). Family treatment of childhood anxiety:
A controlled trial. Journal of Consulting and Clinical Psychology, 64, 333–342.
Barrett, P. M., Rapee, R. M., Dadds, M. M., & Ryan, S. M. (1996). Family enhancement of
cognitive style in anxious and aggressive children. Journal of Abnormal Child Psychology,
24, 187–203.
Barrett, P. M., & Turner, C. (2001). Prevention of anxiety symptoms in primary school
children: Preliminary results from a universal school-based trial. British Journal of Clinical
Beidel, D. C., Turner, S. M., & Morris, T. L. (1999). Psychopathology of childhood social
phobia. Journal of the American Academy of Child and Adolescent Psychiatry, 38, 643–650.
Benjamin, R. S., Costello, E. J., & Warren, M. (1990). Anxiety disorders in a pediatric sample.
Bienvenu, O. J., Hettema, J. M., Neale, M. C., Prescott, C. A., & Kendler, K. S. (2007).
Low extraversion and high neuroticism as indices of genetic and environmental risk for
social phobia, agoraphobia, and animal phobia. American Journal of Psychiatry, 164,
1714–1721.
Bittner, A., Egger, H. L., Erkanli, A., Costello, E. J., Foley, D. L., & Angold, A. (2007). What
do childhood anxiety disorders predict? Journal of Child Psychology and Psychiatry, 48,
1174–1183.
Black, B., & Uhde, T. W. (1992). Elective mutism as a variant of social phobia. Journal of the
Bodden, D. H., Bogels, S. M., Nauta, M. H., De Haan, E., Ringrose, J., Appelboom, C., …
Appelboom-Geerts, K. C. (2008). Child versus family cognitive-behavioral therapy in
clinically anxious youth: An efficacy and partial effectiveness study. Journal of the American
Academy of Child and Adolescent Psychiatry, 47 , 1384–1394.
Bodden, D. H., Dirksen, C. D., & Bogels, S. M. (2008). Societal burden of clinically anxious
youth referred for treatment: A cost-of-illness study. Journal of Abnormal Child Psychology,
36, 487–497.
Bogels, S. M., & Zigterman, D. (2000). Dysfunctional cognitions in children with social phobia,
separation anxiety disorder, and generalized anxiety disorder. Journal of Abnormal Child
Bowen, R. C., Offord, D. R., & Boyle, M. H. (1990). The prevalence of overanxious disorder
and separation anxiety disorder: Results from the Ontario Child Health Study. Journal of
Brown, A. M., Deacon, B. J., Abramowitz, J. S., Dammann, J., & Whiteside, S. P. (2007).
Parents’ perceptions of pharmacological and cognitive-behavioral treatments for childhood
anxiety disorders. Behaviour Research and Therapy, 45, 819–828.
Buckner, J. C., & Bassuk, E. L. (1997). Mental disorders and service utilization among youths
from homeless and low-income housed families. Journal of the American Academy of
Calamari, J. E., Hale, L. R., Heffelfinger, S. K., Janeck, A. S., Lau, J. J., Weerts, M. A., …
Schisler, R. L. (2001). Relations between anxiety sensitivity and panic symptoms in
nonreferred children and adolescents. Journal of Behavior Therapy and Experimental
Cartwright-Hatton, S., Roberts, C., Chitsabesan, P., Fothergill, C., & Harrington, R.
(2004). Systematic review of the efficacy of cognitive behaviour therapies for child-
hood and adolescent anxiety disorders. British Journal of Clinical Psychology, 43,
421–436.
Chorpita, B. F., & Barlow, D. H. (1998). The development of anxiety: The role of control in
the early environment. Psychological Bulletin, 124, 3–21.
Chorpita, B. F., Taylor, A. A., Francis, S. E., Moffitt, C., & Austin, A. A. (2004). Efficacy of
modular cognitive behavior therapy for childhood anxiety disorders. Behavior Therapy,
35, 263–287.
461–470.
Comer, J. S., Furr, J. M., Cooper-Vince, C., Kerns, C., Chan, P. T., Edson, A. L., … Freeman,
J. B. (in press). Internet-delivered treatment for early-onset OCD: A preliminary case
series. Journal of Clinical Child and Adolescent Psychology.
Costello, E. J., & Angold, A. (1995). Anxiety disorders in children and adolescents. In J. S.
March (Ed.), Epidemiology (pp. 109–124). New York, NY: Guilford Press.
Costello, E. J., Angold, A., Burns, B. J., Stangl, D. K., Tweed, D. L., Erkanli, A., & Worthman,
C. M. (1996). The Great Smoky Mountains Study of Youth. Goals, design, methods, and
the prevalence of DSM-III-R disorders. Archives of General Psychiatry, 53, 1129–1136.
Costello, E. J., Egger, H. L., & Angold, A. (2004). Developmental epidemiology of anxiety
disorders. In T. H. Ollendick & J. S. March (Eds.), Phobic and anxiety disorders in
children and adolescents: A clinician’s guide to effective psychosocial and pharmacological
interventions (pp. 61–91). New York, NY: Oxford University Press.
Costello, E. J., Mustillo, S., Erkanli, A., Keeler, G., & Angold, A. (2003). Prevalence and
development of psychiatric disorders in childhood and adolescence. Archives of General
Cunningham, C. E., McHolm, A., Boyle, M. H., & Patel, S. (2004). Behavioral and emotional
adjustment, family functioning, academic performance, and social relationships in children
with selective mutism. Journal of Child Psychology and Psychiatry, 45, 1363–1372.
Doerfler, L. A., Connor, D. F., Volungis, A. M., & Toscano, P. F. Jr. (2007). Panic disorder
in clinically referred children and adolescents. Child Psychiatry and Human Development,
38, 57–71.
Ehrenreich-May, J., & Bilek, E. L. (2012). The development of a transdiagnostic, cognitive

behavioral group intervention for childhood anxiety disorders and co-occurring depression
symptoms. Cognitive and Behavioral Practice, 19, 41–55.
Essau, C. A., Conradt, J., & Petermann, F. (1999a). Frequency and comorbidity of social
phobia and social fears in adolescents. Behaviour Research and Therapy, 37 , 831–843.
Essau, C. A., Conradt, J., & Petermann, F. (1999b). Frequency of panic attacks and panic
disorder in adolescents. Depression and Anxiety, 9, 19–26.
Flannery-Schroeder, E., & Kendall, P. C. (2000). Group and individual cognitive-behavioral
treatments for youth with anxiety disorders: A randomized clinical trial. Cognitive Therapy
and Research, 24, 251–278.
Flessner, C. A., Berman, N., Garcia, A., Freeman, J. B., & Leonard, H. L. (2009). Symptom
profiles in pediatric obsessive-compulsive disorder (OCD): The effects of comorbid
grooming conditions. Journal of Anxiety Disorders, 23, 753–759.
Foley, D. L., Rowe, R., Maes, H., Silberg, J., Eaves, L., & Pickles, A. (2008). The rela-
tionship between separation anxiety and impairment. Journal of Anxiety Disorders, 22,
635–641.
Fox, N. A., & Pine, D. S. (2012). Temperament and the emergence of anxiety disorders.
Freeman, J. B., & Garcia, A. M. (2009). Family-based treatment for young children with OCD.
New York, NY: Oxford University Press.
Fyer, A. J., Mannuzza, S., Chapman, T. F., Martin, L. Y., & Klein, D. F. (1995). Speci-
ficity in familial aggregation of phobic disorders. Archives of General Psychiatry, 52,
564–573.
Ginsburg, G. S., Becker, K. D., Kingery, J. N., & Nichols, T. (2008). Transporting CBT for
childhood anxiety disorders into inner-city school-based mental health clinics. Cognitive
and Behavioral Practice, 15, 148–158.
Ginsburg, G. S., & Drake, K. L. (2002). School-based treatment for anxious African-American
adolescents: A controlled pilot study. Journal of the American Academy of Child and
Greenberg, P. E., Sisitsky, T., Kessler, R. C., Finkelstein, S. N., Berndt, E. R., Davidson,
J. R., … Fyer, A. J. (1999). The economic burden of anxiety disorders in the 1990s.
Gullone, E. (1999). The assessment of normal fear in children and adolescents. Clinical Child
and Family Psychology Review, 2, 91–106.
Hanna, G. L. (1995). Demographic and clinical features of obsessive-compulsive disorder
in children and adolescents. Journal of the American Academy of Child and Adolescent
Hettema, J. M., Neale, M. C., & Kendler, K. S. (2001). A review and meta-analysis of
the genetic epidemiology of anxiety disorders. American Journal of Psychiatry, 158,
1568–1578.
Hudson, J. L., Comer, J. S., & Kendall, P. C. (2008). Parental responses to positive and
negative emotions in anxious and nonanxious children. Journal of Clinical Child and
Adolescent Psychology, 37 , 303–313.
In-Albon, T., & Schneider, S. (2007). Psychotherapy of childhood anxiety disorders: A
meta-analysis. Psychotherapy and Psychosomatics, 76, 15–24.
Kagan, J., Reznick, J. S., Clarke, C., Snidman, N., & Garcia-Coll, C. (1984). Behavioral
inhibition to the unfamiliar. Child Development, 55, 2212–2225.
Kataoka, S. H., Zhang, L., & Wells, K. B. (2002). Unmet need for mental health care among
U.S. children: Variation by ethnicity and insurance status. American Journal of Psychiatry,
159, 1548–1555.
Kearney, C. A., Sims, K. E., Pursell, C. R., & Tillotson, C. A. (2003). Separation anxiety
disorder in young children: A longitudinal and family analysis. Journal of Clinical Child
and Adolescent Psychology, 32, 593–598.
Kendall, P. C. (1994). Treating anxiety disorders in children: Results of a randomized clinical
trial. Journal of Consulting and Clinical Psychology, 62, 100–110.
Kendall, P. C., Gosch, E., Furr, J. M., & Sood, E. (2008). Flexibility within fidelity. Journal of
the American Academy of Child and Adolescent Psychiatry, 47 , 987–993.
Kendall, P. C., & Hedtke, K. (2006a). Cognitive-behavioral therapy for anxious children:
Therapist manual (3rd ed.). Ardmore, PA: Workbook Publishing.
Kendall, P. C., & Hedtke, K. (2006b). Coping cat workbook (2nd ed.). Ardmore, PA: Workbook
Publishing.
Kendall, P. C., Hudson, J. L., Gosch, E., Flannery-Schroeder, E., & Suveg, C. (2008).
Cognitive-behavioral therapy for anxiety disordered youth: A randomized clinical trial
evaluating child and family modalities. Journal of Consulting and Clinical Psychology, 76,
282–297.
Kendall, P. C., & Southam-Gerow, M. A. (1995). Issues in the transportability of treatment:
The case of anxiety disorders in youths. Journal of Consulting and Clinical Psychology, 63,
702–708.
Khanna, M. S., & Kendall, P. C. (2008). Computer-assisted CBT for child anxiety: The Coping
Cat CD-ROM. Cognitive and Behavioral Practice, 15, 159–165.
Khanna, M. S., & Kendall, P. C. (2009). Exploring the role of parent training in the treatment
of childhood anxiety. Journal of Consulting and Clinical Psychology, 77 , 981–986.
Khanna, M. S., & Kendall, P. C. (2010). Computer-assisted cognitive behavioral therapy for
child anxiety: Results of a randomized clinical trial. Journal of Consulting and Clinical
Kindt, M., Bierman, D., & Brosschot, J. F. (1997). Cognitive bias in spider fear and control
children: Assessment of emotional interference by a card format and a single-trial format
of the Stroop task. Journal of Experimental Child Psychology, 66, 163–179.
Kindt, M., Brosschot, J. F., & Everaerd, W. (1997). Cognitive processing bias of children in a
real life stress situation and a neutral situation. Journal of Experimental Child Psychology,
64, 79–97.
Kingery, J. N., Roblek, R. L., Suveg, C., Grover, R. L., & Sherrill, J. T. (1996). They’re not
just “little adults”: Developmental considerations for implementing cognitive-behavioral
therapy with anxious youth. Journal of Cognitive Psychotherapy, 20, 263–173.
Kristensen, H. (2000). Selective mutism and comorbidity with developmental disorder/delay,
anxiety disorder, and elimination disorder. Journal of the American Academy of Child and
La Greca, A. M., & Lopez, N. (1998). Social anxiety among adolescents: Linkages with peer
relations and friendships. Journal of Abnormal Child Psychology, 26, 83–94.
Last, C. G., Perrin, S., Hersen, M., & Kazdin, A. E. (1992). DSM-III-R anxiety disorders in
children: Sociodemographic and clinical characteristics. Journal of the American Academy
of Child and Adolescent Psychiatry, 31, 1070–1076.
Lau, J. J., Calamari, J. E., & Waraczynski, M. (1996). Panic attack symptomatology and anxiety
sensitivity in adolescents. Journal of Anxiety Disorders, 10, 355–364.
Lewinsohn, P. M., Holm-Denoma, J. M., Small, J. W., Seeley, J. R., & Joiner,
T. E., Jr. (2008). Separation anxiety disorder in childhood as a risk factor for future
mental illness. Journal of the American Academy of Child and Adolescent Psychiatry, 47 ,
548–555.
Liber, J. M., Van Widenfelt, B. M., Utens, E. M., Ferdinand, R. F., Van der Leeden, A. J.,
Van Gastel, W., & Treffers, P. D. (2008). No differences between group versus individual
treatment of childhood anxiety disorders in a randomised clinical trial. Journal of Child
Manassis, K., Mendlowitz, S. L., Scapillato, D., Avery, D., Fiksenbaum, L., Freire, M., …
Owens, M. (2002). Group and individual cognitive-behavioral therapy for childhood
anxiety disorders: A randomized trial. Journal of the American Academy of Child and
March, S., Spence, S. H., & Donovan, C. L. (2009). The efficacy of an internet-based
cognitive-behavioral therapy intervention for child anxiety disorders. Journal of Pediatric
Masi, G., Favilla, L., Millepiedi, S., & Mucci, M. (2000). Somatic symptoms in chil-
dren and adolescents referred for emotional and behavioral disorders. Psychiatry, 63,
140–149.
Masi, G., Mucci, M., Favilla, L., Romano, R., & Poli, P. (1999). Symptomatology and
comorbidity of generalized anxiety disorder in children and adolescents. Comprehensive
Masia-Warner, C., Klein, R. G., Dent, H. C., Fisher, P. H., Alvir, J., Albano, A. M., &
Guardino, M. (2005). School-based intervention for adolescents with social anxiety dis-
order: Results of a controlled study. Journal of Abnormal Child Psychology, 33, 707–722.
McCracken, J. T., Walkup, J. T., & Koplewicz, H. S. (2002). Childhood and early-onset
anxiety: Treatment and biomarker studies. Journal of Clinical Psychiatry, 63(Suppl. 6),
8–11.
McLeod, B. D., Wood, J. J., & Weisz, J. R. (2007). Examining the association between par-
enting and childhood anxiety: A meta-analysis. Clinical Psychology Review, 27 , 155–172.
Merikangas, K. R., He, J. P., Burstein, M., Swendsen, J., Avenevoli, S., Case, B., … Olfson, M.
(2011). Service utilization for lifetime mental disorders in U.S. adolescents: Results of the
National Comorbidity Survey-Adolescent Supplement (NCS-A). Journal of the American
Ollendick, T. H., Ost, L. G., Reuterskiold, L., Costa, N., Cederlund, R., Sirbu, C., … Jarrett,
M. A. (2009). One-session treatment of specific phobias in youth: A randomized clinical
trial in the United States and Sweden. Journal of Consulting and Clinical Psychology, 77 ,
504–516.
Ollendick, T. H., Raishevich, N., Davis, T. E., III,, Sirbu, C., & Ost, L. G. (2010). Specific
phobia in youth: Phenomenology and psychological characteristics. Behavior Therapy, 41,
133–141.
Pianta, R. C. (1999). Early childhood. In W. K. Silverman & T. H. Ollendick (Eds.),
Developmental issues in the clinical treatment of children (pp. 88–107). Needham Heights,
MA: Allyn & Bacon.
Pincus, D. B., Chase, R. M., Chow, C., Weiner, C. L., & Pian, J. (2011). Integrating play
into cognitive behavioral therapy in the treatment of child anxiety. In S. Russ & L. Niec
(Eds.), Play in clinical practice: Evidence-based approaches (pp. 218–235). New York, NY:
Guilford Press.
Pincus, D. B., Whitton, S. W., Angelosante, A. G., Buzzella, B., Cheron, D., Weiner,
C. L., … Chow, C. (2010, June). Intensive treatment of adolescents with panic disorder
and agoraphobia. Paper presented at the World Congress of Behavioral and Cognitive
Therapies (WCBCT), Boston, MA.
Pine, D. S., Cohen, P., Gurley, D., Brook, J., & Ma, Y. (1998). The risk for early-adulthood
anxiety and depressive disorders in adolescents with anxiety and depressive disorders.
Pollack, M. H., Otto, M. W., Sabatino, S., Majcher, D., Worthington, J. J., McArdle, E. T.,
& Rosenbaum, J. F. (1996). Relationship of childhood anxiety to adult panic disorder:
Correlates and influence on course. American Journal of Psychiatry, 153, 376–381.
Santucci, L. C., Ehrenreich, J. T., Trosper, S. E., Bennett, S. M., & Pincus, D. B. (2009).
Development and preliminary evaluation of a one-week summer treatment program for
separation anxiety disorder. Cognitive and Behavioral Practice, 16, 317–331.
Silove, D., Manicavasagar, V., Curtis, J., & Blaszczynski, A. (1996). Is early separation anxiety
a risk factor for adult panic disorder?: A critical review. Comprehensive Psychiatry, 37 ,
167–179.
Silverman, W. K., & Ginsburg, G. S. (1998). Anxiety disorders. In T. H. Ollendick &
M. Hersen (Eds.), Handbook of child psychopathology (3rd ed., pp. 239–268). New York,
NY: Plenum Press.
Silverman, W. K., Pina, A. A., & Viswesvaran, C. (2008). Evidence-based psychosocial
treatments for phobic and anxiety disorders in children and adolescents. Journal of
Clinical Child and Adolescent Psychology, 37 , 105–130.
Southam-Gerow, M. A., Weisz, J. R., Chu, B. C., McLeod, B. D., Gordis, E. B., &
Connor-Smith, J. K. (2010). Does cognitive behavioral therapy for youth anxiety outper-
form usual care in community clinics? An initial effectiveness test. Journal of the American
Spence, S. H., Holmes, J. M., March, S., & Lipp, O. V. (2006). The feasibility and outcome of
clinic plus internet delivery of cognitive-behavior therapy for childhood anxiety. Journal
Stein, M. B., Jang, K. L., & Livesley, W. J. (1999). Heritability of anxiety sensitivity: A twin
study. American Journal of Psychiatry, 156, 246–251.
Steinhausen, H. C., & Juzi, C. (1996). Elective mutism: An analysis of 100 cases. Journal of
Storch, E. A., Merlo, L. J., Lehmkuhl, H., Geffken, G. R., Jacob, M., Ricketts, E., … Goodman,
W. K. (2008). Cognitive-behavioral therapy for obsessive-compulsive disorder: A non-
randomized comparison of intensive and weekly approaches. Journal of Anxiety Disorders,
22, 1146–1158.
Strauss, C. C., Frame, C. F., & Forehand, R. (1987). Psychosocial impairment associated with
anxiety in children. Journal of Clinical Child Psychology, 16, 235–239.
Thapar, A., & McGuffin, P. (1995). Are anxiety symptoms in childhood heritable? Journal of
Child Psychology and Psychiatry, 36, 439–447.
Turner, S. M., Beidel, D. C., & Costello, A. (1987). Psychopathology in the offspring of
anxiety disorders patients. Journal of Consulting and Clinical Psychology, 55, 229–235.
Vasey, M. W., & Dadds, M. R. (2001). The developmental psychopathology of anxiety. New York,
Von Korff, M. R., Eaton, W. W., & Keyl, P. M. (1985). The epidemiology of panic attacks and
panic disorder: Results of three community surveys. American Journal of Epidemiology,
122, 970–981.
Walkup, J. T., Albano, A. M., Piacentini, J., Birmaher, B., Compton, S. N., Sherrill, J. T., …
Kendall, P. C. (2008). Cognitive behavioral therapy, sertraline, or a combination in
childhood anxiety. New England Journal of Medicine, 359, 2753–2766.
Weems, C. F., Silverman, W. K., Rapee, R. M., & Pina, A. A. (2003). The role of control in
childhood anxiety disorders. Cognitive Therapy and Research, 27 , 557–568.
Weissman, M. M., Leckman, J. F., Merikangas, K. R., Gammon, G. D., & Prusoff, B. A.
(1984). Depression and anxiety disorders in parents and children: Results from the Yale
family study. Archives of General Psychiatry, 41, 845–852.
Weisz, J. R., Chorpita, B. F., Palinkas, L. A., Schoenwald, S. K., Miranda, J., Bearman,
S. K., … Gibbons, R. D. (2012). Testing standard and modular designs for psychotherapy
treating depression, anxiety, and conduct problems in youth: A randomized effectiveness
Whitaker, A., Johnson, J., Shaffer, D., Rapoport, J. L., Kalikow, K., Walsh, B. T., …
Dolinsky, A. (1990). Uncommon troubles in young people: Prevalence estimates of
selected psychiatric disorders in a nonreferred adolescent population. Archives of General
Psychiatry, 47 , 487–496.
Whiteside, S. P., & Jacobsen, A. B. (2010). An uncontrolled examination of a 5-day intensive
treatment for pediatric OCD. Behavior Therapy, 41, 414–422.
Wilamowska, Z. A., Thompson-Hollands, J., Fairholme, C. P., Ellard, K. K., Farchione, T. J.,
& Barlow, D. H. (2010). Conceptual background, development, and preliminary data
from the unified protocol for transdiagnostic treatment of emotional disorders. Depression
and Anxiety, 27 , 882–890.
Williams, N. L., Reardon, J. M., Murray, K. T., & Cole, T. M. (2005). Anxiety disorders: A
developmental vulnerability-stress perspective. In B. L. Hankin & J. R. Z. Abela (Eds.),
Development of psychopathology: A vulnerability-stress perspective (pp. 289–328). Thousand
Oaks, CA: Sage.
Wood, J. J., McLeod, B. D., Sigman, M., Hwang, W. C., & Chu, B. C. (2003). Parenting
and childhood anxiety: Theory, empirical findings, and future directions. Journal of Child
Woodward, L. J., & Fergusson, D. M. (2001). Life course outcomes of young people with
anxiety disorders in adolescence. Journal of the American Academy of Child and Adolescent
Psychiatry, 40, 1086–1093.
Wu, P., Hoven, C. W., Bird, H. R., Moore, R. E., Cohen, P., Alegria, M., … Roper,
M. T. (1999). Depressive and disruptive disorders and mental health service utilization
Psychiatry, 38, 1081–1090; discussion 1090–1082.
Wuthrich, V. M., Rapee, R. M., Cunningham, M. J., Lyneham, H. J., Hudson, J. L., &
Schniering, C. A. (2012). A randomized controlled trial of the Cool Teens CD-ROM
Computerized Program for Adolescent Anxiety. Journal of the American Academy of
Yehuda, R. (2002). Post-traumatic stress disorder. New England Journal of Medicine, 346,
108–114.
Zohar, A. H. (1999). The epidemiology of obsessive-compulsive disorder in children and
adolescents. Child and Adolescent Psychiatric Clinics of North America, 8, 445–460.
37
School Refusal Behavior
Christopher A. Kearney and Rachele Diliberto
University of Nevada, United States
Introduction
School refusal behavior refers to a child-motivated refusal to attend school and/or

difficulties remaining in classes for an entire day. School refusal behavior thus includes
complete absences, skipped classes, chronic tardiness, morning misbehaviors in an
attempt to miss school, and severe distress about school that precipitates pleas for
future nonattendance (Kearney & Silverman, 1996). School refusal behavior may be
considered part of problematic absenteeism, which includes school-aged youths who
(a) have missed at least 25% of total school time for at least 2 weeks, (b) experience
severe difficulty attending classes for at least 2 weeks with significant interference in a
youth’s or family’s daily routine, and/or (c) are absent for at least 10 days of school
during any 15-week period while school is in session, with an absence defined as 25%
or more of school time missed (Kearney, 2008). School absenteeism may be a singular
problem or one embedded in comorbid behavioral, psychiatric, or familial problems
(McShane, Walter, & Rey, 2001).
School absenteeism is prevalent. A community survey of youths with truancy and
anxiety-based school refusal revealed a prevalence rate of 8.2% (Egger, Costello, &
Angold, 2003). Approximately 19% of fourth-graders and 20% of eighth-graders
missed at least 3 days of school in the past month (National Center for Education
Statistics, 2006). In addition, graduation rates are below 50% in several major Amer-
ican cities (EPE Research Center, 2008). The overall prevalence of school refusal
behavior, which includes absentee-related behaviors such as tardiness, reportedly
ranges from 28 to 35% (Kearney, 2001; Pina, Zerr, Gonzales, & Ortiz, 2009). Prob-
lematic school absenteeism is associated with poor outcomes such as substance abuse,
violence, suicide attempts, risky sexual behavior, pregnancy, delinquency, injury,

DOI: 10.1002/9781118528563.wbcbt37
illness, and school dropout as well as long-term economic deprivation and social,
marital, occupational, and psychiatric problems (Hibbett & Fogelman, 1990, Hibbett,
Fogelman, & Manor, 1990; Kogan, Luo, Murry, & Brody, 2005; Tramontina et al.,
2001).
The substantial prevalence and potential negative consequences of school refusal
behavior have thus provided an impetus for researchers to study this popula-
tion and develop comprehensive assessment and treatment approaches. Indeed,
school refusal behavior has long been a target of clinical child psychologists,
educators, and professionals from multiple disciplines. Treatment approaches for
youths with school refusal behavior can be generally categorized as (a) cognitive
behavioral strategies for anxiety-based cases, (b) cognitive behavioral strategies for
non-anxiety-based cases, and (c) broader strategies that include components of cog-
nitive behavioral treatment and consider the many contextual variables that impact
problematic absenteeism. Each of these treatment approaches is described in this
chapter.
Cognitive Behavioral Treatment for Anxiety-Based School

Refusal Behavior
Psychologists who study school refusal behavior often concentrate on fear- and
anxiety-based absenteeism. Historical examples include psychoneurotic truancy,
school phobia, separation anxiety, or school refusal. These conditions apply to
youths who miss school due to excessive fear of a school-related stimulus (e.g., a
classroom, a teacher), difficulty separating from major attachment figures such as
parents, and anxiety regarding social and evaluative situations at school (e.g., peer
interactions, tests) (Suveg, Aschenbrand, & Kendall, 2005). Many of these anxiety-
based cases include other internalizing behavior problems such as somatic complaints
(e.g., headaches, stomachaches), depression, fatigue, and worry (Kearney & Albano,
2004). Cognitive behavioral treatment approaches for anxiety-based school refusal
behavior generally involve key components such as psychoeducation, somatic con-
trol exercises, cognitive therapy, coping skills training, and gradual exposure to the
school setting. These components, together with supporting evidence, are described
next.
Psychoeducation
Psychoeducation involves educating both youth and parents about the primary
components of a youth’s absentee behaviors and providing a rationale for treatment.
Children can be taught to understand the nature and process of anxiety by giving
personally relevant examples of anxiety-based feelings, thoughts, and actions. In
addition, children can often identify sequences of anxiety-based behavior. For example,
many children with school refusal behavior awake to aversive physical sensations (e.g.,
nervous stomach, jitteriness) that lead to anxiety-based thoughts (e.g., “school is
going to be terrible today”) and then to school refusal behaviors (e.g., dawdling,
noncompliance, absenteeism) (Figure 37.1). Psychoeducation is often integrated with
School Refusal Behavior 877
My head and
Physical stomach hurt;
component of I feel sick;
child’s distress I am so tired;
I am jittery
I do not want
Cognitive to go to
component of school; school
child’s distress will be
terrible; I hate
my classroom
Dawdling,
Behavioral refusal to
component of enter the
child’s distress school
building
Figure 37.1 Sample sequence of school refusal

behaviors for psychoeducation.
rapport-building so a child can gain greater insight into his or her condition and
understand the rationale behind upcoming treatment procedures such as somatic
control exercises, cognitive therapy, or gradual exposure.
Somatic Control Exercises

Somatic control exercises include relaxation training and breathing retraining to
reduce physical symptoms of anxiety associated with school attendance. Relax-
ation training can take several forms but often includes a series of muscle tension
and relaxation exercises, each designed to teach a child to discriminate physical

sensations of tension and calmness. Children are taught to practice relaxation train-
ing before and after school and during school-based situations that cause distress.
Somatic control exercises also include breathing retraining, or diaphragmatic breath-
ing, to prolong relaxation and make it more complete. Breathing retraining often
consists of breathing in slowly through the nose, pushing the fingers into the
diaphragm to enhance depth, and exhaling slowly through the mouth. Children
may be taught to count slowly when exhaling or to imagine inflating and deflat-
ing like a hot air balloon. Relaxation training and breathing retraining scripts are
available (Kearney & Albano, 2007). Somatic control exercises are typically con-
ducted in conjunction with exposure-based practice (which is discussed later in this
chapter).
Cognitive Therapy
Cognitive therapy for school refusal behavior refers to a child-based approach to iden-
tify and modify maladaptive thoughts about peers and other stimuli at school. This
is especially relevant in social and evaluative situations to boost adaptive and realistic
thinking. Many children with school refusal behavior, especially those in middle or
high school, have maladaptive and irrational thoughts regarding performance before
others, examinations, conversations, and other social or evaluative situations. Cogni-
tive therapy is designed to help youths recognize their problematic thoughts, develop
alternative and more realistic thoughts, and self-evaluate the outcome (Reinecke,
Dattilio, & Freeman, 2003).
Cognitive therapy for youths with school refusal behavior relies heavily on the
Socratic method, or questioning a youth so that he or she becomes an active par-
ticipant in the therapy process. Such questioning can initially be used to identify
common cognitive distortions made by youths with school refusal behavior. Such
distortions include certain erroneous beliefs, such as assuming (a) something terri-
ble will happen when actually it will not, (b) incorrectly what others are thinking,
(c) that the consequences of one’s actions will be catastrophic, (d) that embarrass-
ment will linger and be excruciating, (e) that situations will be either wonderful
or awful (with no “gray” areas), and (f) that the child is to blame for a certain
outcome when actually the outcome is beyond his or her control. Such distor-
tions could be conveyed to some adolescents in a more formal fashion so that
they can learn to label a distortion. Examples include all-or-nothing thinking, catas-
trophizing, overgeneralization, negative labeling, absolutist language (e.g., “must,”
“cannot,” “never”) mind reading, fortune telling, and canceling a positive (Kearney,
2005).
Cognitive therapy can then progress to an overall model that a child can use
to identify anxiety-provoking situations and thoughts and develop more realistic
thoughts. The STOP acronym is commonly used in child anxiety treatment to assist
this process (adapted from Silverman & Kurtines, 1996):
• S: Am I Scared or nervous about a certain social or performance situation?

• T: What Thoughts am I having in this situation?
• O: What Other, more realistic thoughts can I have?
• P: Praise myself for thinking more realistic thoughts.
In this process, a child first recognizes if he or she is anxious in a given situation

(the “S” component). Often this includes a specific social or evaluative situation
such as eating in the school cafeteria or speaking to a peer in the hallway. Once
a child has identified such a situation, he or she engages in the “T” component
by recognizing specific cognitive distortions described above. A child who is anxious
about eating in the school cafeteria, for example, may mistakenly assume that everyone
is watching him or her and evaluating him or her harshly. The child is then taught to
extend this process to the “O” component by creating an alternative, more realistic
thought about what is happening in the situation. A child who is anxious about
negative evaluations in the cafeteria, for example, could test this belief by observing
others and then developing a more realistic conclusion, such as the fact that most
people are not looking directly at him or her. If the child successfully develops
an alternative, more realistic thought, he or she praises himself for doing so (the
“P” component) and evaluates the success of the entire process (STOP) on anxiety
reduction.
Dispute handles may be used to assist the cognitive therapy process. Dispute
handles refer to self-statements or questions a child can use to help challenge or refute
unrealistic thoughts. Examples include: “Am I 100% sure that this will happen?,”
“Can I really know what that person thinks of me?,” “What’s the worst thing that
can really happen?,” “Have I ever been in a situation like this before, and was it really
that bad?,” “How many times has this terrible thing actually happened?,” “So what
if I don’t get a perfect grade on this test?,” and “Am I the only person that has ever
had to deal with this situation?” (Kearney & Albano, 2007). A child with school
refusal behavior engaged in cognitive therapy is encouraged to practice these steps
continually to manage anxiety.
Coping Skills Training

Coping skills training refers to a child-based approach to increase problem-solving
ability and assertiveness at school. Coping skills training is sometimes combined
with social skills training for children who require additional assistance with peer
interactions. Coping and social skills training is most often used for youths with
considerable anxiety about school-based social and evaluative situations or for those
who face school-based threats. Key treatment components include modeling, role
play, prompts, practice, and reinforcement to develop important social behaviors
(e.g., eye contact, voice volume) as well as friendship, listening, and problem-solving
skills (see Box 37.1 for common examples). Coping and social skills training is
often combined with cognitive therapy procedures (Spence, Donovan, & Brechman-
Toussaint, 2000).
Box 37.1 Sample coping/social skills training tasks often

pertinent to youth with school refusal behavior
Asking others for help or information

→ Know exactly what information is needed, ask appropriately (“Excuse me”),
be clear in asking for help
Being assertive in saying “no” or when asking for something
→ Make eye contact, be brief in saying no, state your intention clearly and with
good voice volume
Controlling impulses and anger instead of acting quickly upon them
→ Count silently to 10, relax body, exit situation appropriately, talk to someone
Dealing with being sad or anxious
→ Relax body, think about difficult thoughts, understand the feeling is tempo-
rary, talk to someone
Dealing with embarrassing or stressful situations such as teasing
→ Ignore provocation, walk away, go to a safe area, talk to someone if teasing
is severe
Eating appropriately around others
→ Chew food slowly, speak when mouth is empty of food, relax body, listen to
others
Greeting others appropriately
→ Say “hello” and smile, keep head up, speak articulately and with good voice
volume
Initiating and maintaining conversations with others
→ Think about what topic to focus on, make eye contact, speak clearly, ask
questions
Introducing oneself or other people
→ Use appropriate greeting, pick a good time, use full sentence, follow up with
questions
Joining activities with peers
→ Introduce self, ask others if they want another person to join, speak clearly
and with confidence
Keeping head up when speaking to others
→ Maintain eye contact with person, smile, maintain conversation, ask questions
Listening to others appropriately
→ Nod head occasionally, maintain eye contact, smile, do not interrupt
Maintaining eye contact with others during a conversation
→ Keep head up, watch the facial expression of the person talking, smile
Performing athletically before others
→ Stay involved with group activity, try doing your best, talk to others, have
fun
Resisting group pressure to do something inappropriate
→ Think whether someone is asking you to do something inappropriate, say

“no” clearly, give reason for saying no, walk away from the situation, avoid
tempting situations
Resolving conflicts with others
→ Negotiate solutions to problems without force, listen carefully to others’
opinions, think about all sides of the problem, develop a solution agreeable
to everyone
Sharing feelings appropriately
→ Discuss feelings when not angry, use manners, speak articulately and listen
carefully to others’ reactions
Speaking articulately
→ Speak slowly and pronounce each syllable clearly, maintain eye contact, watch
others’ reactions, speak with good voice volume
Speaking in a clear and audible tone of voice
→ Speak slowly, listen to self to see if voice volume is strong, maintain eye
contact, watch others’ reactions
Speaking or reading before others
→ Speak slowly and articulately, speak with good voice volume, relax body,
practice beforehand, be well prepared
Taking the perspective of other people
→ Actively observe and listen to others, think about what others may be
thinking and feeling in a certain situation, ask others what they were thinking
and feeling
Writing before others
→ Relax body and fingers, write slowly and carefully, focus on task at hand
Note. Adapted from Kearney & Albano (2007)
Exposure-Based Practice
A key element of treatment for anxiety-based school refusal behavior is exposure-based
practice, or gradual reintegration of a child into school such as one class or hour at
a time. Exposure-based practice is typically conducted following the development of
an anxiety and avoidance hierarchy. This hierarchy refers to a list of school-related
social and other situations that range from least to most anxiety-provoking and helps
provide structure for exposure-based practice (see Box 37.2 for common examples).
Information on a hierarchy is often organized into gradual steps so a child may begin
with the easiest (or lowest) item and progress toward the most difficult (highest)
hierarchy item. Most children progress through several hierarchies during treatment
until all anxiety-provoking situations or activities are challenged.
Exposure-based practice can take many forms depending on the individual char-
acteristics of a child’s school refusal behavior. However, certain forms are common
in this population. One common example involves entering school and class in the
morning and staying for a limited time, such as an hour, before being allowed to go
Box 37.2 Sample exposure-based tasks for youth with school

refusal behavior
Asking or answering a question in class (e.g., in response to teacher request)
Being in class without one’s parents (e.g., for one or more classes)
Being in school without calling one’s parents (e.g., for lengthier periods of
time)
Eating in the school cafeteria (e.g., with or without friends)
Entering a classroom (e.g., with or without friends)
Going to physical education class (e.g., dressing in the locker room)
Performing before others (e.g., music, academic, athletic performance)
Riding alone on a school bus (e.g., for one or more stops)
Speaking before others (e.g., classroom oral presentation)
Starting or maintaining conversations (e.g., with peers, adults)
Taking tests (e.g., oral, written examinations)
Transitions between classes (e.g., from a special to a regular classroom)
Unpredictable circumstances (e.g., different pick-up times after school)
Walking in hallways at school (e.g., crowded or empty)
Note. Adapted from Kearney (2010)
home. The child is then expected gradually to increase his or her amount of school
time, such as an extra hour every 3 days, until full-time attendance is reached. Other
exposure-based practices are similar but may begin toward the end of the day (and
then working backward), attending school initially for lunch and then increasing class
time, attending successive favorite classes (i.e., most favorite to least favorite over
time), and attending a nonclassroom setting at school (e.g., library, main office) prior
to gradual reintegration to a classroom.
Empirical Support
Several outcome studies reveal that cognitive behavioral treatment approaches are
effective for anxiety-based school refusal behavior. For example, King et al. (1998)
randomly assigned children to cognitive behavioral treatment or wait-list control.
Treatment included (a) child-based rapport-building, coping skills training, relaxation
training, cognitive therapy, and imaginal and in vivo exposure, (b) parent-based
training in behavior management, and (c) a meeting with a child’s teacher regarding
treatment. Treatment for six sessions was superior to control regarding school
attendance, fear, anxiety, and depression. Treatment was especially effective if a
youth returned swiftly to school and if parents and youth were involved in the
intervention.
Last, Hansen, and Franco (1998) found that CBT and education support (control)
over 12 weeks both produced substantial improvements in school attendance, fear,
anxiety, depression, and posttreatment diagnosis. Education support consisted of
allowing youths to express concerns about school. Bernstein et al. (2000) found that
CBT with imipramine was superior to placebo for improving school attendance and
depression over 8 weeks. Better response to treatment was predicted by higher baseline
attendance and less separation anxiety and avoidant disorder (Layne, Bernstein, Egan,
& Kushner, 2003).
Heyne et al. (2002) also examined cognitive behavioral therapy (CBT) across three
groups: child, parent/teacher, and combined. Child-based treatment involved relax-
ation training, social skills training, cognitive therapy, and exposure-based practice.
Parent/teacher-based treatment involved behavior management strategies (discussed
in more detail in next section) and strategies to enhance parent–school communica-
tion. A combined group included both child- and parent/teacher-based CBT. Each
group demonstrated improvements in school attendance and distress, but more so
for the parent/teacher group. Heyne et al. (2011) also designed a treatment program
to blend cognitive behavioral procedures with modules to address key developmental
issues such as comorbid depression, adolescent cognitive capability, adolescent–parent
communication, and problem-solving with respect to school attendance. Treatment
over 13 sessions produced improvements in school attendance, general functioning,
and internalizing and externalizing behavior problems. Cognitive behavioral proce-
dures have also been found useful for treating inpatient youths with school refusal
behavior (Walter et al., 2010).
Cognitive Behavioral Treatment for Non-Anxiety-Based

School Refusal Behavior
Psychologists have often focused on anxiety-based school refusal behavior but many
children refuse school for reasons other than anxiety. Kearney outlined a functional
model of school refusal behavior that includes children with and without anxiety-
based problems (Kearney, 2007; Kearney & Silverman, 1990, 1996). In this model,
children refuse school for one or more of the following reasons, or functions: (a)
avoidance of school-based stimuli that provoke negative affectivity, (b) escape from
aversive school-based social and/or evaluative situations, (c) pursuit of attention from
significant others, and (d) pursuit of tangible rewards outside of school. The first
two functions are anxiety-based and refer to youths who refuse school for negative
reinforcement. Treatment for these youths would include the strategies discussed in
the previous section.
The latter two functions are often non-anxiety-based and refer to youths who refuse
school for positive reinforcement, or to pursue more alluring stimuli outside of school.
Chronic cases of school refusal behavior often involve a combination of these functions
(Evans, 2000). Youths who refuse school for positive reinforcement receive several
cognitive behavioral treatment strategies that are targeted primarily toward parents
and/or family members. These strategies include contingency management and
contingency contracting as well as related practices such as forced school attendance,
communication skills training, peer refusal skills training, attendance journals, and
escorts to school and class. These strategies are described next.
Contingency management is a parent-based approach typically used for children who
refuse school to pursue attention from significant others such as parents. Components
of contingency management for this population include developing regular morning
and daily routines, altering parent commands toward brevity and clarity, ignoring or
extinguishing minor school refusal behaviors such as tantrums, and providing con-
sequences for attendance and nonattendance. Contingency management procedures
may be conducted in conjunction with consultation with school officials.
A key aspect of contingency management for school refusal behavior is to develop
set morning routines that include regular times for tasks such as rising from bed,
eating breakfast, dressing, and preparing school materials. Many families in this group
have chaotic morning routines, so developing a consistent schedule that affords time
for each key task is important. In addition, children may receive immediate and later
rewards for adhering to the morning routine without misbehaviors such as tantrums.
Immediate rewards could include free time and activities before school if all tasks are
completed and later rewards could include later bedtime or extra time spent with a
parent. Failure to adhere to the morning routine would result in loss of free time
and/or some loss of privilege that night. Positive and negative consequences are also
established regarding morning misbehaviors such as tantrums or excessive dawdling.
Another key component of contingency management for this population is to
modify parent commands toward greater brevity and clarity. Parents are discouraged
from negotiating, bribing, lecturing, criticizing, or pleading with their child and
instead encouraged to issue brief, clear commands that focus on school preparation.
In related fashion, parents are encouraged to ignore or extinguish minor inappropriate
behaviors such as complaints about school or persistent requests to remain home.
Parents are also encouraged to reduce excessive reassurance-seeking behavior in their
children by answering a child’s question only once and subsequently ignoring other
pleadings.
Contingency management works well for children whose school refusal behavior
is motivated by attention, but forced school attendance may be used in rare circum-
stances. Forced school attendance involves a procedure whereby parents bring a child
to school and deposit him with school officials who escort the child to his classroom.
Forced school attendance has been advocated in the literature as an effective strategy
(Kennedy, 1965) but is recommended for use only under the following circumstances:
when the child is less than 11 years of age, missing most days of school, understands
the procedure, and refuses school only for attention and without significant distress,
and when there are two parents who are willing to take the child to school, and school
officials who are willing to take the child to class (Kearney & Albano, 2007).
Contingency Contracting
Contingency contracting is a family-based approach involving written contracts
between a youth and his or her parents to increase incentives for school attendance
and disincentives for school nonattendance. Contingency contracting is typically
used for youths who refuse school to pursue tangible rewards outside of school
(e.g., time with friends). Youths in this function tend to have more chronic school
refusal behavior as well as greater absenteeism, family conflict, and externalizing
behavior problems than youths who refuse school for other functions. Contingency
contracting is thus an appropriate method for helping family members improve their
communication and problem-solving skills while focusing on the immediate issue of
school attendance.
Written contracts are commonly constructed between the youth (typically an
adolescent) and his or her parents. Initial contracts may focus on school preparation
behaviors, especially if a child has been out of school for some time and has difficulty
rising in the morning before school. Later contracts may focus on part-time school
attendance (e.g., half-day, three classes) and then full-time school attendance. School
preparation and/or attendance are then reinforced with tangible rewards such as time
with friends on the weekend or payment for completed chores. Tangible disincentives
may be incorporated into the contract as well for absenteeism and may include
fines or loss of privileges. Contracts are generally short (e.g., 1 week) to allow
for modification as the child’s attendance improves. In addition, contracts must be
negotiated with equal input from the adolescent and his or her parents (Kearney &
Albano, 2007).
Other Strategies
Other strategies are often made part of contingency management and contracting
procedures for school refusal behavior. One strategy, especially for older youths and
their parents, is communication skills training. Communication skills training involves
improvements in careful listening, paraphrasing, and appropriate responses in addition
to limits on unhelpful behaviors such as interruptions, insults, and yelling (Khanna &
Kendall, 2009). Communication skills training may be particularly useful during the
contract development phase and for families with longstanding conflict regarding a
child’s school refusal behavior.
Peer refusal skills training is another ancillary strategy for school refusal behavior
whereby a youth is taught methods to refuse offers to miss school or to avoid
high-risk situations that provoke absenteeism. Many youths are lured by friends to
miss school and may not otherwise do so if not tempted. Peer refusal skills training
is thus used to help youths construct appropriate verbal responses to such offers and
avoid embarrassment. In addition, youths are encouraged to avoid places and times
in school where such offers are mostly likely to occur (e.g., the school locker area at
11 a.m.).
Attendance journals are also used to help monitor attendance. A child is required
to attend each class and secure a signature from the teacher confirming his or her
presence. Such logs are then presented to parents for appropriate consequences. In
cases where contracts and attendance journals are insufficient, then escorting a child
to school and from class to class may be implemented. Escorts may involve relatives or
school-based personnel who can ensure the youth attends each class. Escorts usually
must be phased out with time, but are nevertheless useful to help a child secure
tangible rewards that will hopefully produce greater attendance.
Empirical Support
Researchers have found empirical support for a functionally-based, prescriptive treat-
ment approach that includes anxiety-based and non-anxiety-based cases of school
refusal behavior (Chorpita, Albano, Heimberg, & Barlow, 1996; Kearney, 2002;
Kearney, Pursell, & Alvarez, 2001; Kearney & Silverman, 1990; Tolin et al., 2009).
Prescriptive treatment, or intervention administered on the basis of a youth’s primary
function of school refusal behavior, has also been found superior to nonprescriptive
treatment, or intervention administered on the basis of a youth’s least influential
function of school refusal behavior (Kearney & Silverman, 1999).
Pina et al. (2009) conducted a meta-analysis of psychosocial (and largely cognitive
behavioral) interventions for school refusal behavior. Across group design studies,
school attendance improved from 30% at pretest to 75% at posttest (range at posttest:
47–100%). Effect sizes were also calculated for continuous variables associated with
school refusal behavior such as anxiety, fear, and depression. These effect sizes were
quite variable (range: –0.40–4.64), leading the authors to conclude that CBT may
be more effective for some domains (e.g., anxiety) than others (e.g., depression).
These authors contended that further research is needed to pinpoint which specific
interventions are best for individual cases of school refusal behavior, to include a wider
swath of youths who refuse school, to refine interventions to maximize effectiveness,
and to identify which youths are most likely to benefit from treatment. Mediators
of behavior change, such as enhanced self-efficacy for solving school-based problems
and addressing stressors, must also be examined more closely (Pina et al., 2009).
Broader Treatment for School Refusal Behavior
Professionals from disciplines other than psychology have also designed broader
treatment strategies for youths with school refusal behavior that include some cognitive
behavioral components. These strategies are designed to address large numbers of
youth with problematic absenteeism and to account for the many contextual variables
that affect absenteeism (Kearney, 2008). These broader strategies include school-
based truancy courts, other school-based programs, and mental health and related
initiatives. These strategies are described next.
School-Based Truancy Courts

A popular model to reduce absenteeism is to move traditional truancy courts into
school buildings. These “hybrid” efforts are designed to reduce stigmatization and
transportation problems, emphasize a multidisciplinary problem-solving approach to
minimize obstacles to attendance, increase parental involvement, and provide psy-
chosocial and other services. Sanctions from these courts are designed to promote
school attendance and may include school-based community service and extracur-
ricular activities. The courts may also mandate drug testing, family-based and other
therapy, tutoring, and meetings with teacher mentors (Smink & Reimer, 2005).
Several researchers have examined the utility of these school-based truancy court
programs and found them to be successful for reducing absenteeism. These pro-
grams often have elements related to cognitive behavioral practices. Shoenfelt and
Huddleston’s (2006) program involved home visits to investigate factors related
to absenteeism, meetings with a judge, parenting classes, academic tutoring, anger
management, mentoring, and support groups. Richtman’s (2007) program involved
inviting absentee students and their parents to school-based meetings with a county
attorney, school social worker or counselor, or probation officer to create a school
attendance plan. The meetings also included referrals to social services agencies, sub-
stance use and mental health evaluations, and student or family counseling to address
nonattendance. Fantuzzo, Grim, and Hazan (2005) placed court proceedings within
school buildings and linked families with caseworkers from various service organi-
zations. Hendricks, Sale, Evans, McKinley, and Carter (2010) required students to
attend regular truancy court sessions in school, complete assigned work, and avoid
substance use and confrontations with peers.
Other School-Based Programs

Other broader strategies for absenteeism include school-wide initiatives. A good
example is the Check and Connect program, which emphasizes relationship building,
routine monitoring of attendance, school-based support tailored to individual student
needs, academic motivation, conflict resolution skills, and student access to school-
related activities and events. This program has successfully reduced full absences and
tardiness rates (Lehr, Sinclair, & Christenson, 2004).
Another broader strategy is to restructure an existing school to address climate
factors that may be affecting attendance. The Positive Behavioral Intervention and
Supports (PBIS) program is designed to emphasize prosocial skills and behaviors,
monitor student attendance and other disciplinary issues regularly, and imple-
ment evidence-based behavioral practices such as the cognitive behavioral methods
described earlier (Sailor et al., 2006). PBIS is typically implemented by a small,
school-based team of teachers, psychologists, counselors, or social workers, though
some have advocated that the team be expanded to include administrators, parents,
and community members (Sugai & Horner, 2006).
Another broader strategy involves alternative educational programs that emphasize
small class size, project-based and cooperative learning, individualized and interdis-
ciplinary instruction such as vocational or technical skills training, apprenticeships,
and diverse instructional methods such as computers, direct experience, and service-
learning activities. Such programs may also include home study and in-class or
laboratory work, extended class time, summer coursework, work release, or afternoon
or evening classes. Students in these programs are supervised closely, receive extended
instruction for troublesome subjects, obtain specialized training that fits the business
needs of a local community (e.g., finance, tourism), and earn equivalent college course
credit (Detgen & Alfeld, 2011; Dupper, 2008).
Sutphen, Ford, and Flaherty (2010) reviewed 16 studies of truancy interventions
that used group comparison or one-group pretest/posttest designs. Broader inter-
ventions that seemed effective for reducing truancy included school-based structural
changes such as smaller and more independent academic units as well as alternative
educational programs. A meta-analysis of truancy and dropout prevention programs
for middle and high school students also revealed that alternative educational programs
were best for reducing dropout and enhancing attendance, academic achievement, and
graduation rates (Klima, Miller, & Nunlist, 2009). Others have concluded that school
dropout prevention programs are most successful if they involve an individualized
approach that tailors intervention to the academic, health, skills, social, and resource
needs of students and their families (Christenson & Thurlow, 2004; Dynarski &
Gleason, 2002). The most effective programs target students who are behind in grade
level and provide occupational training programs with equivalency diploma assistance
(Mac Iver, 2011).
Mental Health and Related Initiatives

Broader school-based strategies for problematic absenteeism have also included mental
health and related initiatives. These initiatives include strategies to reduce emotional,
learning, and disruptive behavior disorders and substance use or to enhance coping
skills (Weist, Stiegler, Stephan, Cox, & Vaughan, 2010). Other programs focus on
conflict resolution, anger management, peer mediation, coping with divorce or family
conflict, and sex education (Brown & Bolen, 2008). Youth and parent support groups
are sometimes advocated to develop social and family communication and parenting
skills and to reduce obstacles to attendance (White & Kelly, 2010). These initiatives
are sometimes linked to anti-bullying and school safety efforts (Vreeman & Carroll,
2007) as well as academic skills training (e.g., study, organization, time management)
and peer mentoring (Prevatt & Kelly, 2003; Teasley, 2004).
Related to mental health strategies are those that promote social-emotional learning
to reduce absenteeism. Snyder et al. (2010) implemented a character development
program of 140 interactive lessons. These lessons involved (a) self-concept (relation-
ship among thoughts, feelings, and behaviors), (b) physical and intellectual actions
(e.g., hygiene, nutrition, decision-making skills), (c) social and emotional actions
(e.g., self-control, time management), (d) interpersonal skills (e.g., empathy, con-
flict resolution), (e) integrity and self-appraisal, and (f) self-improvement (e.g., goal
setting, problem solving, persistence). Schools using this intervention had signifi-
cantly higher reading and math scores, lower absenteeism, and fewer suspensions and
retentions than control schools.
Conclusion
Cognitive behavioral and related strategies to reduce school absenteeism have garnered
increased empirical support over the past 20 years. Various kinds of problematic
absenteeism in children have been addressed, including children with and without
anxiety symptoms and those in clinical as well as educational settings. However, the
range of mental health, educational, and other professionals who study the assessment
and treatment of this population remains disparate. As such, little consensus has
developed about the best way to address all youths with problematic absenteeism
and the best way to disseminate effective treatment strategies to nonclinical settings.
In addition, researchers are faced with the unenviable task of having to address the
many contextual factors associated with this population. Greater collaboration across
professionals from various disciplines is thus encouraged to help address these unique
challenges.
References
Bernstein, G. A., Borchardt, C. M., Perwein, A. R., Crosby, R. D., Kushner, M. G., Thuras,
P. D., & Last, C. G. (2000). Imipramine plus cognitive-behavioral therapy in the treatment
of school refusal. Journal of the American Academy of Child and Adolescent Psychiatry, 39,
276–283. doi:10.1097/00004583-200003000-00008
Brown, M. B., & Bolen, L. M. (2008). The school-based health center as a resource for preven-
tion and health promotion. Psychology in the Schools, 45, 28–38. doi:10.1002/pits.20276
Chorpita, B. F., Albano, A. M., Heimberg, R. G., & Barlow, D. H. (1996). A systematic repli-
cation of the prescriptive treatment of school refusal behavior in a single subject. Journal
of Behavior Therapy and Experimental Psychiatry, 27 , 281–290. doi:10.1016/S0005-
7916(96)00023-7
Christenson, S. L., & Thurlow, M. L. (2004). School dropouts: Prevention considerations,
interventions, and challenges. Current Directions in Psychological Science, 13, 36–39.
doi:10.1111/j.0963-7214.2004.01301010.x
Detgen, A., & Alfeld, C. (2011). Replication of a career academy model: The Georgia Central
Educational Center and four replication sites. Washington, DC: U.S. Department of
Education, Institute of Education Sciences, National Center for Education Evaluation
and Regional Assistance, Regional Educational Laboratory Southeast.
Dupper, D. R. (2008). Guides for designing and establishing alternative school programs
for dropout prevention. In C. Franklin, M. B. Harris, & P. Allen-Meares (Eds.),
The school practitioner’s concise companion to preventing dropout and attendance prob-
lems (pp. 23–34). New York, NY: Oxford University Press. doi:10.1093/acprof:oso/
9780195370577.003.0003
Dynarski, M., & Gleason, P. (2002). How can we help? What we have learned from recent
federal dropout prevention evaluations. Journal of Education for Students Placed at Risk,
7 , 43–69. doi:10.1207/S15327671ESPR0701_4
Egger, H. L., Costello, E. J., & Angold, A. (2003). School refusal and psychiatric disorders: A
community study. Journal of the American Academy of Child and Adolescent Psychiatry,
42, 797–807. doi:10.1097/01.CHI.0000046865.56865.79
EPE Research Center. (2008). Closing the graduation gap: Educational and economic conditions
in America’s largest cities. Bethesda, MD: Editorial Projects in Education.
Evans, L. D. (2000). Functional school refusal subtypes: Anxiety, avoidance, and malingering.
Psychology in the Schools, 37 , 183–191. doi:10.1002/(SICI)1520-6807(200003)37:2
<183::AID-PITS9>3.0.CO;2–5
Fantuzzo, J., Grim, S., & Hazan, H. (2005). Project START: An evaluation of a community-
wide school-based intervention to reduce truancy. Psychology in the Schools, 42, 657–667.
doi:10.1002/pits.20103
Hendricks, M. A., Sale, E. W., Evans, C. J., McKinley, L., & Carter, S. D. (2010). Evaluation
of a truancy court intervention in four middle schools. Psychology in the Schools, 47 ,
173–183. doi:10.1002/pits.20462
Heyne, D., King, N. J., Tonge, B. J., Rollings, S., Young, D., Pritchard, M., & Ollendick,
T. H. (2002). Evaluation of child therapy and caregiver training in the treatment of
school refusal. Journal of the American Academy of Child and Adolescent Psychiatry, 41,
687–695. doi:10.1097/00004583-200206000-00008
Heyne, D., Sauter, F. M., Van Widenfelt, B. M., Vermeiren, R., & Westenberg, P. M. (2011).
School refusal and anxiety in adolescence: Non-randomized trial of a developmen-
tally sensitive cognitive behavioral therapy. Journal of Anxiety Disorders, 25, 870–878.
doi:10.1016/j.janxdis.2011.04.006
Hibbett, A., & Fogelman, K. (1990). Future lives of truants: Family formation and
health-related behaviour. British Journal of Educational Psychology, 60, 171–179.
doi:10.1111/j.2044-8279.1990.tb00934.x
Hibbett, A., Fogelman, K., & Manor, O. (1990). Occupational outcomes of truancy. British
Journal of Educational Psychology, 60, 23–36. doi:10.1111/j.2044-8279.1990.tb00919.x
Kearney, C. A. (2001). School refusal behavior in youth: A functional approach to assessment and
treatment. Washington, DC: American Psychological Association.
Kearney, C. A. (2002). Case study of the assessment and treatment of a youth with
multifunction school refusal behavior. Clinical Case Studies, 1, 67–80. doi:10.1177/
1534650102001001006
Kearney, C. A. (2005). Social anxiety and social phobia in youth: Characteristics, assessment, and
psychological treatment. New York, NY: Springer.
Kearney, C. A. (2007). Forms and functions of school refusal behavior in youth: An empirical
analysis of absenteeism severity. Journal of Child Psychology and Psychiatry, 48, 53–61.
doi:10.1111/j.1469-7610.2006.01634.x
Kearney, C. A. (2008). An interdisciplinary model of school absenteeism in youth to inform
professional practice and public policy. Educational Psychology Review, 20, 257–282.
doi:10.1007/s10648-008-9078-3
Kearney, C. A. (2010). Helping youths with selective mutism and their parents: A guide for
school-based professionals. New York, NY: Oxford University Press.
Kearney, C. A., & Albano, A. M. (2004). The functional profiles of school refusal
behavior: Diagnostic aspects. Behavior Modification, 28, 147–161. doi:10.1177/
0145445503259263
Kearney, C. A., & Albano, A. M. (2007). When children refuse school: A cognitive-behavioral
therapy approach/therapist guide. New York, NY: Oxford University Press.
Kearney, C. A., Pursell, C., & Alvarez, K. (2001). Treatment of school refusal behavior in
children with mixed functional profiles. Cognitive and Behavioral Practice, 8, 3–11.
doi:10.1016/S1077-7229(01)80037-7
Kearney, C. A., & Silverman, W. K. (1990). A preliminary analysis of a functional model of
assessment and treatment for school refusal behavior. Behavior Modification, 14, 340–366.
doi:10.1177/01454455900143007
Kearney, C. A., & Silverman, W. K. (1996). The evolution and reconciliation of taxonomic
strategies for school refusal behavior. Clinical Psychology: Science and Practice, 3, 339–354.
doi:10.1111/j.1468-2850.1996.tb00087.x
Kearney, C. A., & Silverman, W. K. (1999). Functionally-based prescriptive and nonprescriptive
treatment for children and adolescents with school refusal behavior. Behavior Therapy, 30,
673–695. doi:10.1016/S0005-7894(99)80032-x
Kennedy, W. A. (1965). School phobia: Rapid treatment of 50 cases. Journal of Abnormal
Khanna, M. S., & Kendall, P. C. (2009). Exploring the role of parent training in the treatment
of childhood anxiety. Journal of Consulting and Clinical Psychology, 77 , 981–986.
doi:10.1037/a0016920
King, N. J., Tonge, B. J., Heyne, D., Pritchard, M., Rollings, S., Young, D., … Ollendick,
T. H. (1998). Cognitive-behavioral treatment of school-refusing children: A controlled
evaluation. Journal of the American Academy of Child and Adolescent Psychiatry, 37 ,

395–403. doi:10.1097/00004583-199804000-00017
Klima, T., Miller, M., & Nunlist, C. (2009). What works? Targeted truancy and dropout
programs in middle and high school. Olympia, WA: Washington State Institute for Public
Policy.
Kogan, S. M., Luo, Z., Murry, V. M., & Brody, G. H. (2005). Risk and protective factors
for substance use among African American high school dropouts. Psychology of Addictive
Behaviors, 19, 382–391. doi:10.1037/0893-164X.19.4.382
Last, C. G., Hansen, C., & Franco, N. (1998). Cognitive-behavioral treatment of school
phobia. Journal of the American Academy of Child and Adolescent Psychiatry, 37 , 404–411.
doi:10.1097/00004583-199804000-00018
Layne, A. E., Bernstein, G. A., Egan, E. A., & Kushner, M. G. (2003). Predictors of treatment
response in anxious-depressed adolescents with school refusal. Journal of the American
Academy of Child and Adolescent Psychiatry, 42, 319–326. doi:10.1097/00004583-
200303000-00012
Lehr, C. A., Sinclair, M. F., & Christenson, S. L. (2004). Addressing student engagement
and truancy prevention during the elementary school years: A replication study of the
Check & Connect model. Journal of Education for Students Placed at Risk, 9, 279–301.
doi:10.1207/s15327671espr0903_4
Mac Iver, M. A. (2011). The challenge of improving urban high school graduation outcomes:
Findings from a randomized study of dropout prevention efforts. Journal of Education for
Students Placed at Risk, 16, 167–184. doi:10.1080/10824669.2011.584497
McShane, G., Walter, G., & Rey, J. M. (2001). Characteristics of adolescents with school
refusal. Australian and New Zealand Journal of Psychiatry, 35, 822–826. doi:10.1046/
j.1440–1614.2001.00955.x
National Center for Education Statistics. (2006). The condition of education 2006. Washington,
DC: U.S. Department of Education.
Pina, A. A., Zerr, A. A., Gonzales, N. A., & Ortiz, C. D. (2009). Psychosocial interventions
for school refusal behavior in children and adolescents. Child Development Perspectives, 3,
11–20. doi:10.1111/j.1750-8606.2008.00070.x
Prevatt, F., & Kelly, F. D. (2003). Dropping out of school: A review of intervention programs.
Journal of School Psychology, 41, 377–395. doi:10.1016/S0022-4405(03)00087-6
Reinecke, M. A., Dattilio, F. M., & Freeman, A. (Eds.). (2003). Cognitive therapy with children
and adolescents: A casebook for clinical practice (2nd ed.). New York, NY: Guilford Press.
Richtman, K. S. (2007). The truancy intervention program of the Ramsey County Attorney’s
Office: A collaborative approach to school success. Family Court Review, 45, 421–437.
doi:10.1111/j.1744-1617.2007.00157.x
Sailor, W., Zuna, N., Choi, J.-H., Thomas, J., McCart, A., & Roger, B. (2006). Anchoring
schoolwide positive behavior support in structural school reform. Research and Practice
for Persons with Severe Disabilities, 31, 18–30. doi:10.2511/rpsd.31.1.18
Shoenfelt, E. L., & Huddleston, M. R. (2006). The Truancy Court Diversion Program of
the Family Court, Warren Circuit Court Division III, Bowling Green, Kentucky: An
evaluation of impact on attendance and academic performance. Family Court Review, 44,
683–695. doi:10.1111/j.1744-1617.2006.00119.x
Silverman, W. K., & Kurtines, W. M. (1996). Anxiety and phobic disorders: A pragmatic
approach. New York, NY: Plenum.
Smink, J., & Reimer, M. S. (2005). Fifteen effective strategies for improving student attendance
and truancy prevention. Clemson, SC: National Dropout Prevention Center.
Snyder, F. J., Flay, B. R., Vuchinich, S., Acock, A., Washburn, I. J., Beets, M. W., & Li, K.-K.
(2010). Impact of a social-emotional and character development program on school-level
indicators of academic achievement, absenteeism, and disciplinary outcomes: A matched-

pair, cluster randomized, controlled trial. Journal of Research on Educational Effectiveness,
3, 26–55. doi:10.1080/19345740903353436
Spence, S. H., Donovan, C., & Brechman-Toussaint, M. (2000). The treatment of childhood
social phobia: The effectiveness of a social skills training-based, cognitive-behavioural
intervention, with and without parental involvement. Journal of Child Psychology and
Psychiatry, 41, 713–726. doi:10.1111/1469-7610.00659
Sugai, G., & Horner, R. R. (2006). A promising approach for expanding and sustaining
school-wide positive behavior support. School Psychology Review, 35, 245–259.
Sutphen, R. D., Ford, J. P., & Flaherty, C. (2010). Truancy interventions: A review of
the research literature. Research on Social Work Practice, 20, 161–171. doi:10.1177/
1049731509347861
Suveg, C., Aschenbrand, S. G., & Kendall, P. C. (2005). Separation anxiety disorder, panic
disorder, and school refusal. Child and Adolescent Psychiatric Clinics of North America,
14, 773–795. doi:10.1016/j.chc.2005.05.005
Teasley, M. L. (2004). Absenteeism and truancy: Risk, protection, and best practice implications
for school social workers. Children and Schools, 26, 117–128. doi:10.1093/cs/26.2.117
Tolin, D. F., Whiting, S., Maltby, N., Diefenbach, G. J., Lothstein, M. A., Hardcastle, S., …
Gray, K. (2009). Intensive (daily) behavior therapy for school refusal: A multiple base-
line case series. Cognitive and Behavioral Practice, 16, 332–344. doi:10.1016/j.cbpra.
2009.02.003
Tramontina, S., Martins, S., Michalowski, M. B., Ketzer, C. R., Eizirik, M., Biederman, J.,
& Rohde, L. A. (2001). School dropout and conduct disorder in Brazilian elementary
school students. Canadian Journal of Psychiatry, 46, 941–947.
Vreeman, R. C., & Carroll, A. E. (2007). A systematic review of school-based interven-
tions to prevent bullying. Archives of Pediatric and Adolescent Medicine, 161, 78–88.
doi:10.1001/archpedi.161.1.78
Walter, D., Hautmann, C., Rizk, S., Petermann, M., Minkus, J., Sinzig, J., … Doepfner,
M. (2010). Short term effects of inpatient cognitive behavioral treatment of adolescents
with anxious-depressed school absenteeism: An observational study. European Child and
Adolescent Psychiatry, 19, 835–844. doi:10.1007/s00787-010-0133-5
Weist, M. D., Stiegler, K., Stephan, S., Cox, J., & Vaughan, C. (2010). School mental health
and prevention science in the Baltimore city schools. Psychology in the Schools, 47 , 89–100.
doi:10.1002/pits.20453
White, S. W., & Kelly, F. D. (2010). The school counselor’s role in school dropout prevention.
Journal of Counseling and Development, 88, 227–235.
38
Social Anxiety Disorder
Laura C. Bruce and Richard G. Heimberg
Adult Anxiety Clinic of Temple University, Philadelphia, PA, United States
Social anxiety disorder (SAD), also known as social phobia, is one of the most
prevalent mental disorders, affecting up to 12–13% of the population at some point in
life (Ruscio et al., 2008). SAD is characterized by a marked or persistent fear of one or
more social or performance situations (DSM-IV-TR; American Psychiatric Association
[APA], 2000). The central concern for persons with SAD is that they will say or
do something to elicit negative evaluation from others or that they will demonstrate
excessive symptoms of anxiety. A distinction is also made between generalized SAD,
in which anxiety is present across most social situations, and nongeneralized SAD, in
which anxiety is constrained to a limited number of specific situations (e.g., public
speaking). SAD shows an earlier onset than many other psychiatric disorders (Kessler
et al., 2005). Symptoms typically develop during early childhood or adolescence
(Reich, 1986) and tend to be unremitting without treatment (Bruce et al., 2005).
Social fears and avoidance of social situations appear to be normally distributed
in the population, and SAD represents high levels on a unitary dimension of social
anxiety (Mattick & Clarke, 1998). The widespread presence of subclinical levels of
social anxiety has historically resulted in a minimization of the severity of the disorder.
However, research has shown SAD to be a devastating condition, affecting career,
academic, and general social functioning (Acarturk, de Graaf, van Straten, ten Have,
& Cuijpers, 2008; Schneier et al., 1994). Compared to their nonanxious peers,
individuals with SAD report fewer friends and dating partners (Rodebaugh, 2009;
Wenzel, 2002) and jobs that are less prestigious than would be expected based on
their level of education (Bruch, Fallon, & Heimberg, 2003). They are also less likely
to marry than those suffering from other anxiety disorders (Sanderson, DiNardo,
Rapee, & Barlow, 1990).
Individuals with SAD fear social interaction or performance situations in which oth-
ers may judge them as awkward, inferior, unintelligent, or incompetent. Commonly

Edited by Stefan G. Hofmann. Volume III edited by Jasper A.J. Smits.
DOI: 10.1002/9781118528563.wbcbt38
feared situations include initiating and maintaining conversation, talking to authority

figures or strangers, dating, formal speaking, participating in meetings or classes, and
performing tasks in front of an audience. Individuals with SAD often experience
physical symptoms of anxiety, such as heart palpitations, sweating, trembling, and
abdominal distress. For some, physical symptoms become so intense that they meet
criteria for a panic attack. In contrast to those in panic disorder, however, panic
attacks in SAD are situationally bound and triggered by the fear of negative evalua-
tion. Nevertheless, those with SAD who experience panic attacks tend to have more
severe social anxiety, as well as greater hopelessness (Jack, Heimberg, & Mennin,
1999). Together with cognitions about the likelihood of being judged negatively, the
aversive physical symptoms of social anxiety often compel overt avoidance of feared
situations, subtle avoidance of particular aspects of a situation, deficits in approach
behavior, and submissive social displays.
Theoretical Models of Social Anxiety Disorder
In the 1990s, two similar cognitive behavioral models of social anxiety were advanced
(Clark & Wells, 1995; Rapee & Heimberg, 1997). These models emphasize the
role of cognitive processes during an anxiety-provoking event in maintaining social
fears. In Rapee and Heimberg’s (1997) model, social anxiety first arises with the
perception of an evaluative audience. Subsequently, the individual formulates a mental
representation of the self as seen by the audience. Both models suggest that individuals
with SAD collect information about how they appear to others in maladaptive ways.
Clark and Wells (1995) emphasized the problem of excessive self-focused attention, in
which interoceptive cues (e.g., aversive physiological arousal) are used to gauge how
one must appear to others. This internal monitoring could, for example, lead a socially
anxious man who registers heat in his cheeks to assume that his face appears bright red
to others. Rapee and Heimberg asserted that, in addition to monitoring for internal
symptoms of anxiety, persons with SAD scan the outward environment for signs they
are performing poorly (e.g., signs of boredom from an interactional partner) and
incorporate this potentially inaccurate information into the mental representation of
the self as seen by others.
Once conjured, this mental representation is compared with the audience’s pre-
sumed standards to judge the likelihood of being evaluated (Rapee & Heimberg,
1997; also see Heimberg, Brozovich, & Rapee, 2010). As the discrepancy between
an individual’s self-representation and the audience’s presumed standards grows, so
does the belief that others are forming a negative opinion. The symptoms of anxiety
which follow this estimation attune the individual to negative internal and external
cues, and attention to these cues further distorts the mental representation of the self
as seen by others. This vicious cycle continues, and anxiety climbs as the perceived
probability of evaluation increases. Additionally, because it is a challenge to remain
socially engaged while simultaneously monitoring the self for unacceptable behav-
iors and scanning the environment for signs of threat, this division of attentional
resources has the potential to disrupt social performance and invite true negative
evaluation.
Social Anxiety Disorder 897
Upon perceiving that one is being negatively evaluated, Wells, Clark, Salkovskis,
and Ludgate (1995) and Clark (2001) assert that socially anxious individuals engage
in a range of compensatory “safety behaviors” intended to reduce visible signs of
anxiety and avert negative consequences. For example, the woman who believes no
one at the party is interested in talking to her may play games on her cell phone to
appear busy. Whereas safety behaviors may reduce anxiety in the short term, they may
maintain anxiety in the long term by preventing the unambiguous disconfirmation of
unrealistic beliefs (Wells et al., 1995).
After an anxiety-evoking event has occurred, individuals with SAD typically engage
in postevent processing—the repeated consideration and potential reconstruction
of one’s previous performance. Socially anxious individuals tend to recall selectively
and brood over information which confirms negative assumptions about the self
and others, and this process invariably maintains or worsens the negative mood
state. A growing literature points to the importance of postevent processing in the
maintenance of SAD (Brozovich & Heimberg, 2008).
Since the publication of Clark and Wells’s (1995) and Rapee and Heimberg’s
(1997) theoretical models, numerous studies have refined our understanding of the
cognitive factors implicated in SAD. The tendency for socially anxious individu-
als to selectively process social threat cues in the environment (e.g., angry faces)
has been well established (e.g., Gilboa-Schechtman, Foa, & Amir, 1999; Veljaca
& Rapee, 1998). Persons with SAD also tend to hold high behavioral standards
for themselves and believe that others share these high standards (Hofmann &
Otto, 2008). Although these individuals wish to make a positive impression, they
lack confidence in their ability to do (Leary, 2010) and overestimate the proba-
bility and costs of social mishaps (e.g., Foa, Franklin, Perry, & Herbert, 1996).
Socially anxious individuals also tend to believe they have little control over their
emotions (Hofmann & Barlow, 2002) and display an inability to clearly define
social goals and develop strategies to reach them (Hiemisch, Ehlers, & Wester-
mann, 2002). Based on these findings, Hofmann (2007) put forth an additional
model, which construes social apprehension as the product of unrealistic social
standards and an inability to select specific attainable social goals. According to
Hofmann, when persons with SAD enter anxiety-provoking situations, they shift
their attention toward internal symptoms of anxiety, view themselves as negative
social objects who are unlikely to meet the audience’s high standards, underestimate
their own control over their emotions, and overestimate the costs of negative social
experiences.
Cognitive Behavioral Interventions for

Social Anxiety Disorder
Cognitive behavioral therapy (CBT) is a family of psychosocial techniques and strate-

gies designed to modify distorted cognitions and maladaptive behavior. Theoretical
models of SAD imply that, to reduce social anxiety successfully, treatment must
provide clients with the opportunity to reevaluate old and construct new cognitive
representations of themselves in the presence of others. Consistent with this, the
best-supported cognitive behavioral strategies for SAD involve exposure to feared

situations and the combination of exposure and cognitive restructuring. Social skills
training and relaxation exercises are also commonly used.
Exposure
Broadly, exposure refers to a family of strategies that require contact with the feared
stimulus. In the treatment of SAD, exposure to feared social situations may be
direct or indirect. For example, the man who fears dating could repeatedly visualize
himself asking women out on dates, role play the experience with his therapist, or
speak to and eventually invite out a potential dating partner. From a behavioral
perspective, exposure provides a context for the natural habituation of unpleasant
physiological arousal and increases exposure to reinforcers inherent in the social
environment (McNeil, Lejuez, & Sorrel, 2010). Individuals with SAD may have
long avoided the situations that make them anxious, thereby diminishing their
opportunities to experience physiological habituation or the rewards of nonphobic
behavior.
Avoidance also protects distorted, anxiety-maintaining beliefs. The man who fears
dating may, for example, avoid approaching women because of a belief that his
anxiety will escalate to the point that he will panic and appear foolish. Cogni-
tive behavioral models of SAD assert that exposure presents an opportunity to
experience powerful, corrective feedback, which reduces anxiety by facilitating the
modification of maladaptive beliefs (e.g., that anxiety will increase exponentially if
the feared situation is not avoided). Consistent with this idea, exposure has been
shown to be more effective when clients are instructed to eliminate safety behav-
iors and focus their attention completely on the experience (Wells et al., 1995;
Wells & Papageorgiou, 1998), thereby accessing the full physiological arousal asso-
ciated with the feared situation (Foa & Kozak, 1986). Although research supports
exposure’s efficacy in reducing social anxiety (e.g., Al-Kubaisy, Marks, Logsdail, &
Marks, 1992; Alström, Nordlund, Persson, Hårding, & Ljungqvist, 1984), there
is some question as to the durability of gains when exposure is not coupled
with techniques directly addressing maladaptive cognitions (Heimberg & Juster,
1995).
Current cognitive models of SAD propose that anxiety is largely maintained via
biased information processing and dysfunctional beliefs (e.g., Clark & Wells, 1995;
Heimberg et al., 2010), and most cognitive behavioral treatments for SAD use
cognitive restructuring techniques to address these distortions directly. During cog-
nitive restructuring, the therapist and client collaboratively identify distorted or
maladaptive cognitions and challenge them using strategies such as Socratic ques-
tioning, logical disputation, and behavioral experiments (Hofmann & Admundson,
2008). An important goal of cognitive restructuring is to develop clients’ ability
to regulate their emotions by reappraising the degree of threat present in feared
situations. Research has demonstrated that this ability to reframe emotional events,
often called cognitive reappraisal, is associated with greater psychological flexibility

and successful emotion regulation (Gross, 2007). Cognitive restructuring is also
commonly used to examine the veracity of clients’ deeply held negative beliefs (e.g.,
“I am unlovable,” or “real men do not experience anxiety”) by examining behavioral
evidence and generating alternative explanations for seemingly confirmatory experi-
ences. Although the therapist may initially play a large role in helping clients find
and articulate realistic alternatives to their negative thoughts and beliefs, the greatest
benefit is derived when clients can generate more balanced points of view on their
own.
Combined Exposure and Cognitive Restructuring

A growing body of research shows considerable support for treatments that combine
exposure with cognitive restructuring. In one of the most widely used CBT protocols
for SAD (Hope, Heimberg, & Turk, 2010), cognitive restructuring is used to identify
the evidence for dysfunctional beliefs prior to and after completing an exposure in
order to directly challenge the veracity of these cognitions. Exposures can also provide
evidence that the true cost of appearing anxious, or experiencing a social mishap, is
lower than initially estimated (Hofmann & Otto, 2008). Many CBT protocols for
SAD involve teaching clients to monitor their own anxiety throughout an exposure or
across multiple exposure experiences using the 0–100 Subjective Units of Discomfort
Scale (Wolpe & Lazarus, 1966). This process encourages clients to study their anxiety
objectively and notice how it tends to decrease across time and experience. Through
the repeated combination of cognitive restructuring and exposure, clients learn to
treat their negative thoughts and beliefs as hypotheses and to consider more realistic
or adaptive interpretations. In turn, they are often more willing to engage in activities
that were previously deemed too anxiety-provoking, with less dependence on safety
behaviors. By modifying dysfunctional thinking patterns, cognitive restructuring
can also improve social performance by reducing interference caused by physical
symptoms of anxiety and freeing up attentional resources. Lastly, the use of cognitive
restructuring may be especially important to protect against ruminative postevent
processing after the exposure.
Relaxation Techniques
Because excessive physical symptoms of anxiety can impair social performance in
those with SAD, relaxation techniques are often used to help clients reduce their
physiological arousal. Several variations on the procedure have been developed, with
differing degrees of empirical support. In progressive muscle relaxation, muscle groups
are alternately tensed and released in a sequential fashion. As a stand-alone treatment,
progressive muscle relaxation has shown little efficacy for SAD (Al-Kubaisy et al.,
1992; Alström et al., 1984). Systematic desensitization, a technique which combines
progressive muscle relaxation with the visualization of increasingly anxiety-provoking
scenes, has been associated with some improvements. However, in controlled studies
these improvements were not superior to those observed in wait-list conditions
(Kanter & Goldfried, 1979; Marzillier, Lambert, & Kellett, 1976).
Research suggests that therapies in which clients gain practice applying relaxation
techniques in specific feared social situations are more promising (Jerremalm, Jansson,
& Öst, 1986). In applied relaxation (AR), clients cultivate an awareness of the earliest
symptoms of anxiety and practice relaxation techniques until they reach a state
of moderate relaxation. Once clients are able to achieve a relaxed state relatively
quickly, this practice is transferred to progressively more difficult real-life situations.
One study directly compared a full CBT protocol to exposure plus AR and a
wait-list control condition (Clark et al., 2006). Both treatments fared better than
the control condition; however, CBT was more effective than AR plus exposure.
It is possible that the addition of relaxation techniques could enhance the efficacy
of exposure and CBT protocols more generally, but this has not been empirically
established.
Social Skills Training

Some research suggests that individuals with SAD display social skills deficits (e.g.,
poor eye contact), though findings are mixed (Rapee & Lim, 1992; Stopa &
Clark, 1993). Individuals with SAD often report that they lack the skills to interact
successfully with others. However, observed behavior during exposures or other
behavioral experiments often falls within normal limits (Rapee & Lim, 1992). When
behavioral deficits are observed, it is unclear whether they are due to a lack of social
or procedural knowledge, the interference of physical symptoms of anxiety, or the
effects of anxious thinking.
Social skills training (SST) is an instructional intervention designed to bolster
the interpersonal skills of individuals with SAD, thereby increasing the likelihood
of positive social outcomes. SST strategies include behavioral rehearsal, therapist
modeling and corrective feedback, homework assignments, and social reinforcement.
Some studies indicate that SST is an effective stand-alone treatment for SAD (Mersch,
Emmelkamp, Bögels, & Van der Sleen, 1989; Trower, Yardley, Bryant, & Shaw,
1978; Wlazlo, Schroeder-Hartwig, Hand, & Kaiser, 1990); however, these studies
failed to include adequate control conditions (Ponniah & Hollon, 2008). In the
only controlled study of stand-alone SST, 15 weeks of training did not produce
larger reductions in social anxiety, social skills deficits, or overall adjustment than
those observed in a wait-list condition (Marzillier et al., 1976). One study comparing
group CBT alone to group CBT plus SST showed superior results for the combined
treatment (Herbert et al., 2005). More research is needed to say whether the
addition of SST to standard CBT protocols enhances their efficacy. One possible
explanation for the mixed findings is that the benefits produced by SST are largely
attributable to the repeated confrontation with feared situations (i.e., exposure) or
the corrective feedback about the acceptability of current interpersonal skills (i.e.,
cognitive restructuring), and not the training per se. It is also possible that there is a
subset of socially anxious individuals who are more likely to benefit from SST, and
indeed one study showed that SST is as effective as cognitive therapy for individuals
for whom the predominant fear is the display of bodily symptoms of anxiety (Bögels &
Voncken, 2008).
Well-Supported Cognitive Behavioral Treatments
Since the publication of the DSM-III (APA, 1980), a large body of research supporting
the efficacy of CBT for SAD has accumulated. Several empirically supported treatment
protocols have been developed, in both group (Heimberg & Becker, 2002) and
individual (Clark et al., 2003; Hope et al., 2010) formats. The literature presented
here focuses on treatments containing some combination of the cognitive and
behavioral strategies described above.
One of the most researched and widely disseminated treatments for SAD is Heim-
berg’s cognitive behavioral group therapy (CBGT; Heimberg & Becker, 2002).
Treatment components include (a) psychoeducation about the factors associated with
the onset and maintenance of social fears, (b) in-session and in vivo exposures, (c) cog-
nitive restructuring, (d) identification and modification of dysfunctional core beliefs,
and (e) homework assignments. In 1990, Heimberg and colleagues compared CBGT
to educational-supportive group therapy, which consisted of lectures about social anx-
iety, discussion, and group support. CBGT produced greater reductions in anxiety,
both during a behavioral test and as rated by an independent assessor, and CBGT
treatment gains were better maintained after 5 years (Heimberg, Salzman, Holt, &
Blendell, 1993). CBGT has also been compared to medication known to be effective
for SAD. Heimberg et al. (1998) conducted a multisite study comparing CBGT, the
monoamine oxidase inhibitor phenelzine, educational-supportive group therapy, and
pill placebo. Of those who completed treatment, 75% of those in the CBGT group
and 77% of those who took phenelzine were classified as treatment responders. In
the second phase of the study, responders to both CBGT and phenelzine received 6
additional months of maintenance treatment (Liebowitz et al., 1999). After an addi-
tional 6-month follow-up, 50% of previous responders to phenelzine had relapsed,
compared to only 17% of previous responders to CBGT. Heimberg and colleagues
have since adapted CBGT to an individual format (Hope et al., 2010), which produces
effect sizes similar to those for the group protocol (Ledley et al., 2009).
Another well-studied treatment is Clark’s individual cognitive therapy (CT) for
SAD. Controlled trials of this protocol have also yielded large effect sizes (Clark
et al., 2003, 2006). Consistent with the Clark and Wells (1995) model, CT includes
exposure and cognitive restructuring, with emphasis on the identification and elimi-
nation of safety behaviors. Here, the therapist and client create a personalized version
of the cognitive behavioral model using the client’s idiosyncratic thoughts, images,
safety behaviors, and attentional strategies. Throughout therapy, negatively distorted
mental representations of the self are modified using video-feedback—in which pre-
dicted performance is compared to actual performance—and redirection of attention
from interoceptive cues toward the task at hand. In the 2003 trial, those in the CT
condition responded significantly better than those in a fluoxetine plus self-exposure
condition or a placebo plus self-exposure condition (Clark et al., 2003). In a study
comparing CT to AR, individuals in the CT condition were twice as likely to be
classified as treatment responders (Clark et al., 2006). Additionally, the gains made
during group or individual CT tended to be maintained when assessed at 5-year
follow-up (Mörtberg, Clark, & Bejerot, 2011).
Cognitive Behavioral Treatments with Preliminary Empirical

Support for Social Anxiety Disorder
Internet-Based Cognitive Behavioral Therapy

Internet-delivered CBT has an expanding evidence base (Hedman et al., 2011; Spek
et al., 2007), and shows promising outcomes for those with SAD (Andersson et al.,
2006; Carlbring et al., 2007, 2009; Tillfors et al., 2008). Although effective in-person
treatments exist, research suggests that many individuals with SAD are reluctant to
seek services for a variety of reasons including uncertainty about where to go, fear
of negative evaluation by the treatment provider, and cost (Olfson et al., 2000). In
fact, many individuals with the most severe social anxiety do not present for in-person
treatment; however, they may use the Internet as a resource (Erwin, Turk, Heimberg,
Fresco, & Hantula, 2004). For this severe group, and for those with limited access to
traditional services, Internet-delivered treatment may represent an attractive option.
The first comprehensive Internet-based CBT for SAD was developed by Andersson
et al. (2006). The treatment protocol included moderated online discussion groups,
educational reading modules and activities, minimal contact with a therapist via
e-mail, and quizzes designed to promote learning and assess clients’ understanding
of the treatment procedures. Additionally, clients participated in two voluntary group
exposure sessions, each lasting 3 hours. In the first randomized trial, participants
in the Internet-based CBT group showed significant improvements in symptoms of
social anxiety, depression, and generalized anxiety compared to the wait-list control
group, and gains were maintained at 1-year follow-up (Andersson et al., 2006).
A trial of a similar treatment that did not include group exposures also produced
significant improvements at posttreatment and 6-month follow-up (Carlbring et al.,
2007). Additionally, treatment adherence rose from 62% in the first trial (Andersson
et al., 2006) to 93% in the second trial (Carlbring et al., 2007) when therapists
made weekly 10-minute phone calls to answer clients’ questions and provide support.
These studies suggest that Internet-based self-help with some therapist contact
represents an efficacious treatment for individuals with SAD; however, future studies
should directly compare Internet-based treatments against well-supported, efficacious
in-person treatments.
Mindfulness- and Acceptance-Based Therapies

Mindfulness- and acceptance-based therapies such as mindfulness-based stress reduc-
tion (MBSR; Kabat-Zinn, 1990), mindfulness-based cognitive therapy (MBCT; Segal,
Williams, & Teasdale, 2002), and acceptance and commitment therapy (ACT; S. C.
Hayes, Strosahl, & Wilson, 1999) are increasingly being used to treat a variety of
psychological disorders including SAD. These approaches, sometimes called “third
wave” or “new wave” cognitive behavioral therapies, use strategies similar to tradi-
tional cognitive behavioral approaches, encouraging clients to reduce avoidance of
important situations due to fear (i.e., exposure) and to form a different relationship
with private thoughts and emotions (Hofmann, Sawyer, & Fang, 2010). However,
whereas traditional CBT entails challenging the veracity or helpfulness of negative

thoughts, mindfulness- and acceptance-based therapies encourage clients to adopt a
depersonalized (“decentered”) view of thoughts as naturally occurring mental events
which do not need to be evaluated or judged.
MBSR, MBCT, and ACT emphasize present-moment focus, and a nonjudgmental
awareness of cognitive, emotional, and physiological processes. Particularly in ACT,
emotional distress is seen as the product of reflexive cognitive and behavioral attempts
to control or banish negative internal experience (i.e., experiential avoidance). Here, it
is not the content of thoughts that are thought to drive distress, but rather the struggle
to control and eliminate these thoughts. A major therapeutic goal is to cultivate an
accepting, nonjudgmental, or curious stance toward one’s thoughts, emotions, and
physiological sensations. Practicing mindfulness, which has been defined as “bringing
one’s complete attention to the present experience on a moment-to-moment basis”
(Marlatt & Kristeller, 1999, p. 4), is an important aspect of these treatments. Painful
thoughts and feelings are thought to diminish when attention is held in the present,
instead of worrying about the future or ruminating about the past. Techniques used to
facilitate present-focused attention and reduce sympathetic reactions include mindful
meditation, body scans, and breath-focused attention (Kabat-Zinn, 2003).
Although more well-controlled research is needed, several studies of acceptance-
and mindfulness-based treatments have shown promising results for individuals with
SAD. A pilot study of ACT integrated with in vivo exposures and SST produced
significant improvements in social anxiety symptoms and quality of life posttreatment
and at follow-up (Dalrymple & Herbert, 2007). Experiential avoidance measured
midtreatment emerged as a key predictor of social anxiety reduction at posttreatment.
Results from a more recent open trial of mindfulness- and acceptance-based group
therapy (Kocovski, Fleming, & Rector, 2009)—a protocol which combines elements
of ACT, MBCT, and exposure—indicate that it produced significant increases in
mindfulness and significant decreases in social anxiety, rumination, and depression.
Consistent with the findings of Dalrymple and Herbert (2007), ratings of acceptance
in this study mediated change over the course of treatment.
Two randomized trials have compared mindfulness- and acceptance-based treat-
ments to traditional CBT. Koszyski, Benger, Shlik, and Bradwejn (2007) compared
MBSR, which was not designed to directly target social concerns, to CBGT for SAD
(Heimberg & Becker, 2002). In this study, MBSR consisted of 8 two-and-a-half-
hour group therapy sessions and one full-day meditation retreat. Both treatments
produced improvements in mood, functioning, and quality of life; however, CBGT
was associated with significantly greater reductions in self- and clinician-rated social
anxiety, as well as higher rates of response and remission. Piet, Hougaard, Hecksher,
and Rosenberg (2010) conducted a pilot study comparing MBCT to traditional CBT
in socially anxious young adults aged 18–25. Using a cross-over design, participants
were randomly assigned to eight 2-hour group sessions of MBCT and twelve 2-hour
sessions of CBGT. MBCT produced moderate effects (d = 0.78), which were lower
but not significantly different from those produced by CBGT (d = 1.15), and par-
ticipants continued to improve during the 6-month follow-up period. The authors
concluded that although MBCT is likely less efficacious than CBT, it may represent a
useful, low-cost treatment for SAD.
Attention Bias Modification Programs

The term attention bias refers to the preferential allocation of attention to threatening
stimuli, independent of whether those stimuli are relevant to current goals and
despite competing stimuli that are nonthreatening. The theoretical models discussed
above (Clark & Wells, 1995; Hofmann, 2007; Rapee & Heimberg, 1997) assert
that excessive monitoring for internal cues of threat contributes to the development
and maintenance of SAD. Rapee and Heimberg’s model goes further to suggest that
socially anxious individuals also closely monitor the social environment for external
signs of evaluation. Indeed, a large body of evidence supports the idea that socially
anxious individuals preferentially attend to threatening stimuli in the environment
and that this preference is specific to social threat cues. For example, socially anxious
individuals are faster to detect an angry face in a neutral crowd than a happy face in a
neutral crowd (Gilboa-Schechtman et al., 1999).
Given the presence of attentional biases in individuals with SAD, researchers have
begun to investigate whether training attention away from socially threatening stimuli
can reduce symptoms of social anxiety. The most studied method for attention
retraining uses a variant of the probe detection paradigm (MacLeod, Mathews, &
Tata, 1986). The modified probe detection task presents pairs of nonthreatening
and threatening stimuli and creates a contingency in which correct responding is
associated with preferential allocation of attention to the less threatening stimulus
(for a detailed review of the methodology, see MacLeod, Rutherford, Campbell,
Ebsworthy, & Holker, 2002). Repeated practice on this task is designed to promote
selective processing of neutral cues when cognitive resources are also demanded by
social threat cues.
Two randomized trials support the efficacy of using attention modification programs
(AMPs) as stand-alone treatments for SAD. Using the traditional dot probe task in
which attention is not trained toward threatening or neutral material as a placebo
control, Schmidt, Richey, Buckner, and Timpano (2009) investigated the efficacy of
an AMP condition consisting of sixteen 20-minute computer sessions over 8 weeks,
in which participants were trained to attend to images of neutral faces instead of
faces showing disgust. At posttreatment, symptom differences between the AMP and
placebo groups were detectable but not significant. At 4-month follow-up, group
differences were significant—72% of participants in the AMP group no longer met
criteria for SAD compared to only 11% in the placebo condition. Between-group
effect sizes (d = 0.69–1.59) fell at the lower end of the range of existing empirically
supported treatments for SAD. Amir et al. (2009) conducted a second trial using
materials identical to those used by Schmidt et al. (2009). The results were also
comparable; 50% of participants in the AMP condition no longer met criteria for
SAD at posttreatment, compared to 14% in the placebo condition. Additionally,
the AMP group displayed greater reductions in clinician- and self-rated measures of
social anxiety and disability at posttreatment and 4-month follow-up. In this study,
independent tests of the degree of participants’ attention biases were administered
at baseline, posttreatment, and 4-month follow-up. Further supporting the role of
attention bias in maintaining social anxiety, those in the AMP condition demonstrated
significant gains in their ability to disengage with threatening stimuli, whereas those
in the placebo condition did not. Importantly, a follow-up examination of factors

predicting treatment success showed that AMP was only more effective than placebo
for individuals who exhibited attentional biases toward social threat prior to the start
of treatment (Amir, Taylor, & Donohue, 2011).
Combination of Cognitive Behavioral Therapy

and Pharmacotherapy
Combination of Cognitive Behavioral Therapy

and Antidepressant Medications
Psychosocial and pharmacological treatments have demonstrated similar efficacy for
treating SAD. However, they appear to confer unique benefits. Medication is often
associated with more rapid anxiety reduction (Heimberg et al., 1998), but gains made
through CBT are better maintained following termination (Liebowitz et al., 1999).
Treatments that combine CBT with medication could lead to superior outcomes than
either alone; however, research findings have been mixed.
Blomhoff et al. (2001) conducted a controlled trial examining the efficacy of
exposure and the selective serotonin reuptake inhibitor (SSRI) sertraline. All treatment
conditions (sertraline alone, exposure alone, sertraline plus exposure, and pill placebo
with no exposure) lasted 24 weeks, with patients in the exposure group completing
12 weeks of primary care physician-facilitated exposure and 12 weeks of self-exposure.
After 12 weeks, all active treatment groups were superior to placebo. At posttreatment,
only the sertraline group was superior to placebo. However, by the 1-year follow-up,
participants in the exposure group had demonstrated further improvement, whereas
those receiving sertraline or the combination treatment deteriorated on some measures
(Haug et al., 2003). The results of this study suggest that combined treatment does
not enhance efficacy and may even detract from it; however, the study examined
exposure administered by physicians with minimal CBT training, the pattern of
results was unexpected, and questions have been raised about the interpretations of
the results (e.g., Bandelow, 2004).
A study conducted by Davidson et al. (2004) examined the efficacy of combining
group CBT with the SSRI fluoxetine. In contrast to the study by Blomhoff et al.
(2001), this trial contained a full-blown CBT group, similar to Heimberg’s CBGT
but also including an SST component. All active treatments (fluoxetine alone, CBT
alone, fluoxetine plus CBT, CBT plus placebo) were superior to placebo, but they
were equally efficacious. Combining fluoxetine with group CBT, therefore, did not
provide increased benefit. The authors speculated that physical complaints, which
arise early within medication regimens, might distract from CBT, and that sequential
treatment (SSRI followed or augmented by CBT) may be preferable.
In another study, Blanco et al. (2010) compared CBGT (Heimberg & Becker,
2002), phenelzine, the combination of CBGT and phenelzine, and pill placebo. The
combined treatment was significantly more efficacious than placebo, but surprisingly
this was not the case for phenelzine or CBGT alone. In summary, research findings
are mixed. To date, it is unclear whether combining traditional pharmacotherapy such

as SSRIs with CBT confers any benefit above the use of these treatments alone.
Combination of Nontraditional Pharmacotherapy and Exposure

Recently, basic research on the neural substrates of fear extinction and social bonding
has prompted interest in the use of nontraditional pharmacotherapies that may
enhance the effectiveness of exposure.
D-cycloserine (DCS), a partial NMDA receptor agonist, facilitates extinction of
learned fear in animals (Davis, Ressler, Rothbaum, & Richardson, 2006; Walker,
Ressler, Lu, & Davis, 2002) and in humans (Ressler et al., 2004). Two controlled
trials have investigated whether administering DCS prior to exposure therapy enhances
its efficacy for those with SAD. The first, conducted by Hofmann et al. (2006),
compared the effects of exposure alone (exposure plus pill placebo) to exposure plus
DCS in a sample of socially anxious individuals. The therapy protocol used was an
abbreviated version of an exposure-based protocol for SAD (Hofmann, 2004), which
consisted of one session of psychoeducation and four exposure sessions. Participants
were required to have a fear of public speaking, as exposures focused solely on this
activity. At posttreatment, individuals in the DCS group showed greater reductions on
self-reported symptoms of anxiety. Although clinician-administered ratings of global
severity did not differ between the two groups at posttreatment or follow-up, results
at both time points displayed trends in the same direction as the self-report measures.
The second randomized trial examining the efficacy of combining exposure with
DCS was conducted by Guastella, Richardson, et al. (2008). Procedures were similar
to those used by Hofmann et al. (2006), and the results of that study were largely
replicated. Guastella, Richardson, et al. reported that compared to placebo, DCS pro-
duced significantly greater symptom reductions, and the benefits were maintained at
1-month follow-up. Additionally, DCS moderated the relationship between improved
self-appraisal after a speech task and anxiety reduction. Together, results from the
studies of Hofmann et al. (2006) and Guastella, Richardson, et al. (2008) support
the efficacy of DCS as an adjunct to exposure for SAD. Additionally, these positive
findings underscore the importance of considering how medication might interact
with specific components of CBT in order to enhance overall efficacy.
Another nontraditional pharmacological agent which has been studied in combi-
nation with exposure is oxytocin. Oxytocin, a peptide which acts both hormonally
and as a neurotransmitter in the brain, is thought to play an important role in the
regulation of interpersonal behavior. Oxytocin has been shown to markedly reduce
amygdala reactivity to social stimuli, and this effect is magnified in individuals with
SAD (Labuschagne et al., 2010). Nasal administration of oxytocin has also been
shown to promote processes involved in communication and the encoding of positive
social cues (Guastella, Mitchell, & Mathews, 2008). In a randomized controlled
trial, Guastella, Howard, Dadds, Mitchell, and Carson (2009) administered intranasal
oxytocin or placebo in conjunction with exposure to individuals with SAD who feared
public speaking. Treatment procedures followed those of Hofmann et al. (2006).
Participants who received oxytocin showed more improvement in self-appraisals of
appearance and performance during a speech task; however, these effects did not
generalize to overall improved outcomes. Social anxiety, dysfunctional cognitions,

and disability were not statistically different in the oxytocin and placebo groups. Cur-
rently, there is not enough evidence to support the use of oxytocin in combination
with exposure. More research is needed to determine whether it improves outcomes
if administered more frequently or in closer intervals, in a wider range of situations,
or in conjunction with cognitive interventions.
Factors Influencing Treatment Outcome
Treatment Modality
Several meta-analyses of CBT for SAD suggest that individual and group formats
produce similar effects (e.g., Acarturk, Cuijpers, van Straten, & de Graaf, 2009; Pow-
ers, Sigmarsson, & Emmelkamp, 2008); however, one study (Stangier, Heidenreich,
Peitz, Lauterbach, & Clark, 2003) and one meta-analysis (Aderka, 2009) indicate a
slight advantage for individual therapy. There appear to be costs and benefits to both
formats. By facilitating social contact with other socially anxious individuals, group
therapy reduces isolation and may help to normalize social fears. The group format
also lends itself well to exposure activities, with plenty of people at hand to act as role
players or audience members. This function may be of particular advantage because
high levels of client alliance with their therapist may dampen the arousal of anxiety
during exposure (S. A. Hayes, Hope, VanDyke, & Heimberg, 2007). Furthermore,
group members can help challenge each other’s distorted thinking by providing
objective feedback about social skills and performance. On the other hand, not all
clients are well suited for participation in group therapy. Group treatment may be
contraindicated for clients whose social anxiety symptoms are so severe that they have
difficulty concentrating and learning the concepts in a group context or clients who
exhibit severe personality pathology. Another significant benefit of individual treat-
ment is that it allows for greater flexibility in the pace and duration of therapy and can
address idiosyncratic concerns or symptoms of a comorbid condition. More research
specifically examining client characteristics and how they may moderate response to
group versus individual therapy is needed.
Comorbid Anxiety and Mood Disorders

Because SAD is highly comorbid with other anxiety and mood disorders (Kessler,
Stang, Wittchen, Stein, & Walters, 1999), it is important to understand how comor-
bidity affects the course of treatment. Several studies have examined the impact of
comorbid anxiety and depressive conditions on treatment outcomes among those
with SAD. Findings suggest that higher pretreatment depression is associated with
higher severity, less change in social anxiety symptoms over the course of treatment,
and higher rates of dropout (Ledley et al., 2005). Interestingly, Chambless, Tran,
and Glass (1997) found that higher self-reported depression, but not clinician-rated
depression, was associated with smaller reductions in posttreatment anxiety before a
behavioral task.
Erwin, Heimberg, Juster, and Mindlin (2002) compared the outcomes of

individuals with “uncomplicated” SAD, comorbid anxiety disorders, or comorbid
mood disorders. Those with a comorbid mood disorder had more severe social
anxiety before and after 12 weeks of CBGT, but those with a comorbid anxiety
disorder fared just as well as the uncomplicated group. In another study, Moscovitch,
Hofmann, Suvak, and In-Albon (2005) examined how depression and social anxiety
affect each other during CBGT and found that changes in depression were fully
mediated by changes in social anxiety. Changes in social anxiety accounted for 91%
of the variance in depression scores, but changes in depression only accounted for 6%
of the changes in social anxiety. These findings suggest that changes in depression
track reductions in social anxiety and indicate that SAD-specific protocols should not
be contraindicated for individuals with comorbid depression unless it is severe or
there are additional issues of self-harm.
Expectancy for Improvement

Individuals who seek treatment do so with varying expectations about whether
or how well CBT will “work.” Empirical findings on the relation between the
expectation of good outcomes and response to treatment for SAD are somewhat
mixed (Rapee, Gaston, & Abbott, 2009; Safren, Heimberg, & Juster, 1997). Several
studies have found evidence that higher expectations about treatment are associated
with better outcomes (Chambless et al., 1997; Westra, Dozois, & Marcus, 2007),
even after controlling for differences in initial symptom severity (Safren et al., 1997).
Most of these studies examined expectancy effects within group therapies but did
not account for shared experience. Findings from a more recent study that used
multilevel modeling to control for group-specific variance suggest that initial outcome
expectancies account for 16–33% of the reductions in public-speaking fears (Price &
Anderson, 2012).
Summary
A range of cognitive and behavioral interventions, including several fully articulated

treatment protocols, have been developed since SAD was first acknowledged as a
significant disorder. The most common and best-studied treatments focus on exposure
to feared situations with or without cognitive restructuring, social skills training, and
applied relaxation. The content and structure of these interventions continue to evolve
in response to empirical findings about the cognitive and behavioral processes that
maintain and amplify social anxiety. Currently, the evidence best supports the use of
exposure techniques with the suggestion of adding cognitive restructuring. Newer
mindfulness-/acceptance-based treatments and attention modification programs also
show considerable promise. It is likely that the efficacy of current cognitive behavioral
treatments could be increased by adding newer pharmacological agents; however,
future research must establish these benefits more firmly. Last, it is important for
treatment providers to consider how factors such as treatment modality, comorbidity,
and expectancies about success can affect outcomes for individuals with SAD.
References
Acarturk, C., Cuijpers, P., van Straten, A., & de Graaf, R. (2009). Psychological treat-
ment of social anxiety disorder: A meta analysis. Psychological Medicine, 39, 241–254.
doi:10.1017/S0033291708003590
Acarturk, C., de Graaf, R., van Straten, A., ten Have, M., & Cuijpers, P. (2008). Social
phobia and number of social fears, and their association with comorbidity, health-related
quality of life and help seeking. Social Psychiatry & Psychiatric Epidemiology, 43, 273–279.
doi:10.1007/s00127-008-0309-1
Aderka, I. M. (2009). Factors affecting treatment efficacy in social phobia: The use of video
feedback and individual vs. group formats. Journal of Anxiety Disorders, 23, 12–17.
doi:10.1016/j.janxdis.2008.05.003
Al-Kubaisy, T., Marks, I. M., Logsdail, S., & Marks, M. P. (1992). Role of exposure
homework in phobia reduction: A controlled study. Behavior Therapy, 23, 599–621.
doi:10.1016/S0005-7894(05)80224-2
Alström, J. E., Nordlund, C. L., Persson, G., Hårding, M., & Ljungqvist, C. (1984). Effects
of four treatment methods on social phobic patients not suitable for insight-oriented
psychotherapy. Acta Psychiatrica Scandinavica, 70, 97–110. doi:10.1111/j.1600-0447.
1984.tb01187.x
Amir, N., Beard, C., Taylor, C. T., Klumpp, H., Elias, J., Burns, M., & Chen, X. (2009).
Attention training in individuals with generalized social phobia: A randomized controlled
trial. Journal of Consulting and Clinical Psychology, 77 , 961–973. doi:10.1037/a0016685
Amir, N., Taylor, C. T., & Donohue, M. C. (2011). Predictors of response to an attention
modification program in generalized social phobia. Journal of Consulting and Clinical
Psychology, 79, 533–541. doi:10.1037/a0023808
Andersson, G., Carlbring, P., Holmström, A., Sparthan, E., Furmark, T., Nilsson-Ihrfelt, E., …
Ekselius, L. (2006). Internet-based self-help with therapist feedback and in vivo group
exposure for social phobia: A randomized controlled trial. Journal of Consulting and
Bandelow, B. (2004). Sertraline and exposure therapy in social phobia. British Journal of
Psychiatry, 184, 271–272. doi:10.1192/bjp.184.3.271
Blanco, C., Heimberg, R. G., Schneier, F. R., Fresco, D. M., Chen, H., Turk, C. L., …
Liebowitz, M. R. (2010). A placebo-controlled trial of phenelzine, cognitive behavioral
group therapy, and their combination for social anxiety disorder. Archives of General
Psychiatry, 67 , 286–295. doi:10.1001/archgenpsychiatry.2010.11
Blomhoff, S., Haug, T. T., Hellström, K., Holme, I., Humble, M., Madsbu, H. P., & Wold,
J. E. (2001). Randomised controlled general practice trial of sertraline, exposure therapy
and combined treatment in generalised social phobia. British Journal of Psychiatry, 179,
23–30. doi:10.1192/bjp.179.1.23
Bögels, S. M., & Voncken, M. (2008). Social skills training versus cognitive therapy for social
anxiety disorder characterized by fear of blushing, trembling, or sweating. International
Journal of Cognitive Therapy, 1, 138–150. doi:10.1521/ijct.2008.1.2.138
Brozovich, F., & Heimberg, R. G. (2008). An analysis of post-event processing in social anxiety
disorder. Clinical Psychology Review, 28, 891–903. doi:10.1016/j.cpr.2008.01.002
Bruce, S. E., Yonkers, K. A., Otto, M. W., Eisen, J. L., Weisberg, R. B., Pagano, M., … Keller,
M. B. (2005). Influence of psychiatric comorbidity on recovery and recurrence in gen-
eralized anxiety disorder, social phobia, and panic disorder: A 12-year prospective study.
American Journal of Psychiatry, 162, 1179–1187. doi:10.1176/appi.ajp.162.6.1179
Bruch, M. A., Fallon, M., & Heimberg, R. G. (2003). Social phobia and difficulties in occu-
pational adjustment. Journal of Counseling Psychology, 50, 109–117. doi:10.1037/0022-
0167.50.1.109
Carlbring, P., Gunnarsdóttir, M., Hedensjö, L., Andersson, G., Ekselius, L., & Furmark, T.
(2007). Treatment of social phobia: Randomised trial of Internet-delivered cognitive-
behavioural therapy with telephone support. British Journal of Psychiatry, 190, 123–128.
doi:10.1192/bjp.bp.105.020107
Carlbring, P., Nordgren, L. B., Furmark, T., & Andersson, G. (2009). Long-term outcome of
internet-delivered cognitive-behavioural therapy for social phobia: A 30-month follow-up.
Behaviour Research and Therapy, 47 , 848–850. doi:10.1016/j.brat.2009.06.012
Chambless, D. L., Tran, G. Q., & Glass, C. R. (1997). Predictors of response to cognitive-
behavioral group therapy for social phobia. Journal of Anxiety Disorders, 11, 221–240.
Clark, D. M. (2001). A cognitive perspective on social phobia. In W. R. Crozier, L. E. Alden,
W. R. Crozier, & L. E. Alden (Eds.), International handbook of social anxiety: Concepts,
research and interventions relating to the self and shyness (pp. 405–430). New York, NY:
John Wiley & Sons, Ltd.
Clark, D. M., Ehlers, A., Hackmann, A., McManus, F., Fennell, M., Grey, N., … Wild, J.
(2006). Cognitive therapy versus exposure and applied relaxation in social phobia: A
randomized controlled trial. Journal of Consulting and Clinical Psychology, 74, 568–578.
doi:10.1037/0022-006X.74.3.568
Clark, D. M., Ehlers, A., McManus, F., Hackmann, A., Fennell, M., Campbell, H., … Louis,
B. (2003). Cognitive therapy versus fluoxetine in generalized social phobia: A randomized
placebo-controlled trial. Journal of Consulting and Clinical Psychology, 71, 1058–1067.
doi:10.1037/0022-006X.71.6.1058
Clark, D. M., & Wells, A. (1995). A cognitive model of social phobia. In R. G. Heimberg, M.
R. Liebowitz, D. A. Hope, & F. R. Schneier (Eds.), Social phobia: Diagnosis, assessment,
and treatment (pp. 69–93). New York, NY: Guilford Press.
Dalrymple, K. L., & Herbert, J. D. (2007). Acceptance and commitment therapy for gen-
eralized social anxiety disorder: A pilot study. Behavior Modification, 31, 543–568.
doi:10.1177/0145445507302037
Davidson, J. R. T., Foa, E. B., Huppert, J. D., Keefe, F. J., Franklin, M. E., Compton, J.
S., … Gadde, K. M. (2004). Fluoxetine, comprehensive cognitive behavioral therapy,
and placebo in generalized social phobia. Archives of General Psychiatry, 61, 1005–1013.
doi:10.1001/archpsyc.61.10.1005
Davis, M., Ressler, K., Rothbaum, B. O., & Richardson, R. (2006). Effects of D-cycloserine
on extinction: Translation from preclinical to clinical work. Biological Psychiatry, 60,
369–375. doi:10.1016/j.biopsych.2006.03.084
Erwin, B. A., Heimberg, R. G., Juster, H., & Mindlin, M. (2002). Comorbid anxiety and mood
disorders among persons with social anxiety disorder. Behaviour Research and Therapy,
40, 19–35. doi:10.1016/S0005-7967(00)00114-5
Erwin, B. A., Turk, C. L., Heimberg, R. G., Fresco, D. M., & Hantula, D. A. (2004). The
Internet: Home to a severe population of individuals with social anxiety disorder? Journal
of Anxiety Disorders, 18, 629–646. doi:10.1016/j.janxdis.2003.08.002
Foa, E. B., Franklin, M. E., Perry, K. J., & Herbert, J. D. (1996). Cognitive biases in generalized
social phobia. Journal of Abnormal Psychology, 105, 433–439. doi:10.1037/0021-
843X.105.3.433
information. Psychological Bulletin, 99, 20–35. doi:10.1037/0033-2909.99.1.20
Gilboa-Schechtman, E., Foa, E. B., & Amir, N. (1999). Attentional biases for facial expressions
in social phobia: The face-in-the-crowd paradigm. Cognition and Emotion, 13, 305–318.
doi:10.1080/026999399379294
Gross, J. J. (Ed.). (2007). Handbook of emotion regulation. New York, NY: Guilford Press.
Guastella, A. J., Howard, A. L., Dadds, M. R., Mitchell, P., & Carson, D. S. (2009). A ran-
domized controlled trial of intranasal oxytocin as an adjunct to exposure therapy for social
anxiety disorder. Psychoneuroendocrinology, 34, 917–923. doi:10.1016/j.psyneuen.2009.
01.005
Guastella, A. J., Mitchell, P. B., & Mathews, F. (2008). Oxytocin enhances the encoding of
positive social memories in humans. Biological Psychiatry, 64, 256–258. doi:10.1016/
j.biopsych.2008.02.008
& Dadds, M. R. (2008). A randomized controlled trial of D-cycloserine enhancement
of exposure therapy for social anxiety disorder. Biological Psychiatry, 63, 544–549.
doi:10.1016/j.biopsych.2007.11.011
Haug, T. T., Blomhoff, S., Hellstrøm, K., Holme, I., Humble, M., Madsbu, H. P., & Wold, J. E.
(2003). Exposure therapy and sertraline in social phobia: 1-year follow-up of a randomised
controlled trial. British Journal of Psychiatry, 182, 312–318. doi:10.1192/bjp.182.4.312
Hayes, S. A., Hope, D. A., VanDyke, M. M., & Heimberg, R. G. (2007). Working
alliance for clients with social anxiety disorder: Relationship with session helpfulness
and within-session habituation. Cognitive Behaviour Therapy, 36, 34–42. doi:10.1080/
16506070600947624
Hayes, S. C., Strosahl, K. D., & Wilson, K. G. (1999). Acceptance and commitment therapy:
An experiential approach to behavior change. New York, NY: Guilford Press.
Hedman, E., Andersson, G., Ljótsson, B., Andersson, E., Rück, C., Mörtberg, E., & Lindefors,
N. (2011). Internet-based cognitive behavior therapy vs. cognitive behavioral group
therapy for social anxiety disorder: A randomized controlled non-inferiority trial. PLoS
ONE, 6. doi:10.1371/journal.pone.0018001
Heimberg, R. G., & Becker, R. E. (2002). Cognitive-behavioral group therapy for social phobia:
Basic mechanisms and clinical strategies. New York, NY: Guilford Press.
Heimberg, R. G., Brozovich, F. A., & Rapee, R. M. (2010). A cognitive behavioral model of
social anxiety disorder: Update and extension. In S. G. Hofmann & P. M. DiBartolo (Eds.),
Social anxiety: Clinical, developmental, and social perspectives (2nd ed., pp. 395–422). San
Diego, CA: Elsevier Academic Press.
Heimberg, R. G., Dodge, C. S., Hope, D. A., Kennedy, C. R., Zollo, L. J., & Becker, R.
E. (1990). Cognitive behavioral group treatment for social phobia: Comparison with
a credible placebo control. Cognitive Therapy and Research, 14, 1–23. doi:10.1007/
BF01173521
Heimberg, R. G., & Juster, H. R. (1995). Cognitive-behavioral treatments: Literature review.
In R. G. Heimberg, M. R. Liebowitz, D. A. Hope, & F. R. Schneier (Eds.), Social phobia:
Diagnosis, assessment, and treatment (pp. 261–309). New York, NY: Guilford Press.
Heimberg, R. G., Liebowitz, M. R., Hope, D. A., Schneier, F. R., Holt, C. S., Welkowitz,
L., … Klein, D. F. (1998). Cognitive-behavioral group therapy versus phenelzine
in social phobia: 12-week outcome. Archives of General Psychiatry, 55, 1133–1141.
doi:10.1001/archpsyc.55.12.1133
Heimberg, R. G., Salzman, D. G., Holt, C. S., & Blendell, K. A. (1993). Cognitive-behavioral
group treatment for social phobia: Effectiveness at five-year followup. Cognitive Therapy
and Research, 17 , 325–339. doi:10.1007/BF01177658
Herbert, J. D., Gaudiano, B. A., Rheingold, A. A., Myers, V., Dalrymple, K., & Nolan, E.
M. (2005). Social skills training augments the effectiveness of cognitive behavioral group
therapy for social anxiety disorder. Behavior Therapy, 36, 125–138.
Hiemisch, A., Ehlers, A., & Westermann, R. (2002). Mindsets in social anxiety: A new look at
selective information processing. Journal of Behavior Therapy and Experimental Psychiatry,
33, 103–114. doi:10.1016/S0005-7916(02)00022-8
Hofmann, S. G. (2004). Cognitive mediation of treatment change in social phobia. Journal of
Hofmann, S. G. (2007). Cognitive factors that maintain social anxiety disorder: A comprehen-
sive model and its treatment implications. Cognitive Behaviour Therapy, 36, 193–209.
doi:10.1080/16506070701421313
Hofmann, S. G., & Admundson, G. J. (2008). Acceptance and mindfulness-based therapy: New
wave or old hat? Clinical Psychology Review, 28, 1–16. doi:10.1016/j.cpr.2007.09.003
Hofmann, S. G., & Barlow, D. H. (2002). Social phobia (social anxiety disorder). In D. H.
Barlow (Ed.), Anxiety and its disorders: The nature and treatment of anxiety and panic
(2nd ed., pp. 454–476). New York, NY: Guilford Press.
Hofmann, S. G., Meuret, A. E., Smits, J. A. J., Simon, N. M., Pollack, M. H., Eisenmenger,
K., … Otto, M. W. (2006). Augmentation of exposure therapy with D-cycloserine
for social anxiety disorder. Archives of General Psychiatry, 63, 298–304. doi:10.1001/
archpsyc.63.3.298
Hofmann, S. G., & Otto, M. W. (2008). Cognitive-behavior therapy for social anxiety
disorder: Evidence-based and disorder-specific treatment techniques. New York, NY: Rout-
ledge/Taylor & Francis Group.
Hofmann, S. G., Sawyer, A. T., & Fang, A. (2010). The empirical status of the “new wave”
of cognitive behavioral therapy. Psychiatric Clinics of North America, 33, 701–710.
doi:10.1016/j.psc.2010.04.006
Hope, D. A., Heimberg, R. G., & Turk, C. L. (2010). Managing social anxiety: A cognitive-
behavioral approach (client workbook) (2nd ed.). New York, NY: Oxford University
Press.
Jack, M. S., Heimberg, R. G., & Mennin, D. S. (1999). Situational panic attacks: Impact on
social phobia with and without panic disorder. Depression and Anxiety, 10, 112–118.
doi:10.1002/(SICI)1520-6394(1999)10:3<112::AID-DA4>3.0.CO;2-U
Jerremalm, A., Jansson, L., & Öst, L.-G. (1986). Cognitive and physiological reactivity and
the effects of different behavioral methods in the treatment of social phobia. Behaviour
Research and Therapy, 24, 171–180. doi:10.1016/0005-7967(86)90088-4
Kabat-Zinn, J. (1990). Full catastrophe living: Using the wisdom of your body and mind to face
stress, pain, and illness. New York, NY: Dell.
Kabat-Zinn, J. (2003). Mindfulness-based stress reduction (MBSR). Constructivism in the
Human Sciences, 8, 73–107.
Kanter, N. J., & Goldfried, M. R. (1979). Relative effectiveness of rational restructuring and
self-control desensitization in the reduction of interpersonal anxiety. Behavior Therapy,
10, 472–490. doi:10.1016/S0005-7894(79)80051-9
Kessler, R. C., Berglund, P., Demler, O., Jin, R., Merikangas, K. R., & Walters, E. E.
(2005). Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the
National Comorbidity Survey Replication. Archives of General Psychiatry, 62, 593–602.
doi:10.1001/archpsyc.62.6.593
Kessler, R. C., Stang, P., Wittchen, H.-U., Stein, M., & Walters, E. E. (1999). Lifetime
comorbidities between social phobia and mood disorders in the US National Comorbidity
Survey. Psychological Medicine, 29, 555–567. doi:10.1017/S0033291799008375
Kocovski, N. L., Fleming, J. E., & Rector, N. A. (2009). Mindfulness and acceptance-based
group therapy for social anxiety disorder: An open trial. Cognitive and Behavioral Practice,
16, 276–289. doi:10.1016/j.cbpra.2008.12.004
Koszycki, D., Benger, M., Shlik, J., & Bradwejn, J. (2007). Randomized trial of a meditation-
based stress reduction program and cognitive behavior therapy in generalized social anxiety
disorder. Behaviour Research and Therapy, 45, 2518–2526. doi:10.1016/j.brat.2007.
04.011
Labuschagne, I., Phan, K. L., Wood, A., Angstadt, M., Chua, P., Heinrichs, M., … Nathan,
P. J. (2010). Oxytocin attenuates amygdala reactivity to fear in generalized social anxiety
disorder. Neuropsychopharmacology, 35, 2403–2413. doi:10.1038/npp.2010.123
Leary, M. R. (2010). Social anxiety as an early warning system: A refinement and extension of
the self-presentation theory of social anxiety. In S. G. Hofmann & P. M. DiBartolo (Eds.),
Social anxiety: Clinical, developmental, and social perspectives (2nd ed., pp. 471–486). San
Diego, CA: Elsevier Academic Press.
Ledley, D. R., Heimberg, R. G., Hope, D. A., Hayes, S. A.., Zaider, T. I., Van
Dyke, M., … Fresco, D. M. (2009). Efficacy of a manualized and workbook-driven
individual treatment for social anxiety disorder. Behavior Therapy, 40, 414–424.
doi:10.1016/j.beth.2008.12.001
Ledley, D. R., Huppert, J. D., Foa, E. B., Davidson, J. R. T., Keefe, F. J., & Potts, N. L. S.
(2005). Impact of depressive symptoms on the treatment of generalized social anxiety
disorder. Depression and Anxiety, 22, 161–167. doi:10.1002/da.20121
Liebowitz, M. R., Heimberg, R. G., Schneier, F. R., Hope, D. A., Davies, S., Holt, C. S., …
Klein, D. F. (1999). Cognitive-behavioral group therapy versus phenelzine in social pho-
bia: Long term outcome. Depression and Anxiety, 10, 89–98. doi:10.1002/(SICI)1520-
6394(1999)10:3<89::AID-DA1>3.0.CO;2–5
MacLeod, C., Mathews, A., & Tata, P. (1986). Attentional bias in emotional disorders. Journal
of Abnormal Psychology, 95, 15–20. doi:10.1037/0021-843X.95.1.15
MacLeod, C., Rutherford, E., Campbell, L., Ebsworthy, G., & Holker, L. (2002). Selective
attention and emotional vulnerability: Assessing the causal basis of their association
through the experimental manipulation of attentional bias. Journal of Abnormal Psychology,
111, 107–123. doi:10.1037/0021-843X.111.1.107
Marlatt, G. A., & Kristeller, J. L. (1999). Mindfulness and meditation. In
W. R. Miller & W. R. Miller (Eds.), Integrating spirituality into treatment: Resources
for practitioners (pp. 67–84). Washington, DC: American Psychological Association.
doi:10.1037/10327-004
Marzillier, J. S., Lambert, C., & Kellett, J. (1976). A controlled evaluation of systematic desen-
sitization and social skills training for socially inadequate psychiatric patients. Behaviour
Research and Therapy, 14, 225–238. doi:10.1016/0005-7967(76)90015-2
Mattick, R. P., & Clarke, J. C. (1998). Development and validation of measures of social
phobia scrutiny fear and social interaction anxiety. Behaviour Research and Therapy, 36,
455–470. doi:10.1016/S0005-7967(97)10031-6
McNeil, D. W., Lejuez, C. W., & Sorrel, J. T. (2010). Basic behavioral mechanisms and
processes in social anxieties and social anxiety disorders. In S. G. Hofmann & P. M.
DiBartolo (Eds.), Social anxiety: Clinical, developmental, and social perspectives (2nd ed.,
pp. 347–372). San Diego, CA: Elsevier Academic Press.
Mersch, P. P., Emmelkamp, P. M., Bögels, S. M., & Van der Sleen, J. (1989). Social phobia:
Individual response patterns and the effects of behavioral and cognitive interventions.
Behaviour Research and Therapy, 27 , 421–434. doi:10.1016/0005-7967(89)90013-2
Mörtberg, E., Clark, D. M., & Bejerot, S. (2011). Intensive group cognitive therapy and
individual cognitive therapy for social phobia: Sustained improvement at 5-year follow-up.
Journal of Anxiety Disorders, 25, 994–1000. doi:10.1016/j.janxdis.2011.06.007
Moscovitch, D. A., Hofmann, S. G., Suvak, M. K., & In-Albon, T. (2005). Mediation
of changes in anxiety and depression during treatment of social phobia. Journal of
Olfson, M., Guardino, M., Struening, E., Schneier, F. R., Hellman, F., & Klein, D. F. (2000).
Barriers to the treatment of social anxiety. American Journal of Psychiatry, 157 , 521–527.
doi:10.1176/appi.ajp.157.4.521
Piet, J., Hougaard, E., Hecksher, M. S., & Rosenberg, N. K. (2010). A randomized pilot
study of mindfulness-based cognitive therapy and group cognitive-behavioral therapy
for young adults with social phobia. Scandinavian Journal of Psychology, 51, 403–410.
doi:10.1111/j.1467-9450.2009.00801.x
Ponniah, K., & Hollon, S. D. (2008). Empirically supported psychological interventions for
social phobia in adults: A qualitative review of randomized controlled trials. Psychological
Powers, M. B., Sigmarsson, S. R., & Emmelkamp, P. M. G. (2008). A meta-analytic review
of psychological treatments for social anxiety disorder. International Journal of Cognitive
Therapy, 1, 94–113. doi:10.1521/ijct.2008.1.2.94
Price, M., & Anderson, P. L. (2012). Outcome expectancy as a predictor of treatment response
in cognitive behavioral therapy for public speaking fears within social anxiety disorder.
Psychotherapy, 49, 173–179. doi:10.1037/a0024734
Rapee, R. M., Gaston, J. E., & Abbott, M. J. (2009). Testing the efficacy of theoretically
derived improvements in the treatment of social phobia. Journal of Consulting and
Clinical Psychology, 77 , 317–327. doi:10.1037/a0014800
Rapee, R. M., & Heimberg, R. G. (1997). A cognitive-behavioral model of anxiety in
social phobia. Behaviour Research and Therapy, 35, 741–756. doi:10.1016/S0005-
7967(97)00022-3
Rapee, R. M., & Lim, L. (1992). Discrepancy between self- and observer ratings of performance
in social phobics. Journal of Abnormal Psychology, 101, 727–731. doi:10.1037/0021-
843X.101.4.728
Reich, J. (1986). The epidemiology of anxiety. Journal of Nervous and Mental Disease, 174,
129–136. doi:10.1097/00005053-198603000-00001
Davis, M. (2004). Cognitive enhancers as adjuncts to psychotherapy: Use of D-cycloserine
in phobic individuals to facilitate extinction of fear. Archives of General Psychiatry, 61,
1136–1144. doi:10.1176/appi.ajp.2007.07121871
Rodebaugh, T. L. (2009). Social phobia and perceived friendship quality. Journal of Anxiety
Disorders, 23, 872–878. doi:10.1016/j.janxdis.2009.05.001
Ruscio, A. M., Brown, T. A., Chiu, W. T., Sareen, J., Stein, M. B., & Kessler, R. C. (2008).
Social fears and social phobia in the USA: Results from the National Comorbidity Survey
Replication. Psychological Medicine, 38, 15–28. doi:10.1017/S0033291707001699
Safren, S. A., Heimberg, R. G., & Juster, H. R. (1997). Clients’ expectancies and their
relationship to pretreatment symptomatology and outcome of cognitive-behavioral group
treatment for social phobia. Journal of Consulting and Clinical Psychology, 65, 694–698.
doi:10.1037/0022-006X.65.4.694
Sanderson, W. C., DiNardo, P. A., Rapee, R. M., & Barlow, D. H. (1990). Syndrome comor-
bidity in patients diagnosed with a DSM-III-R anxiety disorder. Journal of Abnormal
Psychology, 99, 308–312. doi:10.1037/0021-843X.99.3.308
Schmidt, N. B., Richey, J. A., Buckner, J. D., & Timpano, K. R. (2009). Attention training
for generalized social anxiety disorder. Journal of Abnormal Psychology, 118, 5–14.
doi:10.1037/a0013643
Schneier, F. R., Heckelman, L. R., Garfinkel, R., Campeas, R., Fallon, B. A., Gitow, A., …
Liebowitz, M. R. (1994). Functional impairment in social phobia. Journal of Clinical
Segal, Z. V., Williams, J. M., & Teasdale, J. D. (2002). Mindfulness-based cognitive therapy for
depression: A new approach to preventing relapse. New York, NY: Guilford Press.
Spek, V., Cuijpers, P., Nykl ı́ček, I., Riper, H., Keyzer, J., & Pop, V. (2007). Internet-based
cognitive behaviour therapy for symptoms of depression and anxiety: A meta-analysis.
Psychological Medicine, 37 , 319–328. doi:10.1017/S0033291706008944
Stangier, U., Heidenreich, T., Peitz, M., Lauterbach, W., & Clark, D. M. (2003). Cognitive
therapy for social phobia: Individual versus group treatment. Behaviour Research and
Therapy, 41, 991–1007.
Stopa, L., & Clark, D. M. (1993). Cognitive processes in social phobia. Behaviour Research
and Therapy, 31, 255–267. doi:10.1016/0005-7967(93)90024-O
Tillfors, M., Carlbring, P., Furmark, T., Lewenhaupt, S., Spak, M., Eriksson, A., … Andersson,
G. (2008). Treating university students with social phobia and public speaking fears:
Internet delivered self-help with or without live group exposure sessions. Depression and
Anxiety, 25, 708–717. doi:10.1002/da.20416
Trower, P., Yardley, K., Bryant, B. M., & Shaw, P. (1978). The treatment of social failure: A
comparison of anxiety-reduction and skills-acquisition procedures on two social problems.
Behavior Modification, 2, 41–60. doi:10.1177/014544557821003
Veljaca, K., & Rapee, R. M. (1998). Detection of negative and positive audience
behaviours by socially anxious subjects. Behaviour Research and Therapy, 36, 311–321.
doi:10.1016/S0005-7967(98)00016-3
Walker, D. L., Ressler, K. J., Lu, K., & Davis, M. (2002). Facilitation of conditioned fear
extinction by systemic administration or intra-amygdala infusions of D-cycloserine as
assessed with fear-potentiated startle in rats. Journal of Neuroscience, 22, 2343–2351.
Wells, A., Clark, D. M., Salkovskis, P., & Ludgate, J. (1995). Social phobia: The role of
in-situation safety behaviors in maintaining anxiety and negative beliefs. Behavior Therapy,
26, 153–161. doi:10.1016/S0005-7894(05)80088-7
Wells, A., & Papageorgiou, C. (1998). Social phobia: Effects of external attention of anxiety,
negative beliefs, and perspective taking. Behavior Therapy, 29, 357–370.
Wenzel, A. (2002). Characteristics of close relationships in individuals with social phobia:
A preliminary comparison with nonanxious individuals. In J. H. Harvey & A. Wenzel
(Eds.), A clinician’s guide to maintaining and enhancing close relationships (pp. 199–214).
Westra, H. A., Dozois, D. J. A., & Marcus, M. (2007). Expectancy, homework compliance,
and initial change in cognitive-behavioral therapy for anxiety. Journal of Consulting and
Wlazlo, Z., Schroeder-Hartwig, K., Hand, I., & Kaiser, G. (1990). Exposure in vivo vs. social
skills training for social phobia: Long-term outcome and differential effects. Behaviour
Research and Therapy, 28, 181–193. doi:10.1016/0005-7967(90)90001-Y
Wolpe, J., & Lazarus, A. A. (1966). Behavior therapy techniques: A guide to the treatment of
neuroses. Elmsford, NY: Pergamon Press.
39
Panic Disorder
Norman B. Schmidt, Kristina J. Korte,
and Aaron M. Norr
Florida State University, United States
Meghan E. Keough
University of Washington, United States
Background
The anxiety response is an innate, adaptive “alarm system” that prepares humans to act
and ensure safety. However, this “alarm system” can have problematic consequences
when it is triggered without the presence of a true environmental threat, or for exag-
gerated periods of time. Panic responses (intense fight-or-flight emotional arousal)
represent the most intense activation of the “alarm system.” More formally defined by
the Diagnostic and Statistical Manual of Mental Disorders, a panic attack is described
as a discrete period of intense fear or discomfort accompanied by four or more somatic
and/or cognitive symptoms (e.g., sweating, fear of dying) (DSM-IV-TR; American
Psychiatric Association [APA], 2000). When triggered at inappropriate times, panic
responses can become feared and may result in the development of panic disorder,
though panic attacks have also been shown to be associated with a diverse array of
psychiatric disorders (Craske et al., 2010).
A diagnosis of panic disorder is merited when the individual experiences recurrent,
unexpected panic attacks, and at least one of the attacks is followed by one month
(or longer) of worry around having future attacks or the implications of the
attacks, or the individual exhibits a significant change of behavior as a result of the
attacks (APA, 2000). When fear of panic attacks results in substantial avoidance
behaviors, a specifier of agoraphobia (i.e., panic disorder with agoraphobia) is added
(APA, 2000). Individuals with panic disorder with or without agoraphobia suffer
intensely and often chronically. Fortunately, treatments for panic psychopathology
are well researched, such that we now have a variety of established and efficacious
interventions for those suffering from panic disorder. Of all available treatment
options for panic disorder, cognitive behavioral therapy (CBT) is the clear favorite
(Schmidt & Keough, 2010). These treatments constitute the focus of this chapter.

DOI: 10.1002/9781118528563.wbcbt39
Conceptual Models of Panic Psychopathology
Contemporary CBT owes much to conceptual models of panic attacks that were
advanced in the mid-to-late 1980s. At that time, a variety of cognitively focused,
learning-based accounts of panic were advanced. We briefly highlight three highly
influential models that directly impacted the most common CBT procedures in use
for panic disorder today. Contemporary conceptualizations of panic have focused on
cognitive models that detail the relationships between fear and cognitive appraisal,
and the external factors that affect the appraisal process. The development of cognitive
and behavioral interventions for panic has been heavily influenced by Barlow’s (2002)
emotion-based model, Clark’s (1986) cognitive model, and Reiss’s (1991) expectancy
model.
The central tenet of each of these models is that individuals with panic disorder have
acquired exaggerated, fearful beliefs that were critical in the genesis and maintenance
of the disorder. As illustrated by the cognitive model of panic advanced by Clark
(1986), panic evolves from a positive feedback loop model involving the catastrophic
misinterpretation of anxiety-related symptoms. Clark posits that individuals perceive
the presence of anxiety-related symptoms to be indicative of a more serious medical
or cognitive condition. For example, an individual may interpret arousal such as
heart palpitations as an impending cardiac arrest, or difficulty concentrating as a sign
of a mental breakdown. These catastrophic misinterpretations lead to greater fear,
increased arousal symptoms, and the possibility of panic.
The emotion-based model of panic (Barlow, 2002) is a diathesis–stress model in
which the etiology of panic is seen as the result of biological and psychological vulner-
abilities that interact with environmental stressors. Individuals who are predisposed
to the development of panic disorder may be neurobiologically overreactive to stress,
have a sense that emotions and external events are uncontrollable and unpredictable,
or both. One of the unique processes outlined by Barlow’s model is that, as stress-
related arousal and panic transpire, the individual associates this “panic alarm” with
salient internal sensations through a classical conditioning framework referred to as
interoceptive conditioning. For example, specific bodily sensations associated with
arousal (e.g., rapid heart rate) become conditioned to panic and may serve to trigger
subsequent panic attacks. Thus, interoceptive conditioning is believed to play a critical
role in the development and exacerbation of panic disorder.
The expectancy model (Reiss, 1991) proposes that panic attacks and panic disorder
result from elevated levels of a cognitive risk factor described as anxiety sensitivity.
Anxiety sensitivity is a fear of anxiety symptoms due to beliefs that dire consequences
can result from experiencing anxiety (Reiss, 1991). Expectancy theory suggests that
although bodily sensations do not cause panic in everyone, individual difference levels
in anxiety sensitivity will determine whether an individual will panic in response
to bodily arousal (Reiss & McNally, 1985). Anxiety sensitivity is thought to be
a relatively stable belief system that results from many different paths, suggesting
that an individual can develop high anxiety sensitivity without having personally
experienced anxiety or panic. Whereas Clark’s model suggests that some individuals
may misinterpret arousal, thereby leading to panic, expectancy theory suggests that
Panic Disorder 919
misinterpretation may not be necessary for some, as arousal per se is sufficient to

engender a fear response. The construct of anxiety sensitivity appears to nicely capture
what is thought to be at the core of panic disorder, that is, the acquisition of “fear of
fear.”
Prior to the development of these more cognitively focused models of panic,
the treatment of anxiety disorders (including panic disorder) focused on encour-
aging patients to confront situations that cause them intense fear and avoidance
behaviors (i.e., in vivo exposure; Mathews et al., 1981). However, the development
of these cognitive models has led to a shift from straightforward exposure-based
treatments to interventions that attempt to reduce the patient’s hypersensitivity
to arousal sensations and correct the tendency to believe these sensations (and
their consequences) to be threatening. The result has been the development of
cognitively oriented treatment protocols, which tend to focus on correcting misin-
terpretations of anxiety sensations (Beck, 1988; Beck & Emery, 1985; Clark, 1986).
Conversely, newer behaviorally oriented treatments have highlighted the importance
of identification and repeated induction of feared bodily sensations (i.e., intero-
ceptive exposure) as a means to reduce anxiety sensitivity, or the set of beliefs
a patient holds with regard to anxiety-related bodily sensations (Barlow et al.,
1989).
Elements of a Cognitive Behavioral Therapy Protocol

for Panic Disorder
In the following section, an outline of current CBT protocols for panic is provided.
This outline is intended to provide a description of the key elements involved in
treating panic rather than as a step-by-step guide for panic treatment. CBT manuals
that serve this purpose are readily available. One such manual that has been widely
utilized and empirically supported is Mastery of your Anxiety and Panic, which is
currently in its fourth edition (Barlow & Craske, 2007).
Assessment
Because panic attacks occur across a number of anxiety disorders, the first step
in the treatment of panic disorder is to conduct a thorough assessment to obtain
an accurate diagnosis. The gold standard, certainly for research purposes, begins
with a structured diagnostic interview such as the Structured Clinical Interview
for DSM-IV (SCID-IV; First, Spitzer, Gibbon, & Williams, 1994) or the Anxiety
Disorders Interview Schedule for DSM-IV (ADIS-IV; DiNardo, Brown, & Bar-
low, 1994). These interviews facilitate the development of an accurate diagnostic
impression by ruling out differential diagnoses and assessing for comorbidity. While
both are excellent interviews, the ADIS provides more detailed information about
anxiety psychopathology beyond establishing the presence or absence of DSM-IV
criteria (APA, 1994). At our academic anxiety clinic, we routinely receive refer-
rals from the community with inaccurate diagnoses and much of this stems from
a lack of appreciation that the central feature of panic disorder is not the mere
presence or history of panic attacks, but the development of a clear pattern of
worry and impairment created by fear of additional panic. These structured inter-
views will often assist in the assessment of panic-related worry and disability, but
clinicians should remind themselves of the importance of these criteria when con-
ducting their assessments. As noted by Barlow, Raffa, and Cohen (2002), a key
to accurate assessment of anxiety psychopathology goes beyond simply noting the
presence of fear, anxiety, avoidance, and panic. Differential diagnosis of anxiety
should focus on the nature of the anxious apprehension. When this focus is on
panic per se, then it is highly likely that the individual is suffering from panic
disorder.
In addition to information gathered from the diagnostic interview, further analysis
of panic and related symptomatology can be achieved through a number of brief
measurement instruments. These instruments can serve to facilitate an accurate
diagnosis as well as aid in the development of a treatment plan and provide baseline
data for later comparison of treatment progress. A thorough guide to relevant measures
is beyond the scope of this chapter but one excellent resource is the Practitioner’s
Guide to Empirically Based Measures of Anxiety (Antony, Orsillo, & Roemer, 2001)
or the Handbook of Clinical Interviewing with Adults (Hersen & Thomas, 2007).
However, we provide a few suggestions for measures of specific domains related to
panic disorder. First, panic attack severity can be assessed using a clinician-administered
scale such as the Panic Disorder Severity Scale (PDSS; Shear et al., 1997) or the self-
administered Panic Disorder Self-Report (Newman, Holmes, Zuellig, Kachin, &
Behar, 2006). Panic-related (or agoraphobic) avoidance should either be assessed
through a clinician’s questioning about commonly seen panic avoidance, or be
more systematically assessed with the Mobility Inventory (Chambless, Caputo, Jasin,
Gracely, & Williams, 1985), which is a self-report measure that queries respondents
about 26 different situations that are commonly the focus of phobic avoidance.
Anxiety sensitivity has been shown to mediate treatment outcome (Smits, Powers,
Cho, & Telch, 2004) and therefore we recommend monitoring it on a regular basis.
The most commonly utilized measure of anxiety sensitivity is the Anxiety Sensitivity
Index, a 16-item self-report measure (Peterson & Reiss, 1993). A newer measure of
anxiety sensitivity is the 18-item Anxiety Sensitivity Index–3 (ASI-3; Taylor et al.,
2007). The ASI-3 was developed to address some of the psychometric deficiencies
observed with the ASI, especially in regard to measuring its subfactors (e.g., social
concerns, cognitive concerns, physiological concerns) of anxiety sensitivity (Zinbarg,
Barlow, & Brown, 1997). Use of the ASI-3 is recommended when there is particular
interest in monitoring change in the anxiety sensitivity subfactors during the course
of treatment.
An important part of the assessment and diagnostic phase of treatment is providing
the client with diagnostic feedback. Individuals with panic disorder have often spent
significant time and resources seeking a diagnosis for and understanding of their
symptoms. Patients with panic disorder often repeatedly present to medical settings
such as emergency departments thinking that their panic symptoms are a manifestation
of a serious physical illness and in such settings they rarely receive an accurate diagnosis
(e.g., Deacon, Lickel, & Abramowitz, 2008; Foldes-Busque et al., 2011). Thus, before
Panic Disorder 921
beginning the specific techniques of CBT, time should be set aside to explain the
diagnosis of panic disorder and how the client’s particular symptoms and experiences
fit the diagnosis.
Education
Building upon the diagnostic feedback, CBT should begin with psychoeducation
regarding the patient’s role in this type of therapy, the CBT model of panic, and the
physiological nature of panic. As with the CBT treatment of any disorder, therapy
should start with a discussion of the patient’s role in the therapeutic process. Patients
come to therapy with different levels of therapeutic experience and expectations.
Those who have a history of supportive or dynamic therapy may have expectations
about their role in therapy and the therapeutic process that are discordant with CBT.
Because CBT is necessarily challenging, it is helpful for patients to understand that
treatment is collaborative, that sessions will be structured and follow a mutually
agreed upon agenda, and that treatment gains will be more readily seen if they attend
sessions on a regular basis and complete the home practice that is assigned between
sessions.
Orienting patients to the CBT conceptualization of the panic cycle also helps to
set the foundation for therapy. Patients are likely to achieve a deeper understanding
of the processes involved if the therapist and patient work together to personalize
the cycle to the patient’s experience. This can be done by first asking patients what
they noticed during some of their initial, or more severe, panic attacks. Some of the
important data to highlight include physical symptoms that may be salient. Finally,
the patient is asked how he or she has tended to react to panic. For example, a trip
to the emergency room is a pretty clear sign that the individual believed they were
experiencing some type of catastrophic medical emergency. If patients have difficulty
recalling such information, the clinician can prompt them by providing examples that
were mentioned during the assessment (see an example of a personalized panic cycle
in Figure 39.1). The clinician then uses the specific examples to engage the patient in
a discussion of how physical symptoms lead to anxiety-provoking thoughts that then
lead to anxious behaviors. This discussion should illustrate that this cycle serves to
reinforce and exacerbate anxiety and panic. Finally, it should then be explained that
the goal of CBT is to alleviate panic through disrupting this cycle.
Patients with panic disorder necessarily experience a significant amount of distress
regarding the specific physiological presentation of their panic attacks. It is crucial for
patients to come to the understanding that while the symptoms may be uncomfortable
they are not dangerous or a sign of some impending physical or cognitive catastrophe
(Barlow & Craske, 2007). To ameliorate this distress, clinicians should provide
patients with an explanation of the fight-or-flight response and how this response
serves to protect us when faced with harm. It is helpful to emphasize that this is an
adaptive, evolutionary system designed to protect us, as well as to review with patients
their particular physical symptoms and how those symptoms fit into the fight-or-flight
response. For example, anxiety will create unpleasant cardiac sensations because of
increased heart rate. However, the reason for these sensations is that the body is
preparing itself (to fight or flee) by ensuring increased delivery of oxygen to our
Physical symptoms
• Shaking
• Sweating
• Nauseous
• Heart racing
• Dizziness
• Difficulty breathing
Behaviors Thoughts
• Avoid crowds • I am going to pass out and hurt myself.
• Avoid situations where panic has • People are going to think I am weird
occurred because my hands are shaking.
• Sit by the exit in class and movies • My throat is closing.
• Make sure I always have my medicine • I am going crazy.
and cell phone with me
Figure 39.1 Personalized panic cycle example.
major muscle groups. For some patients, such explanations may mitigate their fear of
physical symptoms, but for most psychoeducation is just the starting point for more
active and challenging CBT interventions.
Exposure
Exposure, that is, repeated and systematic provocation of fear by placing the patient
in fear-producing situations, is the central intervention in the treatment of anxiety
psychopathology (Craske, Rowe, Lewin, & Noriega-Dimitri, 1997). In the case of
panic disorder, therapists utilize both in vivo exposure and interoceptive exposure.
In vivo exposure is focused on exposing clients to places, people, and situations
that they actively avoid in their day-to-day lives due to fears and distress about
panicking. Situational exposure is informed by assessments focused on bringing to
light avoidance. In addition to specifying more overt and obvious avoidance behaviors
such as avoiding driving on certain roads or going to crowded stores, this assessment
needs to help identify more subtle coping strategies, which we typically refer to as
safety behaviors (Schmidt & Telch, 1994; Schmidt et al., 2012), such as bringing
companions or objects (e.g., water bottle, pill bottle) with them to places in an effort
to make themselves feel more secure. The use of these safety behaviors may serve to
undermine exposure since use of safety aids may prevent the induction of fear, or
patients may perceive that the safety aids were critical in allowing them to manage
Panic Disorder 923
the situation. In both instances, the patient fails to receive a potent disconfirmation
of the beliefs underlying the avoidance behaviors.
Whereas in vivo exposure has long been employed in the treatment of anxiety
problems, cognitive models of panic suggest that addressing the fear of anxiety-
related physiological arousal may be even more critical to effective treatment of
panic disorder (Clark, 1986). To address these concerns, interoceptive exposure (IE)
is utilized. Just as in vivo exposure is designed to mitigate fears of situations, the
basic premise of IE is that repeated, deliberate exposure to internal anxiety-related
sensations will reduce fear of internal sensations. To begin IE, an assessment is
conducted which involves the therapist guiding the patient through a number of
exercises (e.g., breathing through a coffee stirrer, running in place, spinning in an
office chair) intended to provoke strong physical sensations. Following each exercise,
the patient is asked to rate the fear provoked by the particular exercise as well as
its similarity to the panic-induced sensations. Exercises that elicit distress are then
selected for repeated practice both in session and for homework. Further information
on these procedures can be found elsewhere (e.g., Craske & Barlow, 2007; Schmidt
& Trakowski, 2004).
While exposure-based techniques address many of the physical and behavioral sequelae
of panic disorder, cognitive restructuring serves to directly address the fear-provoking
thoughts that are believed to be central to the condition. The first step in the
restructuring is identifying anxiety-provoking thoughts. Some patients are more
aware of their thoughts than others but probing as well as the assessment will
typically identify many of the key anxiogenic thoughts. When these methods are
insufficient, therapist-assisted exposure will often reveal such thoughts when sufficient
anxiety is generated. The goal of cognitive restructuring is to examine and correct
maladaptive thoughts as well as to enable the patient to generate alternatives. The
themes of panic-related anxious thoughts vary; however, they regularly fall into two
categories—probability overestimation and catastrophization.
Probability overestimation involves greatly overestimating the likelihood of an
event (e.g., “Being dizzy means I will pass out”). In many instances, education
about the physical effects of arousal (e.g., anxiety causes hyperventilation, which in
turn often creates dizziness) is a critical starting point to cognitive restructuring.
However, behavioral experiments including IE exercises are often important in
providing compelling disconfirmation of the threatening thought (e.g., having the
patient repeatedly hyperventilate until very dizzy to see that these intense symptoms
do not lead to passing out).
The second type of thinking that is common for panic clients is catastrophization
and typically involves prediction that the consequences of panic are far worse than
reality. For example, patients may believe that they will panic at work and make a
“complete fool of themselves.” Careful examination of prior panic attacks as well as
planned exposure is useful in illuminating the more accurate outcomes of panic (e.g.,
“No one even noticed when I panicked”). Of course, cognitive restructuring, in vivo
exposure, and IE as well as other techniques often are designed in conjunction to

provide a compelling disconfirmation of the ideas that maintain and exacerbate panic.
Efficacy and Effectiveness
Efficacy
CBT is viewed as the most efficacious form of treatment for most anxiety disorders and
is generally considered to be the ideal type of treatment modality for panic disorder
(Barlow et al., 2002). Randomized controlled trials (RCTs) have clearly indicated
the efficacy of CBT in the treatment of panic disorder (Barlow, Gorman, Shear, &
Woods, 2000). RCTs examining the use of CBT for panic disorder have consistently
found impressive effect sizes with a mean effect size of 0.68 in meta-analyses (Gould,
Otto, & Pollack, 1995) with the majority of patients being classified as treatment
responders (Mitte, 2005). These effects have been demonstrated in tightly controlled
trials by independent research teams, showing the efficacy of CBT for panic disorder
in comparison to placebo (Barlow et al., 2000; Sharp, Power, Simpson, & Swanson,
1996), applied relaxation (Clark et al., 1994), nondirective supportive therapy (Craske,
Maidenberg, & Bystritsky, 1995), and the use of pharmacotherapy, especially when
considering long-term treatment gains (Otto & Deveney, 2005). As a result, CBT has
been listed as an empirically supported treatment for panic disorder by the American
Psychological Association Task Force (Chambless & Ollendick, 2001).
Recent meta-analytic examinations of the effects of singular and combined treatment
approaches have shown that the combination of CBT and pharmacotherapy tends to
provide beneficial effects in the treatment of panic disorder in the short-term, acute
treatment phase; however, when examining the long-term maintenance of treatment
gains, the effects of CBT are believed to be more enduring (Hofmann, Sawyer, Korte,
& Smits, 2009), particularly once medication has been discontinued. In fact, it has
been suggested that the discontinuation of pharmacotherapy may actually have a
deleterious effect on prior treatment gains (Schmidt, Koselka, & Woolaway-Bickel,
2001), thereby underscoring the potential difficulties associated with discontinuing
this treatment approach over time. For example, the use of benzodiazepines has been
shown to be efficacious in the acute treatment of anxiety; however, discontinuation
of these medications is associated with significant withdrawal sensations (Roy-Byrne
& Hommer, 1988) which tend to mirror the symptoms of anxiety and result in
rebound anxiety (Fontaine, Chouinard, & Annable, 1984). Fortunately, evidence
has emerged showing that CBT can assist with reducing the distress associated with
withdrawal sensations experienced when tapering benzodiazepines among those with
panic disorder (Otto et al., 2010; Otto et al., 1993).
While older, primarily exposure-based interventions and newer CBT-based inter-
ventions have reliably been shown to be efficacious in RCTs, a recent review paper
revealed some interesting findings regarding historical trends in the efficacy of CBT
for anxiety (Öst, 2008). Specifically, Öst (2008) reviewed over 400 RCTs for panic
and other anxiety disorders and found that the average effect size for panic disorder
treatment trials has decreased from an effect size of 2.40 for cognitive therapy in the
Panic Disorder 925
1990s to an effect size of 1.23 for cognitive behavioral therapy in the 2000s, thereby
demonstrating the negative associations between year of publication and effect sizes
for the primary outcome measures used in the studies. These findings may be due to
a number of factors, such as an increase in symptom severity in more recent trials;
however, this review raises a significant question about whether the integration of
cognitive therapy and interoceptive exposure has significantly enhanced efficacy in the
treatment of panic. Öst, Thulin, and Ramnerö (2004) conducted a dismantling study
illustrating this effect, in which panic disorder patients were randomized to receive
either in vivo exposure or CBT. Results revealed that while both groups evidenced
significant improvements across a wide range of treatment outcomes, there were no
differences in treatment outcome between the groups, 67% of the in vivo exposure
group and 79% of the CBT group having significant reductions in the primary out-
come at posttreatment. At follow-up, 74% of the in vivo exposure group and 76% of
the CBT group had significant treatment gains. So while it is fair to say that CBT for
panic disorder has demonstrated high efficacy, it is also important to note that the use
of interoceptive techniques and cognitive restructuring may not significantly enhance
treatments that rely on basic exposure.
Effectiveness
While considerable research has supported the use of CBT as an efficacious treatment
for panic disorder, less work has examined the dissemination and effectiveness of
CBT for panic disorder in real-world settings, such as primary care and community
mental health centers. The majority of patients with panic disorder initially seek
treatment for their symptoms in primary care settings (Kessler et al., 2006; Wang
et al., 2005), which underscores the need for effectiveness trials in real-world settings
to address this public health concern. As such, primary care physicians are commonly
the first to see individuals suffering from panic disorder, with 85% of panic disorder
patients initially seeking medical attention for their symptoms (Katerndahl & Realini,
1995). At the onset of panic attacks, many patients will present at medical centers
since their symptoms (e.g., racing heart, shortness of breath, numbness) tend to
be misinterpreted as symptoms of an impending medical condition such as having
a heart attack or a stroke. Unfortunately, it appears that a minority of patients in
primary care settings are recognized as having an anxiety condition when presenting
for treatment in a primary care setting (Ormel, Koeter, van den Brink, & van de
Willige, 1991) and it has been estimated that 70% of panic disorder patients have an
average of 10 contacts with a physician before receiving a correct diagnosis (Sheehan,
1982). Moreover, Roy-Byrne, Katon, Cowley, and Russo (2001) found that of those
correctly diagnosed with panic disorder in a primary care setting, only 12% received
psychotherapy containing some elements of CBT.
Despite the lack of recognition of panic and anxiety conditions and the low
percentage of those receiving efficacious treatment for panic in these settings, there
are some promising effectiveness trials examining the integration of CBT into primary
care settings. These trials have used a variety of strategies, including training primary
care physicians in CBT, using self-help and computer-assisted treatments in these
settings, and using collaborative care models that involve the integration of CBT-
trained mental health therapists into primary care settings (Grey, Salkovskis, Quigley,
Clark, & Ehlers, 2008; Roy-Byrne et al., 2005; Roy-Byrne et al., 2010). These
effectiveness trials suggest significant patient improvement can be achieved when
CBT is incorporated into primary care settings.
Effectiveness trials examining the use of CBT for panic disorder have also been
conducted in community mental health centers. Based on the limited reports available,
research has shown that manualized CBT protocols for the treatment of panic disorder
can be administered effectively at community mental health centers with high rates
of treatment responders at posttreatment (87%) and at 1-year follow-up (89%),
suggesting that the treatment gains at posttreatment (Wade, Treat, & Stuart, 1998)
and at 1-year follow-up (Stuart, Treat, & Wade, 2000) tend to be comparable to those
reported for efficacy trials conducted at research centers. Likewise, reports evaluating
the use of empirically supported CBT protocols in managed care settings also suggest
that CBT protocols result in improvements over treatment as usual (Addis et al.,
2006).
Cognitive Behavioral Therapy for Panic Disorder with

Comorbid Disorders
Treatment in the Context of Comorbidity

Like most psychiatric conditions, panic disorder has been shown to have substantial
overlap with other mental health disorders. Specifically, panic disorder has been asso-
ciated with high rates of comorbidity with anxiety, mood, and substance use disorders
(Brown, Campbell, Lehman, Grisham, & Mancill, 2001; Kessler, Chiu, Demler, &
Walters, 2005). Panic disorder has also been shown to be highly comorbid with per-
sonality disorders (Mennin & Heimberg, 2000; Telch, Kamphuis, & Schmidt, 2011).
Because patients with panic disorder commonly present with comorbid disorders,
there has been increased attention paid to examining the effect of comorbidity on the
treatment of panic disorder.
Most studies examining the effect of comorbidity in panic disorder tend to evaluate
the treatment response of patients with comorbid conditions when using CBT
protocols focusing on the treatment of panic disorder. The results of these studies
tend to be variable, with a number of studies providing evidence for the reduction
of comorbid symptoms during the course of CBT, while other studies suggest
that CBT for panic disorder does not lead to a reduction in comorbid symptoms.
While treatment of panic disorder per se is relatively straightforward, in most clinical
settings panic disorder will not be present in isolation, thereby leading to a more
complex set of issues for the clinician to deal with. In this section, we will review
the literature examining treatment for panic disorder in the context of comorbid
conditions.
Some research has suggested that treatment effects of CBT for panic disorder
may be attenuated in those with comorbid personality disorders and depression
(Mennin & Heimberg, 2000). Recently, Telch et al. (2011) found that patients with
Panic Disorder 927
panic disorder with comorbid Cluster A and Cluster C personality disorders tended
to have elevated severity of symptoms at baseline and posttreatment, and poorer
treatment outcome, after controlling for baseline panic disorder and personality
disorder severity.
Other reports have also found that certain comorbid diagnoses are not affected
even when CBT is generally efficacious for panic disorder. For example, comorbid
alcohol use disorders and posttraumatic stress disorder (PTSD) may not be impacted
by CBT for panic (Bowen, D’Arcy, Keegan, & Senthilselvan, 2000; Teng et al.,
2008). Teng et al. (2008) conducted an investigation examining the use of CBT
for panic disorder or a supportive psychoeducation control in a group of individuals
with a principal PTSD diagnosis and comorbid panic. The intervention resulted in a
more substantial reduction in panic frequency, severity, and distress than the control
treatment; however, the symptom severity for PTSD and other comorbid conditions
was not reduced in either condition.
Still other evidence suggests that comorbid conditions may benefit from CBT
for panic disorder. Tsao et al. (2002, 2005) assessed the use of a CBT-based
panic intervention for panic disorder patients with a broad spectrum of comorbid
diagnoses. These investigations suggest that the panic-focused intervention resulted
in reductions in the severity of the comorbid diagnoses as well as the number
of comorbid conditions that met diagnostic criteria at posttreatment. Recently,
Emmrich et al. (2012) examined the impact of CBT for panic disorder in comorbid
depression, finding depressive symptoms to be significantly reduced at posttreatment.
These investigations are consistent with the idea that certain comorbid conditions are
secondary to panic disorder, or it may be the case that CBT skills for panic disorder
effectively generalize to other conditions.
It has also been suggested that comorbidity may actually be associated with
enhanced treatment outcome for some panic disorder patients (Chambless,
Renneberg, Goldstein, & Gracely, 1992). Recently, Olatunji, Cisler, and Tolin
(2010) conducted a meta-analytic investigation examining the effect of comorbidity
on treatment outcome in patients with anxiety disorders, finding positive effect sizes
for panic disorder patients with comorbid conditions (k = 13, z = 3.81, p < .001).
As suggested by Olatunji et al., it is possible that panic disorder patients with
comorbid conditions may have a differential treatment response, possibly having an
enhanced response to treatment. It is not clear exactly why panic disorder patients
with comorbid conditions show larger effect sizes. One explanation is that these
individuals may have greater overall severity pretreatment because of the comorbid
conditions and therefore have more room to change in the context of treatment,
or they have more room to regress to the mean while at the same time being less
responsive to control conditions (Olatunji et al., 2010).
Overall, results of these investigations examining the effects of comorbidity in
the treatment of panic disorder appear to be complex and potentially contradictory.
Although there are considerable methodological differences across studies, it appears
that at least some of the incongruous findings are due to differences in the type and
severity of the comorbid conditions examined. Further investigation is needed to
clarify this situation.
Pharmacotherapy
Pharmacotherapy is also commonly used in the treatment of panic disorder. A

comprehensive review of medication treatment for panic disorder is beyond the scope
of this chapter, but we will provide a few salient findings since the majority of patients
with panic disorder presenting for CBT will be medicated. A wide range of classes
of medication, including selective serotonin reuptake inhibitors (SSRIs), serotonin
and norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants, tetracyclic
antidepressants, and benzodiazepines, have all been shown to be efficacious for panic
disorder (Mitte, 2005; Pull & Damsa, 2008). All these classes of medication have
similar efficacy when taken as prescribed, though SSRIs and SNRIs have emerged as the
frontline treatments due to their more tolerable side effects (Pull & Damsa, 2008). In
fact, meta-analyses have found CBT and pharmacotherapy to have comparable efficacy
with regard to panic symptom reduction (Mitte, 2005; Westen & Morrison, 2001).
However, studies have also found that upon discontinuation of pharmacotherapy,
many patients relapse within 6 months (Roy-Byrne & Cowley, 2002).
In an effort to improve treatment outcomes, researchers have also investigated
the combination of CBT and pharmacotherapy for panic disorder (Schmidt et al.,
2001). A consistent and somewhat surprising finding indicates that across various
combinations of medications and CBT, there is no added efficacy by supplementing
CBT with pharmacotherapy other than a slight short-term advantage of combined
treatment (Hofmann et al., 2009). Previous work suggests that the lack of additive
long-term benefits may be due to specific medication dose levels, sequencing of the
treatments, and relapse from medication cessation (Schmidt et al., 2001; Schmidt &
Smith, 2005). Although a combined treatment approach can be considered for panic
disorder, it is important for clinicians to be reminded that monotherapy (CBT alone)
may very well be more efficacious, though individual client factors such as motivation
and treatment history should be taken into account when determining a treatment
plan (Schmidt et al., 2001).
Treatment Innovations
Computerized Interventions
Computerized treatments for panic disorder have begun to appear over the past
decade. The advantages of computerized treatments are similar to those previously
seen with more traditional self-help book therapy (or bibliotherapy) as they require
little to no involvement from a trained mental health professional, reducing the cost
of treatment and the burden to the mental health system. However, computerized
treatments offer additional advantages over bibliotherapy as they can be interactive,
which can provide the user with a more engaging, personally tailored therapy
experience. An engaging protocol should lead to greater compliance and decreased
attrition. Additionally, more sophisticated, computer-based platforms can provide a
means of assessing treatment compliance, comprehension, and clinical progress.
Panic Disorder 929
To date, there have been approximately 20 studies evaluating computer- and

Internet-based treatments for panic disorder, including a number of well-controlled
RCTs with large sample sizes. Recent reviews of these protocols have found significant
improvements compared to control groups as well as comparable treatment gains as
compared to individual and group therapy (mean d = 0.93; Andrews et al., 2010;
Reger & Gahm, 2009). For example, Carlbring et al. (2006) evaluated a 10-week
Internet-based CBT protocol supplemented with phone calls versus a wait-list control.
At the end of treatment, approximately 80% of patients no longer met criteria for
a diagnosis of panic disorder, whereas there were no remitted cases in the control
group. These treatment gains were maintained after a follow-up period. Studies
have also compared the effect of computerized CBT to live CBT (Bergstrom et al.,
2010; Carlbring et al., 2005; Kiropoulos et al., 2008). These studies suggest roughly
comparable effect sizes for computerized and in-person CBT protocols (between
groups d = 0.00–0.16), although these comparisons were certainly underpowered
and lack tests of statistical equivalence. As would be expected, research shows that
Internet CBT is more cost-effective than group CBT (Bergstrom et al., 2010), which
is often used to reduce the expense of individual treatment.
Researchers have also investigated the effectiveness of computerized CBT protocols
within primary care settings. In Australia, a study found that treatment gains in
patients with panic disorder did not differ between patients supervised by a psycholo-
gist or general medical practitioner in a 12-week open trial utilizing an online program
highlighting CBT techniques (Shandley et al., 2008). A similar study implemented a
computer-assisted CBT program in primary care settings designed for use with rela-
tively inexperienced therapists (Craske et al., 2009). In this study, patients interacted
with novice therapists and used a computer program that facilitated their learning
of typical CBT skills. According to preliminary data, patients found this treatment
to be tolerable and effective at significantly reducing their symptoms (Craske et al.,
2009).
Another interesting technological advancement has been the incorporation of
virtual reality to facilitate the exposure component of CBT for panic disorder.
The use of virtual reality as an exposure tool has a lot of benefits, such as being
able to produce distinct scenarios quickly rather than having to take the time to
travel physically to different locations. Furthermore, virtual reality allows therapists
to tightly control relevant exposure parameters (e.g., the number of people in the
scenario), and gives patients the ability to conduct exposures that would otherwise
be too difficult or expensive (e.g., sitting on an airplane). Preliminary accounts of
virtual reality exposure are encouraging (Martin, Botella, Garc ı́a-Palacios, & Osma,
2007); however, most reports are case studies or small RCTs (Botella et al., 2007;
Meyerbröker & Emmelkamp, 2010).
Dissemination and Transdiagnostic Approaches

Dissemination of empirically established treatments for mental health disorders is a
significant challenge (Stirman, Crits-Christoph, & DeRubeis, 2004). Unfortunately,
most individuals with psychiatric problems do not receive efficacious, evidence-based
treatments (U.S. Department of Health and Human Services, 1999). This issue
is especially important in the treatment of panic disorder patients, most of whom

present for treatment in primary care settings, tend to be misdiagnosed, and do
not receive evidence-based treatments once they do receive an accurate diagnosis. It
seems that these issues could be partially resolved through improved dissemination of
CBT.
Typically, CBT is delivered with disorder-specific treatment manuals. This approach
works well in research settings, where therapists are generally trained by highly skilled
treatment outcome researchers. While research settings are ideal for testing the
efficacy of a novel treatment in a highly controlled environment, it creates a problem
for the dissemination and generalizability of efficacious treatments to the community.
The challenges associated with the dissemination of evidence-based treatments from
research centers to the community invariably raise a number of questions. What is
the best approach to train clinicians in the community? Is it feasible to train clinicians
on efficacious treatment protocols for each disorder treated? How should community
clinicians approach treatment when dealing with severely affected clients who may
have complex comorbidity issues?
CBT protocols tend to be fairly complex and require clinicians to receive extensive
training and to be competent in the use of these protocols. The complexity and
training requirements of CBT protocols have resulted in underlying issues with
the dissemination of these treatments. One attempt at addressing the issue of
dissemination has been the development of transdiagnostic treatment approaches
(Barlow et al., 2011; Norton, 2008; Schmidt et al., 2012). These approaches provide
a parsimonious approach to treatment by creating protocols designed to treat multiple
disorders. Transdiagnostic approaches have been developed to treat disorders that
are deemed to be similar in nature, are viewed to have the same underlying or
maintaining factors, and tend to be responsive to the same treatment mechanisms.
These approaches provide an attractive alternative to the complex, disorder-specific
treatment CBT protocols.
Barlow et al. (2011) developed a transdiagnostic treatment approach designed to
treat the emotional disorders (i.e., anxiety and unipolar depressive disorders). This
treatment approach integrates emotion regulation strategies with traditional cognitive
behavioral strategies that have been shown to be efficacious in the treatment of
the emotional disorders. The primary advantage of this protocol is that it provides
clinicians with one treatment protocol to concurrently treat multiple anxiety disorders
and depression. Farchione et al. (2012) conducted an RCT in a group of patients with
anxiety disorders and unipolar depression. The authors reported large reductions in
anxiety disorder diagnoses at posttreatment across the anxiety disorders (β = −0.58,
p < .001, Hedges’ g = 1.39) and also reported a decrease in comorbid depressive
symptoms (β = −0.46, p < .001, Hedges’ g = 1.11). Given the high rate of
comorbidity among panic disorder and additional anxiety disorders and depression,
the Unified Protocol may be beneficial for clinicians to use when dealing with panic
disorder patients with depression comorbidity.
Schmidt et al. (2012) have also developed a transdiagnostic treatment approach
for the anxiety disorders called False Safety Behavior Elimination Treatment (F-SET).
F-SET was designed to treat multiple anxiety disorders through the identification
and elimination of avoidance and coping strategies utilized by anxiety patients.
Panic Disorder 931
These strategies, called safety aids, are ubiquitous across anxiety conditions and
play a central role in the maintenance of anxiety conditions. A major strength of
F-SET is the straightforward nature of the intervention, which focuses on iden-
tification and elimination of safety aids, which tend to be similar across anxiety
disorders. The F-SET protocol is especially helpful for clients with multiple anxiety
conditions, who tend to use the same safety behaviors with each diagnosed anxi-
ety condition. For example, Schmidt et al. (2012) found that 88% of participants
in the F-SET condition, which included patients with panic disorder, social anx-
iety disorder, and generalized anxiety disorder, demonstrated clinically significant
improvement.
Attrition and Nonresponders
Adjuncts to Cognitive Behavioral Therapy for Panic Disorder

Despite the effectiveness of CBT in the treatment of panic disorder, treatment
outcome studies have shown that a substantial portion of panic disorder patients drop
out of treatment prematurely, have a marginal response to treatment, or are classified
as nonresponders by the end of treatment. It has been estimated that 26% of panic
disorder patients drop out of treatment prematurely in community settings (Wade
et al., 1998), and that of the patients completing treatment, there are still a number
of patients that are classified as nonresponders at posttreatment. The high rates of
attrition and treatment nonresponders in CBT for panic disorder raise the question of
how best to treat these individuals. That is, are there additional treatment techniques
that can be added to CBT for panic disorder to enhance treatment outcome in these
individuals?
One approach to ameliorate low treatment response has been to augment CBT by
incorporating techniques from additional forms of treatment to maximize treatment
response, including the use of mindfulness techniques (Roemer & Orsillo, 2002),
emotion regulation techniques (Barlow, Allen, & Choate, 2004; Moses & Barlow,
2006), and D-cycloserine (DCS; Hofmann et al., 2006). Although the use of DCS as
an adjunct to CBT for panic disorder is in the initial stages, some preliminary reports
are encouraging. Otto et al. (2010) examined the augmentation of a brief CBT for
panic disorder with DCS in a randomized, double-blind, placebo-controlled trial.
The use of DCS enhanced treatment outcome, resulting in larger effect sizes than for
those receiving CBT alone (Otto et al., 2010).
There has also been an increased interest in developing methods to address the
high rate of dropout in panic disorder patients. Low motivation has been identified
as one factor that may influence treatment dropout rates. Keijsers, Kampman, and
Hoogduin (2001) reported that of 161 panic disorder patients enrolling in CBT
treatment at an anxiety clinic approximately 20% dropped out of treatment. Of the
variables examined (i.e., education level, motivation, personality psychopathology, and
symptom severity), only education level and low motivation were significant predictors
of dropout. These findings may point to the potential benefit of augmenting CBT for
panic disorder with techniques to enhance motivation for treatment.
Recently, the utility of adding motivational interviewing (MI; Miller & Rollnick,
2002) techniques to CBT in the treatment of anxiety disorders has been examined.
Preliminary research has suggested that incorporating MI techniques into CBT
enhances treatment outcome for anxiety disorders (Buckner, Ledley, Heimberg, &
Schmidt, 2008; Maltby & Tolin, 2005; Merlo et al., 2010; Westra, Arkowitz, &
Dozois, 2009). Westra and Dozois (2006) examined the use of a three-session MI
pretreatment before group CBT in a mixed anxiety sample of patients with panic
disorder, generalized anxiety disorder, and social anxiety disorder. Those receiving MI
were found to have increased homework compliance, higher expectancy for anxiety
control, and a significantly higher level of responders at posttreatment. This provides
preliminary evidence for the potential benefits of using MI as an adjunct to CBT in
the treatment of panic disorder.
Conclusions
Panic disorder can be a chronic and highly debilitating condition. Fortunately, there
are a number of scientifically established treatments for this disorder, with CBT being
a clear treatment of choice. As reviewed in the chapter, CBT has vast empirical
support for its efficacy in treating panic disorder. Moreover, strides have been made
to disseminate CBT for panic in primary care and other settings. However, there
is some concern that we have reached something of an “efficacy plateau” as newer
CBT interventions do not appear to clearly outperform older, exposure-focused
interventions. Moreover, dissemination remains a critical challenge as the majority of
individuals suffering from panic do not receive CBT. On the positive side, there is
promise in these areas. For example, the use of transdiagnostic treatment approaches
and computerized interventions are likely to speed dissemination, and researchers have
begun to examine different approaches to enhance outcomes through augmentation
of protocols with other treatment strategies as well as certain substances (e.g.,
D-cycloserine, motivational interviewing, emotion regulation).
References
Addis, M. E., Hatgis, C., Cardemil, E., Jacob, K., Krasnow, A. D., & Mansfield, A. (2006).
Effectiveness of cognitive-behavioral treatment for panic disorder versus treatment as usual
in a managed care setting: 2-year follow-up. Journal of Consulting and Clinical Psychology,
74, 377–385. doi:10.1037/0022-006X.74.2.377
(4th ed.).Washington, DC: Author.
Andrews, G., Cuijpers, P., Craske, M. G., McEvoy, P., & Titov, N. (2010). Computer therapy
for the anxiety and depressive disorders is effective, acceptable and practical health care: A
meta-analysis. PLoS ONE, 5, e13196. doi:10.1371/journal.pone.0013196
Antony, M. M., Orsillo, S. M., & Roemer, L. (2001). Practitioner’s guide to empirically based
measures of anxiety. New York, NY: Plenum.
Panic Disorder 933
Barlow, D. H. (2002). Anxiety and its disorders: The nature and treatment of anxiety and panic.
disorders. Behaviour Therapy, 35, 205–230. doi:10.1016/S0005-7894(04)80036-4
Barlow, D. H., & Craske, M. G. (2007). Mastery of your anxiety and panic: Workbook (4th ed.).
panic disorder. Behaviour Therapy, 20, 261–282. doi:10.1016/S0005-7894(89)80073-5
Barlow, D. H., Farchione, T. J., Fairholme, C. P., Ellard, K. K., Boisseau, C. L., & Ehrenreich-
May, J. (2011). The unified protocol for the transdiagnostic treatment of emotional disorders:
Therapist guide. New York, NY: Oxford University Press.
Barlow, D. H., Gorman, J. M., Shear, M. K., & Woods, S. W. (2000). Cognitive-behavioral
therapy, imipramine, or their combination for panic disorder: A randomized controlled
trial. Journal of the American Medical Association, 283, 2529–2536. doi:10.1001/
jama.283.19.2529
Barlow, D. H., Raffa, S. D., & Cohen, E. M. (2002). Psychosocial treatments for panic
disorders, phobias, and generalized anxiety disorder. In P. E. Nathan & J. M. Gorman
(Eds.), A guide to treatments that work (pp. 301–335). New York, NY: Oxford University
Press.
Beck, A. T. (1988). Cognitive approaches to panic disorder: Theory and therapy. In S. Rachman
& J. Maser (Eds.), Panic: Psychological perspectives (pp. 91–109). Hillsdale, NJ: Erlbaum.
Beck, A. T., & Emery, G. (1985). Anxiety disorders and phobias: A cognitive perspective.
New York, NY: Basic Books.
Beck, A. T., Kovacs, M., & Weissman, A. (1979). Assessment of suicidal intention: The
Scale for Suicide Ideation. Journal of Consulting and Clinical Psychology, 47 , 343–352.
doi:10.1037/0022-006X.47.2.343
Bergstrom, J., Andersson, G., Ljotsson, B., Ruck, C., Andreewitch, S., Karlsson, A., Lin-
defors, N. (2010). Internet-versus group-administered cognitive behaviour therapy for
panic disorder in a psychiatric setting: A randomised trial. BMC Psychiatry, 10, 54.
doi:10.1186/1471-244X-10-54
Botella, C., Garc ı́a-Palacios, A., Villa, H., Baños, R. M., Quero, S., Alcañiz, M., & Riva,
G. (2007). Virtual reality exposure in the treatment of panic disorder and agoraphobia:
A controlled study. Clinical Psychology & Psychotherapy, 14, 164–175. doi:10.1002/
cpp.524
Bowen, R. C., D’Arcy, C., Keegan, D., & Senthilselvan, A. (2000). A controlled trial of
cognitive behavioral treatment of panic in alcoholic inpatients with comorbid panic
disorder. Addictive Behaviors, 25, 593–597. doi:10.1016/S0306-4603(99)00017-9
Brown, T. A., Campbell, L. A., Lehman, C. L., Grisham, J. R., & Mancill, R. B. (2001).
Current and lifetime comorbidity of the DSM-IV anxiety and mood disorders in a
large clinical sample. Journal of Abnormal Psychology, 110, 585–599. doi:10.1037/0021-
843X.110.4.585
Buckner, J. D., Ledley, D. R., Heimberg, R. G., & Schmidt, N. B. (2008). Treating
comorbid social anxiety and alcohol use disorders. Clinical Case Studies, 7 , 208–223.
doi:10.1177/1534650107306877
Carlbring, P., Bohman, S., Brunt, S., Buhrman, M., Westling, B. E., Ekselius, L., & Andersson,
G. (2006). Remote treatment of panic disorder: A randomized trial of Internet-based
cognitive behavior therapy supplemented with telephone calls. American Journal of
Psychiatry, 163, 2119–2125. doi:10.1176/appi.ajp.163.12.2119
Carlbring, P., Nilsson-Ihrfelt, E., Waara, J., Kollenstam, C., Buhrman, M., Kaldo, V., …
Andersson, G. (2005). Treatment of panic disorder: Live therapy vs. self-help via the Inter-
net. Behaviour Research and Therapy, 43, 1321–1333. doi:10.1016/j.brat.2004.10.002
Chambless, D. L., Caputo, G. C., Jasin, S. E., Gracely, E. J., & Williams, C. (1985).
The Mobility Inventory for Agoraphobia. Behavior Research and Therapy, 23, 35–44.
doi:10.1016/0005-7967(85)90140-8
Chambless, D. L., & Ollendick, T. H. (2001). Empirically supported psychological inter-
ventions: Controversies and evidence. Annual Review of Psychology, 52, 685–716.
doi:10.1146/annurev.psych.52.1.685
Chambless, D. L., Renneberg, B., Goldstein, A., & Gracely, E. J. (1992). MCMI-diagnosed
personality disorders among agoraphobic outpatients: Prevalence and relationship to sever-
ity and treatment outcome. Journal of Anxiety Disorders, 6, 193–211. doi:10.1016/0887-
6185(92)90033-4
461–470. doi:10.1016/0005-7967(86)90011-2
Clark, D. M., Salkovskis, P. M., Hackmann, A., Middleton, H., Anastasiades, P., & Gelder,
M. (1994). A comparison of cognitive therapy, applied relaxation and imipramine in the
treatment of panic disorder. British Journal of Psychiatry, 164, 759–769. doi:10.1192/
bjp.164.6.759
Craske, M. G., & Barlow, D. H. (2007). Mastery of your anxiety and panic (4th ed.).
Craske, M. G., Kircanski, K., Epstein, A., Wittchen, H. U., Pine, D. S., Lewis-Fernandez, R.,
& Hinton, D. (2010). Panic disorder: A review of DSM-IV panic disorder and proposals
for DSM-V. Depression and Anxiety, 27 , 93–112. doi:10.1002/da.20654
Craske, M. G., Maidenberg, E., & Bystritsky, A. (1995). Brief cognitive-behavioral versus
nondirective therapy for panic disorder. Journal of Behavior Therapy and Experimental
Psychiatry, 26, 113–120. doi:10.1016/0005-7916(95)00003-I
Craske, M. G., Rose, R. D., Lang, A., Welch, S. S., Campbell-Sills, L., Sullivan, G., …
Roy-Byrne, P. P. (2009). Computer-assisted delivery of cognitive behavioral therapy
for anxiety disorders in primary-care settings. Depression and Anxiety, 26, 235–242.
doi:10.1002/da.20542
versus breathing retraining within cognitive behavioural therapy for panic disorder with
Deacon, B. J., Lickel, J., & Abramowitz, J. S. (2008). Medical utilization across the anxiety
disorders. Journal of Anxiety Disorders, 22, 344–350. doi:10.1016/j.janxdis.2007.03.004
DiNardo, P. A., Brown, T. A., & Barlow, D. H. (1994). Anxiety disorders interview schedule
for DSM-IV: Lifetime version (ADIS-IV-L). New York, NY: Oxford University Press.
Emmrich, A., Beesdo-Baum, K., Gloster, A. T., Knappe, S., Hofler, M., Arolt, V., …
Wittchen, H. U. (2012). Depression does not affect the treatment outcome of CBT for
panic and agoraphobia: Results from a multicenter randomized trial. Psychotherapy and
Psychosomatics, 81, 161–172. doi:10.1159/000335246
Farchione, T. J., Fairholme, C. P., Ellard, K. K., Boisseau, C. L., Thompson-Hollands, J.,
Carl, J. R., … Barlow, D. H. (2012). Unified protocol for transdiagnostic treatment of
emotional disorders: A randomized controlled trial. Behavior Therapy, 43, 666–678. doi:
10.1016/j.beth.2012.01.001
First, M., Spitzer, R., Gibbon, M., & Williams, J. (1994). Structured clinical interview for
DSM-IV Axis I disorders: Non-patient edition. New York, NY: Biometrics Research
Department.
Panic Disorder 935
Foldes-Busque, G., Marchand, A., Chauny, J. M., Poitras, J., Diodati, J., Denis, I., … Fleet,
R. (2011). Unexplained chest pain in the ED: Could it be panic? American Journal of
Emergency Medicine, 29, 743–751. doi:10.1016/j.ajem.2010.02.021
Fontaine, R., Chouinard, G., & Annable, L. (1984). Rebound anxiety in anxious patients after
abrupt withdrawal of benzodiazepine treatment. American Journal of Psychiatry, 141,
848–852.
Gould, R. A., Otto, M. W., & Pollack, M. H. (1995). A meta-analysis of treatment
outcome for panic disorder. Clinical Psychology Review, 15, 819–844. doi:10.1016/0272-
7358(95)00048-8
Grey, N., Salkovskis, P., Quigley, A., Clark, D. M., & Ehlers, A. (2008). Dissemination
of cognitive therapy for panic disorder in primary care. Behavioural and Cognitive
Hersen, M., & Thomas, J. C. (2007). Handbook of clinical interviewing with adults. Thousand
Oaks, CA: Sage.
Hofmann, S. G., Meuret, A. E., Smits, J. A. J., Simon, N. M., Pollack, M. H., Eisen-
menger, K., … Otto, M. W. (2006). Augmentation of exposure therapy with D-
cycloserine for social anxiety disorder. Archives of General Psychiatry, 63, 289–304.
doi:10.1001/archpsyc.63.3.298
Hofmann, S. G., Sawyer, A. T., Korte, K. J., & Smits, J. A. J. (2009). Is it beneficial to
add pharmacotherapy to cognitive-behavioral therapy when treating anxiety disorders? A
meta-analytic review. International Journal of Cognitive Therapy, 2, 162–178.
Katerndahl, D. A., & Realini, J. P. (1995). Where do panic attack sufferers seek care? Journal
of Family Practice, 40, 237–243.
Keijsers, G. P., Kampman, M., & Hoogduin, C. A. (2001). Dropout prediction in cognitive
behavior therapy for panic disorder. Behavior Therapy, 32, 739–749. doi:10.1016/S0005-
7894(01)80018-6
Kessler, R. C., Chiu, W. T., Demler, O., & Walters, E. E. (2005). Prevalence, severity,
and comorbidity of 12-month DSM-IV disorders in the national comorbidity survey
replication. Archives of General Psychiatry, 62, 617–627. doi:10.1001/archpsyc.62.6.617
Kessler, R. C., Chiu, W. T., Jin, R., Ruscio, A. M., Shear, K., & Walters, E. E.
(2006). The epidemiology of panic attacks, panic disorder, and agoraphobia in the
national comorbidity survey replication. Archives of General Psychiatry, 62, 415–424.
doi:10.1001/archpsyc.63.4.415
Kiropoulos, L. A., Klein, B., Austin, D. W., Gilson, K., Pier, C., Mitchell, J., & Ciechom-
ski, L. (2008). Is Internet-based CBT for panic disorder and agoraphobia as effective
as face-to-face CBT? Journal of Anxiety Disorders, 22, 1273–1284. doi:10.1016/
j.janxdis.2008.01.008
Maltby, N., & Tolin, D. (2005). A brief motivational intervention for treatment-
refusing OCD patients. Cognitive Behavioral Therapy, 34, 176–184. doi:10.1080/
16506070510043741
Martin, H. V., Botella, C., Garc ı́a-Palacios, A., & Osma, J. (2007). Virtual reality exposure in
the treatment of panic disorder with agoraphobia: A case study. Cognitive and Behavioral
Mathews, A. M., Teasdale, J., Munby, M., Johnston, D., & Shaw, P. (1981). Agoraphobia:
Nature and treatment. New York, NY: Guilford Press.
Mennin, D. S., & Heimberg, R. G. (2000). The impact of comorbid mood and personality
disorders in the cognitive-behavioral treatment of panic disorder. Clinical Psychology
Review, 20, 339–357. doi:10.1016/S0272-7358(98)00095-6
Merlo, L. J., Storch, E. A., Lehmkul, H. D., Murphy, T. K., Goodman, W. K., & Geffken, G. R.
(2010). Cognitive behavioral therapy plus motivational interviewing improves outcome
for pediatric obsessive-compulsive disorder: A preliminary study. Cognitive Behaviour

Therapy, 39, 24–27. doi:10.1080/16506070902831773
Meyerbröker, K., & Emmelkamp, P. M. G. (2010). Virtual reality exposure therapy in anxiety
27 , 933–944. doi:10.1002/da.20734
Miller, W. R., & Rollnick, S. (Eds.). (2002). Motivational interviewing: Preparing people for
change (2nd ed.). New York, NY: Guillford Press.
Mitte, K. (2005). A meta-analysis of the efficacy of psycho- and pharmacotherapy in panic
disorder with and without agoraphobia. Journal of Affective Disorders, 88, 27–45.
doi:10.1016/j.jad.2005.05.003
Moses, E. B., & Barlow, D. H. (2006). A new unified treatment approach for the emotional
disorder based on emotion science. Current Directions in Psychological Science, 15,
146–150. doi:10.1111/j.0963-7214.2006.00425.x
Newman, M. G., Holmes, M., Zuellig, A. R., Kachin, K. E., & Behar, E. (2006). The reliability
and validity of the Panic Disorder Self-Report: A new diagnostic screening measure of
panic disorder. Psychological Assessment, 18, 49–61. doi:10.1037/1040-3590.18.1.49
Norton, P. J. (2008). An open trial of a transdiagnostic cognitive-behavioral group therapy for
anxiety disorder. Behavior Therapy, 39, 242–250. doi:10.1016/j.beth.2007.08.002
Olatunji, B. O., Cisler, J. M., & Tolin, D. F. (2010). A meta-analysis of the influence of
comorbidity on treatment outcome in the anxiety disorders. Clinical Psychology Review,
30, 642–654. doi:10.1016/j.cpr.2010.04.008
Ormel, J., Koeter, M. W. J., van den Brink, W., & van de Willige, G. (1991). Recognition,
management, and course of anxiety and depression in general practice. Archives of General
Psychiatry, 48, 700–706. doi:10.1001/archpsyc.1991.01810320024004
Öst, L.-G. (2008). Cognitive behavior therapy for anxiety disorders: 40 years of progress.
Nordic Journal of Psychiatry, 62, 5–10. doi:10.1080/08039480802315590
Öst, L.-G., Thulin, U., & Ramnerö, J. (2004). Cognitive behavior therapy vs. exposure in vivo
in the treatment of panic disorder with agoraphobia. Behavior Research and Therapy, 42,
1105–1127.
Otto, M. W., & Deveney, C. (2005). Cognitive-behavioral therapy and the treatment of panic
disorder: Efficacy and strategies. Journal of Clinical Psychiatry, 66, 28–32.
Otto, M. W., McHugh, R. K., Simon, N. M., Farach, F. J., Worthington, J. J., & Pollack,
M. H. (2010). Efficacy of CBT for benzodiazepine discontinuation in patients with
panic disorder: Further evaluation. Behaviour Research and Therapy, 48, 720–727.
doi:10.1016/j.brat.2010.04.002
Otto, M. W., Pollack, M. H., Sachs, G. S., Reiter, S. R., Meltzer-Brody, S., & Rosenbaum, J.
F. (1993). Discontinuation of benzodiazepine treatment: Efficacy of cognitive-behavior
therapy for patients with panic disorder. American Journal of Psychiatry, 150, 1485–1490.
Peterson, R. A., & Reiss, S. (1993). Anxiety sensitivity index revised test manual. Worthington,
OH: IDS.
Pull, C. B., & Damsa, C. (2008). Pharmacotherapy of panic disorder. Neuropsychiatric Disease
and Treatment, 4, 779–795. doi:10.2147/NDT.S1224
Reger, M. A., & Gahm, G. A. (2009). A meta-analysis of the effects of Internet- and computer-
based cognitive-behavioral treatments for anxiety. Journal of Clinical Psychology, 65,
53–75. doi:10.1002/jclp.20536
Reiss, S. (1991). Expectancy model of fear, anxiety, and panic. Clinical Psychology Review, 11,
141–153. doi:10.1016/0272-7358(91)90092-9
Reiss, S., & McNally, R. J. (1985). The expectancy model of fear. In S. Reiss & R. R. Bootzin
(Eds.), Theoretical issues in behavior therapy (pp. 107–121). New York, NY: Academic
Press.
Panic Disorder 937
Reiss, S., Peterson, R. A., Gursky, D. M., & McNally, R. J. (1986). Anxiety sensitivity, anxiety
frequency and the predictions of fearfulness. Behaviour Research and Therapy, 24, 1–8.
doi:10.1016/0005-7967(86)90143-9
Roemer, L., & Orsillo, S. M. (2002). Expanding our conceptualization of and treatment for
generalized anxiety disorder: Integrating mindfulness/acceptance-based approaches with
existing cognitive-behavioral models. Clinical Psychology: Science and Practice, 9, 54–68.
doi:10.1093/clipsy/9.1.54
Roy-Byrne, P. P., & Cowley, D. S. (2002). Pharmacologic treatment for panic disorder,
generalized anxiety disorder, specific phobia and social anxiety disorders. In P. Nathan &
J. M. Gorman (Eds.), A guide to treatments that work (pp. 337–365). New York, NY:
Roy-Byrne, P. P., Craske, M. G., Stein, M. B., Sullivan, G., Bystritsky, A., Katon, W.,
& Sherbourne, C. D. (2005). A randomized effectiveness trial of cognitive-behavioral
therapy and medication for primary care panic disorder. Archives of General Psychiatry,
62, 290–298. doi:10.1001/archpsyc.62.3.290
Roy-Byrne, P. P., Craske, M. G., Sullivan, G., Rose, R. D., Edlund, M. J., Lang, A. J.,
… Stein, M. B. (2010). Delivery of evidence-based treatment for multiple anxiety
disorders in primary care. Journal of the American Medical Association, 303, 1921–1928.
doi:10.1001/jama.2010.608
Roy-Byrne, P. P., & Hommer, D. (1988). Benzodiazepine withdrawal: Overview and impli-
cations for the treatment of anxiety. American Journal of Medicine, 84, 1041–1052.
doi:10.1016/0002-9343(88)90309-9
Roy-Byrne, P. P., Katon, W., Cowley, D., & Russo, J. (2001). A randomized effectiveness trial
of collaborative care for patients with panic disorder in primary care. Archives of General
Psychiatry, 58, 869–876. doi:10.1001/archpsyc.58.9.869
Schmidt, N. B., Buckner, J. D., Pusser, A., Woolaway-Bickel, K., Preston, J. L., & Norr, A.
M. (2012). Randomized controlled trial of False Safety Behavior Elimination Therapy
(F-SET): A unified cognitive behavioral treatment for anxiety psychopathology. Behavior
Therapy, 43, 518–532. doi:10.1016/j.beth.2012.02.004
Schmidt, N. B., & Keough, M. E. (2010). Treatment of panic. Annual Review of Clinical
Psychology, 6, 241–256. doi:10.1146/annurev.clinpsy.121208.131317
Schmidt, N. B., Koselka, M., & Woolaway-Bickel, K. (2001). Cognitive behavioral and phar-
macological treatment strategies for phobic anxiety disorders. In M. T. Sammons & N. B.
Schmidt (Eds.), Rational psychopharmacology: Combined behavioral and pharmacological
treatments for mental distress (pp. 81–110). Washington, DC: American Psychological
Association.
Schmidt, N. B., & Smith, J. D. (2005). Do medications matter in the context of cognitive
behavior therapy for panic disorder? Journal of Cognitive Psychotherapy, 19, 353–360.
doi:10.1891/jcop.2005.19.4.347
Schmidt, N. B., & Telch, M. J. (1994). The role of safety information and fear of bodily
sensations in moderating responses to a hyperventilation challenge. Behavior Therapy, 25,
197–208.
Schmidt, N. B., & Trakowski, J. (2004). Interoceptive assessment and exposure in
panic disorder: A descriptive study. Cognitive and Behavioral Practice, 11, 81–92.
doi:10.1016/S1077-7229(04)80010-5
Shandley, K., Austin, D. W., Klein, B., Pier, C., Schattner, P., Pierce, D., & Wade, V.
(2008). Therapist-assisted, Internet-based treatment for panic disorder: Can general
practitioners achieve comparable patient outcomes to psychologists? Journal of Medical
Internet Research, 10, e14. doi:10.2196/jmir.1033
Sharp, D. M., Power, K. G., Simpson, R. J., & Swanson, V. (1996). Fluvoxamine,
placebo, and cognitive behaviour therapy used alone and in combination in the treat-
ment of panic disorder and agoraphobia. Journal of Anxiety Disorders, 10, 219–242.
doi:10.1016/0887-6185(96)00008-4
Shear, M. K., Brown, T. A., Barlow, D. H., Money, R., Sholomskas, D. E., Woods, S. W., …
Papp, L. A. (1997). Multicenter collaborative panic disorder severity scale. American
Sheehan, D. (1982). Current concepts in psychiatry: Panic attacks and phobias. New England
Journal of Medicine, 307 , 156–158.
Smits, J. A. J., Powers, M. B., Cho, Y., & Telch, M. J. (2004). Mechanism of change
in cognitive-behavioral treatment of panic disorder: Evidence for the fear of fear
mediational hypothesis. Journal of Consulting and Clinical Psychology, 72, 646–652.
doi:10.1037/0022-006X.72.4.646
Stirman, S. W., Crits-Christoph, P., & DeRubeis, R. J. (2004). Supported psychotherapies: A
synthesis of dissemination theory. Clinical Psychology: Science and Practice, 11, 343–359.
Stuart, G. L., Treat, T. A., & Wade, W. A. (2000). Effectiveness of an empirically based
treatment for panic disorder delivered in a service clinic setting: 1-year follow-up. Journal
Taylor, S., Zvolensky, M. J., Cox, B. J., Deacon, B., Heimberg, R. G., Ledley Roth,
D., … Jurado, S. (2007). Robust dimensions of anxiety sensitivity: Development and
initial validation of the Anxiety Sensitivity Index-3 (ASI-3). Psychological Assessment, 19,
176–188. doi:10.1037/1040-3590.19.2.176
Telch, M. J., Kamphuis, J. H., & Schmidt, N. B. (2011). The effects of comorbid personality
disorders on cognitive behavioral treatment for panic disorder. Journal of Psychiatric
Research, 45, 469–474. doi:10.1016/j.jpsychires.2010.08.008
Teng, E. J., Bailey, S. D., Chaison, A. D., Petersen, N. J., Hamilton, J. D., & Dunn,
N. J. (2008). Treating comorbid panic disorder in veterans with posttraumatic stress
disorder. Journal of Consulting and Clinical Psychology, 76, 704–710. doi:10.1037/0022-
006X.76.4.710
Tsao, J. C., Mystkowski, J. L., Zucker, B. G., & Craske, M. G. (2002). Effects of cognitive-
behavioral therapy for panic disorder on comorbid conditions: Replication and extension.
Behavior Therapy, 33, 493–509. doi:10.1016/S0005-7894(02)80013-2
Tsao, J. C., Mystkowski, J. L., Zucker, B. G., & Craske, M. G. (2005). Impact of
cognitive-behavioral therapy for panic disorder on comorbidity: A controlled investigation.
U.S. Department of Health and Human Services. (1999). Mental health: A report of the Surgeon
General. Rockville, MD: U.S. Department of Health and Human Services, National
Institutes of Health, National Institute of Mental Health.
Wade, W. A., Treat, T. A., & Stuart, G. L. (1998). Transporting an empirically supported
treatment for panic disorder to a service clinic setting: A benchmarking strategy. Journal
of Consulting and Clinical Psychology, 66, 231–239. doi:10.1037/0022-006X.66.2.231
Wang, P. S., Berglund, P., Olfson, M., Pincus, H. A., Wells, K. B., & Kessler, R. C. (2005).
Failure and delay in initial treatment contact after first onset of mental disorders in the
national comorbidity survey replication. Archives of General Psychiatry, 62, 603–613.
doi:10.1001/archpsyc.62.6.603
Westen, D., & Morrison, K. (2001). A multidimensional meta-analysis of treatments for
depression, panic, and generalized anxiety disorder: An empirical examination of the
status of empirically supported treatments. Journal of Consulting and Clinical Psychology,
69, 875–899. doi:10.1037/0022-006X.69.6.875
Panic Disorder 939
Westra, H. A., Arkowitz, H., & Dozois, D. J. A. (2009). Adding motivational interview-
ing pretreatment to cognitive behavioral therapy for generalized anxiety disorder: A
preliminary randomized controlled trial. Journal of Anxiety Disorders, 23, 1106–1117.
doi:10.1016/j.janxdis.2009.07.014
Westra, H. A., & Dozois, D. J. A. (2006). Preparing clients for cognitive behavioral therapy:
A randomized pilot study of motivational interviewing for anxiety. Cognitive Therapy and
Research, 30, 481–498. doi:10.1007/s10608-006-9016-y
Zinbarg, R. E., Barlow, D. H., & Brown, T. A. (1997). Hierarchical structure and general
factor saturation of the Anxiety Sensitivity Index: Evidence and implications. Psychological
Assessment, 9, 277–284. doi:10.1037/1040-3590.9.3.277
40
Agoraphobia
Michael J. Telch, Adam R. Cobb,
and Cynthia L. Lancaster
Laboratory for the Study of Anxiety Disorders, The University of Texas at Austin
History of Agoraphobia
The term agoraphobia was first coined by Westphal (1871) in his description of three
males who experienced intense anxiety when walking across open spaces. Westphal also
noted the physiological symptoms of anxiety (i.e., palpitations, blushing, trembling,
and sensations of heat) and the intense subjective anxiety that is elicited upon
anticipating entering a feared situation. Today, agoraphobia remains one of the
most disabling phobias and one of the most challenging to treat (Wittchen, Gloster,
Beesdo-Baum, Fava, & Craske, 2010).
In the third edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-III; American Psychiatric Association [APA], 1980), agoraphobia was char-
acterized as a “marked fear and avoidance of being alone, or in public places from
which escape might be difficult, or help not available in case of sudden incapacitation”
(p. 227). However, even the DSM-III recognized the linkage between agoraphobia
and panic attacks by stipulating that a diagnosis of agoraphobia with panic attacks
should be coded if the onset of the disorder included recurring panic attacks. In the
third revised edition of the DSM (DSM-III-R; APA, 1987) and subsequently in the
fourth edition (DSM-IV; APA, 1994; DSM-IV-TR; APA, 2000), agoraphobia was
reconceptualized as a common complicating feature of panic, thus relegating agora-
phobia to a panic disorder “subtype” status. In the DSM-IV, the diagnosis “agorapho-
bia” no longer exists; rather, in cases of “pure” agoraphobia, clinicians are instructed to
use the diagnosis “agoraphobia without history of panic disorder.” It is interesting to
note that the diagnostic criteria for agoraphobia in the International Statistical Clas-
sification of Diseases and Related Health Problems (10th ed.; ICD-10; World Health
Organization, 1992)—the diagnostic system used in many other countries outside the
United States—still recognizes agoraphobia as taking precedence over panic disorder.
There continues to be considerable controversy surrounding the current diagnostic
status of agoraphobia. The crux of this controversy concerns whether agoraphobia

DOI: 10.1002/9781118528563.wbcbt40
should be conceptualized as a complication of panic attacks/panic disorder as outlined

in the DSM-IV-TR or whether agoraphobia should be treated as a distinct, phobic
syndrome independent of panic disorder as outlined in the ICD-10. The interested
reader is referred to Wittchen et al. (2010) for an excellent review of this controversial
issue, which has profound implications for both researchers and clinicians.
Epidemiology
Prevalence of Agoraphobia
Data from a community survey in Vermont predating the DSM-III (Agras, Sylvester,
& Oliveau, 1969) estimated the prevalence of agoraphobia to be 6 per 1,000 indi-
viduals. Since that early report, numerous high quality epidemiological investigations
using standard diagnostic criteria have appeared (Adler et al., 2006; Eaton, Kessler,
Wittchen, & Magee, 1994; Kessler et al., 2006; Wittchen & Essau, 1991). Prevalence
rates from these studies vary somewhat as a function of sample, diagnostic criteria,
and diagnostic instrument, but a reasonably conservative estimate of the lifetime
prevalence of agoraphobia with and without panic across studies is approximately 5%.
Further, agoraphobia with and without panic disorder is about 2 and 1.3 times more
likely to occur in women, respectively, and has a mean age of onset in the early 20s
(Kessler et al., 2006).
First Generation Treatment Studies
The first series of research reports on the treatment of agoraphobia appeared almost
50 years ago. These first generation studies share several common features. First,
they all predated the DSM-III and consequently it is not clear what proportion
of the patients in these studies would have met current DSM-IV criteria for panic
disorder with agoraphobia, or agoraphobia without panic disorder, or neither diag-
nosis. Second, the treatments included in this first group all targeted reductions in
situational avoidance and phobic anxiety, as opposed to reductions in panic attacks,
or fear of panic attacks. Third, despite a number of different treatment variations
and labels, they all had a common procedural element, namely having the patient
confront fear-eliciting situations repeatedly with the goal of eliminating the patients’
phobic anxiety and avoidance. Finally, most would not meet the methodological
standards of contemporary treatment outcome investigations; that is, the studies were
underpowered, lacked treatment fidelity assessments, and focused their analyses on
treatment completers only.
The specific treatments studied in these early investigations include systematic
desensitization (Gelder & Marks, 1966; Gillan & Rachman, 1974), imaginal flooding
(Gelder et al., 1973; Marks, Boulougouris, & Marset, 1971), reinforced practice
(Agras, Leitenberg, & Barlow, 1968; Crowe, Marks, Agras, & Leitenberg, 1972),
self-observation (Emmelkamp, 1974), group in vivo flooding (Hand, Lamontagne,
& Marks, 1974; Stern & Marks, 1973; Teasdale, Walsh, Lancashire, & Mathews,
Agoraphobia 943
1977; Watson, Mullett, & Pillay, 1973), and participant modeling/guided mastery
(Bandura, Jeffery, & Wright, 1974; Williams, 1990). As mentioned earlier, these
treatments all shared the central procedural element of having the patient repeat-
edly confront fear-provoking situations. They differ mainly with respect to certain
parameters of exposure, namely, mode of presentation (imaginal vs. in vivo), intensity
(graded vs. ungraded), and mode of facilitation (therapist-aided, partner-aided, or
self-directed).
The primary focus of systematic desensitization in the treatment of agoraphobia has
been to teach the patient to produce inhibitory physiological responses (i.e., deep
muscle relaxation) in order to inhibit the anxiety response to increasingly threatening
situations. Gelder and Marks (1966) compared desensitization with attention placebo
control in treating 20 inpatients with agoraphobia. Despite the trend in favor of
desensitization, differences between the two groups at posttreatment and follow-
up were not statistically significant. Similarly, Gelder, Marks, and Wolff (1967)
found systematic desensitization only slightly more effective than individual or group
psychotherapy in reducing phobic symptoms in 14 patients with agoraphobia. Further,
Wolpe (1974) reported that desensitization is contraindicated in the treatment of
agoraphobia except for those who suffer from a specific fear of open space.
Imaginal Flooding
Imaginal flooding involves exposing the patient in imagination to high levels of
feared situations for prolonged durations. Research investigating its application in
the treatment of agoraphobia first appeared in an article by Watson, Gaind, and
Marks (1971) in which they reported significant reductions in phobic symptoms
as measured by clinical ratings and heart rate response to phobic imagery among
10 agoraphobics. Other investigations of imaginal flooding have been conducted in
the context of comparisons with systematic desensitization (Boulougouris, Marks,
& Marset, 1971). Boulougouris et al., for instance, showed that imaginal flooding
significantly outperformed imaginal desensitization in a mixed sample of patients with
agoraphobia and specific phobias.
In an attempt to assess the role of anxiety experienced during flooding, Chambless,
Foa, Groves, and Goldstein (1979) compared imaginal flooding alone, flooding plus a
relaxant drug, and a control group with 27 outpatient agoraphobics. Results indicated
that imaginal flooding decreased phobic symptoms as measured by client and therapist
ratings, and physiological and behavioral measures. They found some support for the
hypothesis that patients who experienced higher levels of anxiety during treatment
benefited more from the treatment. This finding is in sharp contrast to results reported
by Hussain and Nolan (1971), who treated 40 outpatients diagnosed with anxiety
neurosis with either imaginal flooding with thiopental infusions or imaginal flooding
with saline. Hussain and Nolan suggest that the use of a short-acting barbiturate
(e.g., thiopental) protects against the possibility that exposure therapy may exacerbate
anxiety.
Self-Observation
The self-observation procedure for treating agoraphobia was introduced by
Emmelkamp and colleagues (Emmelkamp, 1974; Emmelkamp & Emmelkamp-
Benner, 1975). Like successive approximation, self-observation requires patients to
gradually enter feared situations. Upon experiencing undue anxiety, the patient is
instructed to return immediately. This procedure is repeated for a number of trials,
with the usual session length being approximately 90 minutes. Unlike successive
approximation, however, patients are not given social reinforcement by the therapist.
Instead, patients are provided with a stopwatch and instructed to record the time
they spend outside. It should be noted that both self-observation and successive
approximation differ from flooding in that they do not require the patient to
experience a reduction in anxiety before terminating the trial.
Emmelkamp (1974) compared the relative effectiveness of self-observation, flood-
ing, a combination of flooding and self-observation, and a wait-list control in treating
20 outpatient agoraphobics. Patients in the first three conditions received a total
of 12 sessions (90 minutes each) over a 4-week period (three sessions per week).
In the flooding sessions, patients received 45 minutes of flooding in imagination
immediately followed by 45 minutes of flooding in vivo. Patients in the combined
flooding/self-observation condition received flooding during the first three sessions
and self-observation for the remaining nine sessions. Results indicated that patients in
all three treatment conditions significantly improved on measures of phobic anxiety,
phobic avoidance (rated by patient, therapist, and observer), and a behavioral in vivo
measure. While no differences were found between self-observation and flooding,
the combined flooding/self-observation treatment was shown to be more effective
than either of the individual treatments. It is possible that the combined treatment
proved more credible to the patients and thus increased their expectation for change.
Unfortunately, credibility assessment was not carried out to test this hypothesis.
Everaerd, Rijken, and Emmelkamp (1973) compared self-observation and succes-
sive approximation in a cross-over design with 16 agoraphobic outpatients. Patients
in both treatment conditions received six 90-minute sessions over a 3-week period
(two sessions per week). Results indicated that both treatments produced significant
improvement in phobic anxiety (rated by client and therapist) and in vivo mea-
surement (number of minutes spent outside). Between-group comparisons yielded
no significant differences on any of the measures. The findings suggest that social
reinforcement administered by the therapist is not an essential component of in vivo
treatments for agoraphobia.
Using a 2 x 2 factorial design, Emmelkamp and Emmelkamp-Benner (1975) tested
the effects of historically portrayed modeling and group versus individual format
on the outcome of self-observation treatment. Thirty-four agoraphobic outpatients
were randomly assigned to one of the following four conditions: (a) video film plus
individual treatment, (b) video film plus group treatment, (c) individual treatment (no
film), and (d) group treatment (no film). Patients in all conditions received four 90-
minute sessions of self-observation. Half of the patients were treated in small groups
of 4 to 6 patients, while the other half were seen individually. The video film, which
lasted 23 minutes, showed three ex-agoraphobics discussing their experiences with
Agoraphobia 945
self-observation treatment. The film stressed that clients had improved by practicing
in the phobic situations. Patients in all conditions were instructed to carry out the
procedure at home. Results showed a significant improvement for all conditions,
as measured by in vivo client and observer ratings of phobic anxiety and phobic
avoidance. Group treatment proved just as effective as individual treatment and the
video film had no effect on treatment outcome. The present findings support the
conclusion that self-observation treatment administered in a group setting is both
effective and cost-efficient in treating agoraphobia.
Participant Modeling/Guided Mastery

Participant modeling was first introduced by Bandura and his colleagues in a series
of elegant experiments investigating cognitive change mechanisms governing the
reduction of pathological fear (Bandura, Adams, Hardy, & Howells, 1980; Bandura,
Jeffery, & Gajdos, 1975; Bandura et al., 1974). As in other exposure-based treatments,
in participant modeling, later renamed guided mastery, the phobic patient confronts
actual fear-provoking situations. However, in guided mastery, the therapist plays
a very active role in incorporating specific mastery enhancing strategies to help
the patient overcome his or her fear. These enhancement elements include: (a)
the therapist modeling coping behavior in the feared situation, (b) the systematic
introduction and subsequent fading of performance aids (e.g., the therapist sits next
to the driving phobic patient and then gradually fades his or her presence), (c)
setting proximal goals and mastering subtasks to help the patient manage challenging
tasks (e.g., having the phobic patient drive only one exit on the highway prior to
tackling multiple exits), (d) identification and elimination of defensive maneuvers
(e.g., having the patient loosen his or her vice grip on the steering wheel), and (e)
encouraging the patient to vary his or her performance (e.g., venture into different
grocery stores).
The first controlled investigation of guided mastery in the treatment of agoraphobia
was reported by Williams, Dooseman, and Kleifield (1984). Thirty-two patients dis-
playing severe driving and height phobias were randomly assigned to one of three con-
ditions: (a) guided mastery, (b) in vivo exposure alone, and (c) no-treatment control.
Total amount of exposure time in the two active treatments was carefully controlled.
At posttreatment, both active treatments outperformed no treatment; however, partic-
ipants receiving guided mastery showed significantly greater improvement than those
receiving in vivo exposure alone on multiple indices of outcome including performance
on behavioral approach tests, and patient ratings of anxiety and coping self-efficacy.
Subsequent studies of guided mastery have provided consistent support for its efficacy
in the treatment of agoraphobia (Hoffart, 1995, 1998; Williams & Zane, 1989).
Self-Directed Exposure
For almost four decades, anxiety disorder researchers have speculated that exposure
to feared situations is the crucial procedural element in the successful treatment
of agoraphobia (Marks, 1978). If this assumption is true, agoraphobia sufferers
should be able to achieve considerable therapeutic benefit on their own through
self-directed practice entering feared situations with guidance coming from a ther-
apist, family member, or self-help manual. Several studies have examined the
effects of simply providing agoraphobia patients with instructions for self-directed
practice.
The first systematic evaluation of a self-directed home-based treatment program
for agoraphobia was conducted by Mathews, Teasdale, Munby, Johnston, and Shaw
(1977). Twelve married agoraphobia patients were seen at their homes and were
provided with manuals which described (a) the development and maintenance of
agoraphobia, (b) principles of target behavior selection, (c) self-monitored practice,
and (d) panic management. In addition, patients’ spouses were provided with a
detailed manual describing the same material with additional sections covering the
spouse’s role in reinforcing phobic behavior and use of contingent attention to
reinforce patients’ practice. A therapist visited patients on eight occasions during the
4-week program. During the home visits, the therapist stressed the importance of
daily practice, gave advice about overcoming specific difficulties encountered during
practice, ensured that future targets had been agreed upon between partners, and
encouraged the use of contingent reinforcement for achieving proximal goals. Results
of the program were quite encouraging. Data obtained from patients’ diaries revealed
a twofold increase in the time spent out of the house. Significant improvement was
also shown on ratings of phobic anxiety, phobic severity, and psychiatric ratings
of overall improvement. Comparison of the present results with those achieved in
earlier studies by the same authors using the same measures, therapists, and assessors
(Mathews et al., 1976) revealed a similar or even greater effect for the home-based
program. A notable finding was that patients showed further improvements on most
measures during the follow-up.
A replication of the Mathews et al. home-based treatment program (Jannoun,
Munby, Catalan, & Gelder, 1980) provided additional evidence for the efficacy
of this self-directed exposure treatment. Twenty-eight women with agoraphobia
were randomly assigned to the self-directed exposure program or a problem-solving
control condition. Self-directed exposure led to a significantly greater increase in
the number of weekly journeys out of the home compared to the problem-solving
treatment. However, the authors also noted the unexpected improvement achieved
in the problem-solving control treatment. This latter finding raises the question as
to whether exposure to phobic situations is a crucial procedural component for fear
reduction to occur as well as the possibility that both treatments may be mediated by
a mechanism other than exposure-facilitated habituation to feared situations.
Several early studies have examined the efficacy of self-directed exposure to
feared situations without the involvement of family members (Greist, Marks, Berlin,
Gournay, & Noshirvani, 1980; McDonald et al., 1979). In McDonald et al., 19
patients with agoraphobia were randomly assigned to a self-exposure homework con-
dition or a nonexposure discussion control. Results revealed a small but statistically
significant superiority of the self-exposure condition on patients’ ratings of phobic
severity and assessors’ ratings of target problems. It should be noted that the supe-
riority of the self-exposure condition was obtained despite evidence from patients’
diaries showing that the groups did not differ in the frequency of outings (McDonald
et al., 1979).
Agoraphobia 947
Summary of Early First Generation Behavioral Treatment Studies

Results of these early behavioral treatment studies are of great historical significance
because they provided compelling evidence, albeit without the rigor of today’s ran-
domized controlled trials (RCTs), that agoraphobics receiving treatments employing
in vivo exposure to fear-provoking situations can achieve significant therapeutic ben-
efit as measured by clinically meaningful reductions in situational avoidance and
phobic anxiety. They also provide some very preliminary data to suggest that exposure
treatments can be enhanced through the systematic addition of certain therapeutic
strategies—a topic we address later in this chapter.
Second Generation Treatment Studies
This next group of treatment studies includes single-site RCTs in which patients
meeting for agoraphobia with panic attacks (DSM-III) were randomly assigned to
a psychological treatment that was compared to either another active treatment, a
nonspecific treatment (attention/placebo control), or delayed treatment (wait-list
control). As a group, the studies in this generation tend to be methodologically
superior to those in the first generation by virtue of their (a) larger sample size,
(b) use of structured diagnostic interviews to ensure patients met the threshold for
agoraphobia, (c) use of psychometrically validated outcome measures, (d) greater
attention to issues of treatment fidelity, (e) greater attention to patient dropouts
in their outcome analyses, and (f) greater attention to the clinical significance of
the changes brought about by the treatments. The treatments investigated in this
generation of studies tend to be exposure-based treatments or attempts to enhance
exposure treatments through one or more augmentation strategies. Representative
studies in this generation (Michelson, Marchione, Greenwald, Testa, & Marchione,
1996; Öst, Thulin, & Ramnero, 2004; van den Hout, Arntz, & Hoekstra, 1994)
are described later in this chapter in the section entitled, “Exposure Augmentation
Strategies in the Treatment of Agoraphobia.”
Third Generation Treatment Studies
This next group of treatment studies includes single-site RCTs in which patients
met DSM-III-R or DSM-IV criteria for panic disorder with agoraphobia. As a
group, the studies in this generation tend to be of high quality and share the same
methodological strengths outlined above. Unlike second generation studies, which
focused primarily on situational exposure treatments alone or in combination with
other treatment augmentation strategies, the treatments investigated in this generation
include therapeutic elements that specifically target panic attacks and panic-related
apprehension. The three most widely researched treatments in this generation are
panic-focused cognitive behavioral therapy (Barlow, Craske, Cerny, & Klosko, 1989;
Craske et al., 2005; Margraf, Barlow, Clark, & Telch, 1993; Telch et al., 1993;
Telch, Schmidt, Jaimez, Jacquin, & Harrington, 1995), cognitive therapy (Clark
et al., 1994; Clark et al., 1999), and applied relaxation training (Öst, 1987, 1988).
Most studies of this generation include mixed samples of panic disorder with and
without agoraphobia. To avoid duplication with Chapter 39 (“Panic Disorder”), we
have limited this review to representative third generation treatment studies focusing
on agoraphobia outcome.
In a comparative study of several widely established treatments for panic disorder
with agoraphobia (PDA), Öst, Westling, and Hellstrom (1993) randomized 45
patients meeting DSM-III-R criteria for panic disorder with moderate to severe
agoraphobia to applied relaxation, in vivo exposure, or cognitive therapy. Patients
in all three conditions received self-exposure homework instructions. The three
treatments yielded significant pre- to posttreatment improvements across behavioral
and self-report measures of agoraphobia with no appreciable differences between the
treatments. On a behavioral assessment of agoraphobia, 86.7% in the applied relaxation
group, 80% in the in vivo exposure group, and 60% in the cognitive therapy group
met criteria for clinically significant improvement at posttreatment. On a self-report
assessment of agoraphobia, 53.3% in the applied relaxation group, 46.7% in the in
vivo exposure group, and 60% in the cognitive therapy group met criteria for clinically
significant improvement at posttreatment. Between-group comparisons revealed no
statistically significant differences in the percentage of participants demonstrating
clinically significant improvement. All three treatments maintained their gains at
1-year follow-up, although only patients assigned to cognitive therapy (26.7%)
sought additional treatment during the follow-up period.
Craske, DeCola, Sachs, and Pontillo (2003) investigated the efficacy of augmenting
panic control treatment (PCT) with in vivo exposure. Patients meeting DSM-IV
criteria for panic disorder with moderate to severe agoraphobia were assigned to
either PCT alone (in which they were encouraged to approach avoided situations, but
were not provided with instruction or feedback) or PCT with formal in vivo exposure
(in which they were encouraged to approach avoided situations and were provided
with instruction and feedback). At posttreatment and at follow-up, both treatments
were deemed equally effective for both panic disorder and agoraphobia. Clinically
significant improvement at posttreatment was achieved in 42% of the PCT-only
group and 32% of the PCT plus exposure group. At 6-month follow-up, 58% of the
PCT-only group and 50% of the PCT plus exposure group met criteria for clinically
significant improvement. There were no statistically significant between-group
differences in the percentage meeting criteria for clinically significant improvement.
Results overall suggest that adding formal in vivo exposure to standard PCT does not
enhance therapeutic outcome in patients displaying moderate to severe agoraphobia.
Unfortunately, the failure to include a treatment arm in which patients receive only
in vivo exposure limits conclusions drawn from this study regarding the relative
benefits of PCT versus in vivo exposure in the treatment of agoraphobia.
In a study designed to address whether cognitive therapy, exposure therapy, and
their combination vary in efficacy depending on the patient’s level of agoraphobia,
Williams and Falbo (1996) randomized 48 panic patients with varying levels of
agoraphobic avoidance to one of four conditions: (a) cognitive therapy, (b) guided
performance mastery, (c) combined cognitive therapy plus guided mastery, and (d)
wait-list. Between-group comparisons of the three active treatments for the full
Agoraphobia 949
sample showed equally large effects across the primary measures of panic attacks,
and agoraphobic avoidance. However, comparison of patients with high and low
levels of agoraphobia revealed that all three treatments were significantly less effective
for reducing panic attacks for those with high levels of agoraphobia (88% vs. 39%,
respectively, at the 2-year follow-up). Accordingly, Williams et al. suggest that
panic disorder treatment studies that exclude patients with agoraphobia may be
overestimating the efficacy of cognitive behavioral therapy (CBT) for panic attacks
and argue that exposure-based treatments that do not directly target panic attacks are
as effective for reducing panic as cognitive therapy.
Investigation of Exposure Parameters in the

Treatment of Agoraphobia
Because in vivo exposure is a cornerstone therapeutic strategy in the treatment of

agoraphobia, it makes sense to examine the parameters of exposure that optimize its
efficacy. In this next section we review studies examining several distinct parameters
of exposure therapy implementation.
Massed versus Spaced Exposure Sessions

What is the optimal frequency of exposure therapy sessions? Are sessions conducted
weekly more effective than sessions occurring every day? In the first study to address
this issue, Foa, Jameson, Turner, and Payne (1980) used a counterbalanced crossover
design to compare the effects of 10 daily sessions with 10 weekly sessions in a
small sample of agoraphobics (N = 11). At posttreatment, the massed condition
outperformed the weekly spaced condition on independent assessor ratings of phobic
anxiety and avoidance.
In the only other study to compare massed versus spaced exposure treatment for
agoraphobia, Chambless (1990) used a between-subjects design to compare massed
versus spaced therapist-assisted in vivo exposure. Agoraphobic patients (N = 19)
received 10 daily or 10 weekly sessions of in vivo exposure along with several
anxiety control strategies including respiratory control training, thought-stopping,
and paradoxical intention. Exposure homework was not given due to the obvious
advantage that would give to patients assigned to the spaced condition. Results
revealed no significant differences in outcome at either posttreatment or 6-month
follow-up. Moreover, they found no evidence to support the claim that massed
sessions would lead to more dropouts and significantly higher relapse relative to spaced
sessions. However, it should be noted that the failure to find differences may have
been due to insufficient statistical power as a result of the relatively small sample size.
Brief versus Standard Treatments for Agoraphobia

Reducing length of treatment has several potential advantages including lower
treatment offset costs and increased accessibility of care. However, these potential
advantages hinge on the assumption that standard empirically supported treatments

for panic disorder with agoraphobia can be condensed without a loss of therapeutic
efficacy. Fortunately, there is now converging evidence across laboratories that brief
CBT confers significant therapeutic benefit over control conditions, including wait-list
(Clark et al., 1999) and nondirective treatment (Craske, Maidenberg, & Bystritsky,
1995). Moreover, studies comparing brief versus standard CBT also suggest that
brief treatments tend to be as effective overall as standard length treatments (Côté,
Gauthier, Laberge, Cormier, & Plamondon, 1994; Gould, Clum, & Shapiro, 1993;
Hecker, Losee, Fritzler, & Fink, 1996).
One limitation of the above studies is that patients exhibited minimal or no
agoraphobia, and thus they do not directly address the efficacy of brief treatments
for agoraphobia symptoms per se. However, there is encouraging evidence that the
efficacy of condensed CBT interventions can also benefit patients with agoraphobia.
Goisman et al., (1987) randomly assigned 40 patients with agoraphobia to receive
self-exposure instructions from a psychiatrist, a self-help book, or a computer. All
three groups improved substantially and continued to maintain those gains through a
6-month follow-up (Goisman et al., 1987). These data are encouraging and suggest
that providing exposure instructions, regardless of the delivery modality, affords major
therapeutic benefits despite only brief contact with a clinician.
In a more ambitious study, Roberge, Marchand, Reinharz, and Savard (2008)
randomized 100 patients meeting DSM-IV criteria for panic disorder with agoraphobia
to 14-session standard CBT (n = 33), 14-session group CBT (n = 35), or 7-session
brief CBT (n = 32). Patients received a self-study manual and were assigned weekly
readings and exercises. The results indicate that regardless of the treatment condition,
CBT for moderate to severe panic disorder with agoraphobia is beneficial in the
intermediate and long term. To this effect, all three treatment conditions significantly
improved quality of life and reduced the intensity of symptoms, producing large
within-group effect sizes (d ranging from 1.13 to 1.68) on the Panic and Agoraphobia
Scale (Bandelow, 1995), and on a clinician-rated index of global severity (d ranging
from 1.41 to 1.65) at 3-month follow-up. A 2-year follow-up report revealed large
within-group effect sizes (d = 1.67 to 1.89) on the primary agoraphobia outcome
measure across the three treatments, which supports the durability of treatment
gains (Marchand, Roberge, Primiano, & Germain, 2009). Not surprisingly, patients
receiving brief individual CBT and group CBT had superior cost-effectiveness relative
to standard individual CBT. The implication of these findings is clear—CBT can be
delivered in more cost-effective formats without reduced efficacy. Future research will
hopefully address two important follow-up questions: (a) Could group CBT also be
delivered in fewer sessions to improve its efficiency? and (b) What are the patient
prognostic factors that predict differential response to brief versus group CBT?
Group versus Individually Administered Treatment

Although several investigators have demonstrated the efficacy of group behavioral
treatment of agoraphobia (Telch, Agras, Taylor, Roth, & Gallen, 1985; Telch et al.,
1993; Telch et al., 1995), few studies have conducted a head-to-head comparison
of individual- versus group-administered treatments for agoraphobia. Sharp, Power,
Agoraphobia 951
and Swanson (2004) compared group with individual CBT in 97 patients meeting
DSM-IV criteria for panic disorder either with or without agoraphobia. On the major
index of agoraphobia treatment outcome, both groups showed statistically equal
symptom reduction at 3-month follow-up; 40% of the participants receiving group
CBT and 58% of the participants receiving individual CBT met criteria for clinically
significant improvement. However, two additional findings are worth noting. First,
47% of the participants assigned to the group treatment condition dropped out of the
study, which is four times higher than that observed in previous group administered
CBT (Telch et al., 1985; Telch et al., 1993; Telch et al., 1995). Second, when
wait-listed patients were given the choice of receiving group or individual treatment,
the majority chose individual treatment.
Therapist-Assisted versus Self-Directed Exposure

Does the presence of the therapist during in vivo exposure to agoraphobic situations
offer advantages over therapist-unaccompanied exposure? Those working directly
with agoraphobics know full well the tremendous dread that many display while
anticipating and performing in vivo exposure procedures. There are several reasons to
believe that therapeutic outcome might be enhanced for patients when the therapist
is present to offer instructions, guidance, and moral support, and to assist the patient
in problem-solving obstacles encountered during in vivo exposure. Until recently,
there have been few data that speak directly to this important issue. Fortunately,
an impressive eight-site clinical trial has been completed that directly addresses the
impact of therapist assistance during in vivo exposure (Gloster et al., 2011). Patients
(N = 369) meeting DSM-IV criteria for panic disorder with moderate to severe
agoraphobia were randomized to a wait-list control group or to group CBT in which
they either (a) completed all situational confrontations as homework, or (b) had a
therapist present for one-third of the situational confrontations. For sessions involving
in vivo exposure in the latter condition, the therapist accompanied the participant for
one in vivo exposure and then assigned two independent exposures for homework.
Results suggest that both CBT interventions were beneficial for patients; however,
those who received therapist-assisted in vivo exposure exhibited superior outcomes,
particularly for agoraphobic avoidance (Cohen’s d = 0.32). This finding supports
the conclusion that the presence of a therapist during the initial exposures to feared
situations enhances the effectiveness of exposure therapy for agoraphobia.
Exposure Augmentation Strategies in the

Treatment of Agoraphobia
In this next section we provide a brief overview of research examining efforts to

enhance the efficacy of exposure-based treatments for agoraphobia by integrating
additional procedural elements. For an excellent in-depth review of the research on
exposure augmentation in agoraphobia, see Meuret, Wolitzky-Taylor, Twohig, and
Craske (2012).
Cognitive Strategies
Several studies have investigated whether cognitive restructuring interventions
enhance the efficacy of exposure-based therapies for agoraphobia (Michelson et al.,
1996; Öst et al., 2004; van den Hout et al., 1994). In a well-crafted, two-phase
design by van den Hout et al. (1994), 24 agoraphobia patients were randomized to
one of two groups: Group 1 received four sessions of cognitive therapy (CT) without
exposure followed by eight sessions of CT plus exposure. Group 2 received four
sessions of a placebo psychotherapy (“associative therapy”) followed by exposure
without CT. At the conclusion of the first 4-week phase, CT resulted in reductions
in panic, but not avoidance, whereas those assigned to the attention control showed
no significant change in panic or avoidance. At the conclusion of 8 weeks of either
exposure therapy or exposure therapy plus CT, no differences were observed, thus
showing that CT did not enhance the effects of exposure.
Öst et al. (2004) randomized 73 patients meeting DSM-IV criteria for panic
disorder with agoraphobia to (a) in vivo exposure alone, (b) in vivo exposure plus
CT, or (c) wait-list control. The two active treatments were equated for both number
of sessions (12–15) and duration of each session (45–90 minutes). Both active
treatments showed large pre-to-post effect sizes and maintenance of improvement
at the follow-up assessment. Comparisons between the two active treatments were
consistent with the earlier findings of van de Hout et al. (1994) showing that those
receiving the combination of CT plus exposure therapy fared no better than patients
receiving exposure therapy alone. The percentage of patients no longer meeting
criteria for a diagnosis of panic disorder with agoraphobia at the end of treatment
was 76% among those receiving CT plus exposure, 62% receiving exposure alone,
and 0% among wait-listed patients. At follow-up, 86% of patients receiving exposure
alone and 74% receiving exposure plus CT no longer met DSM-IV criteria for panic
disorder with agoraphobia (follow-up results include wait-list patients who had been
randomized to an active treatment condition).
In the only study to show a significant exposure enhancement effect of cognitive
therapy, Michelson et al. (1996) randomized 92 patients meeting DSM-III criteria
for agoraphobia with panic attacks to one of three treatment arms: (a) group-
administered graded exposure (GE) alone, (b) GE plus CT, and (c) GE plus relaxation
training (RT). Experienced doctoral-level clinicians delivered the treatments and total
treatment time (48 hours) was equated across the three conditions. Results revealed
that patients assigned to CT plus GE were significantly more likely to achieve high
end-state functioning (44% at posttreatment; 71% at follow-up) relative to GE alone
(22% at posttreatment; 38% at follow-up) or GE plus RT (22% at posttreatment;
33% at follow-up). The observed enhancement effect brought about by CT in this
study raises the obvious question: Why did CT enhance the effects of exposure in
this study but not in the two studies reviewed above (Öst et al., 2004; van den
Hout et al., 1994)? One possibility, although unlikely, is that the increased sample
size led to greater statistical power to detect a CT enhancement effect. A more likely
possibility is that the markedly increased “dose” of CT used by Michelson et al. (i.e.,
at least a threefold increase in therapy hours over other studies) was responsible for
the observed exposure enhancement effects of CT.
Agoraphobia 953
Respiratory Training
For over 25 years, aberrant respiratory functioning has been implicated in the
pathogenesis of panic disorder with agoraphobia (Klein, 1993; Ley, 1985). Reduced
levels of pCO2 (i.e., partial pressure of CO2) brought about through hyperventilation
can lead to a positive feedback loop in which heightened levels of anxiety lead to
increased respiration resulting in further lowering of pCO2 and panic-like symptoms.
Consequently, many of the CBT packages for panic disorder with agoraphobia have
included a breathing retraining component (BRT) designed to normalize pCO2
levels, thus reducing somatic perturbations and, presumably, anxiety and panic.
Several studies have examined whether adding BRT enhances the efficacy of exposure
treatment for panic disorder with agoraphobia (Bonn, Readhead, & Timmons, 1984;
Hibbert & Chan, 1989) or whether BRT contributes to the efficacy of multi-
component CBT interventions for panic/agoraphobia (Schmidt et al., 2000).
In the study by Bonn et al. (1984), patients with panic disorder with agoraphobia
received either two sessions of BRT followed by seven weekly sessions of in vivo
exposure, or nine weekly sessions of in vivo exposure with no BRT. Findings at
posttreatment showed no differences, but an advantage of BRT-augmented exposure
emerged at the 6-month follow-up. In the Hibbert and Chan (1989) study, patients
with panic and agoraphobia received 2 weeks of BRT followed by 3 weeks of in vivo
exposure, or 2 weeks of supportive therapy followed by 3 weeks of in vivo exposure.
At the end of the in vivo exposure treatment, patients receiving BRT showed greater
improvement on clinician ratings of improvement, but not on patient self-report
ratings.
In a dismantling study of group CBT, Schmidt et al. (2000) randomized panic
disorder patients with and without agoraphobia to CBT either with or without
BRT. At the end of the trial there were no significant differences in outcome,
suggesting that BRT did not significantly contribute to the efficacy of group CBT.
These findings are in accord with those reported by Craske, Rowe, Lewin, and
Noriega-Dimitri (1997), who found no differences on measures of agoraphobic
avoidance between an individual-administered CBT treatment consisting of cognitive
restructuring (CR), interoceptive exposure, and in vivo exposure relative to a treatment
package combining CR plus BRT plus in vivo exposure. Taken together, these findings
provide little evidence that BRT enhances the efficacy of either exposure treatment or
multicomponent CBT interventions for panic disorder with agoraphobia.
Involvement of Spouses in Treatment

Several studies have explored whether involving spouses in treatment enhances the
outcome of exposure therapy for agoraphobia. Theoretically, involving spouses in
therapy may augment the effectiveness of interventions for two reasons: (a) spouses
can reinforce the development of skills for managing anxiety and the completion of
exposure exercises, and (b) spouses can be educated about actions they can take to
stop reinforcing or perpetuating agoraphobic symptoms (Byrne, Carr, & Clark, 2004;
Oatley & Hodgson, 1987).
In one of the earlier investigations in this area, Cobb, Mathews, Childs-Clarke,

and Blowers (1984) assigned patients to receive home-based exposure therapy with
or without the participation of their spouse. Therapists visited the homes of clients
for each session and provided a total of 5 hours of therapy over the course of
treatment. The group without spouse involvement received a therapeutic manual
during the first session, and completed one therapist-assisted in vivo exposure session.
Additional sessions were spent planning and discussing independent in vivo exposure
assignments. In this group, spouses only attended the first therapy session and were
otherwise uninvolved in therapy. The group with spouse involvement differed in that
spouses attended each session of therapy, received a therapy manual, were instructed
to assist clients in completion of homework assignments, and were told to promote
self-help in lieu of dependence from the client. Results indicated that both treatments
led to improvements on agoraphobic symptoms that were maintained at 6-month
follow-up; however, between-group comparisons did not reveal an advantage for
involvement of spouses. Thus, the authors concluded that while the involvement of a
spouse is not detrimental, it also does not appear to enhance outcome.
Similarly, Emmelkamp et al. (1992) randomized agoraphobia patients to receive
in vivo exposure therapy with or without the involvement of their spouse. In the
spouse-assisted condition, spouses attended each treatment session and received a
manual describing how to support the client. However, the authors explicitly stated
that relationship problems were not discussed until after the experimental trial, which
may suggest that any communication skills regarding coping with agoraphobic symp-
toms were not actively discussed during treatment. Though overall both treatments
improved agoraphobic symptoms, there was no clear advantage of spouse-assisted
treatment. However, other studies have produced conflicting results.
In contrast to the above findings, Barlow, O’Brien, and Last (1984) found a
treatment enhancement effect for including spouses in treatment. In their study,
women with agoraphobia were randomly assigned to a group CBT intervention
consisting of coping skills training, in vivo exposure, and cognitive restructuring, with
or without the attendance of their husbands. The spouse-assisted condition included
discussion of methods for the husband to assist the client in anxiety management and
reduction of avoidance behaviors, and discussion about the possible roles of spouses
in maintaining agoraphobia. Additionally, husbands were instructed to assist with in
vivo exposure exercises, but to allow the client to complete at least one exposure
independently for each feared situation. Furthermore, partners worked on strategies
for communicating when the client was anxious or panicked and agreed upon
strategies for managing anxiety in these situations. Results indicated that significantly
more participants in the spouse versus no spouse group (i.e., 12 out of 14 vs. 6 out
of 14, respectively) were classified as treatment responders at posttreatment based
on a composite index of treatment outcome. Furthermore, the advantage of spouse
involvement was maintained at 2-year follow-up (Cerny, Barlow, Craske, & Himadi,
1987).
Similarly, research by Arnow, Taylor, Agras, and Telch (1985) also suggests that
the involvement of spouses can enhance treatment outcomes. In contrast to previous
studies, in which the partner primarily supported the client in completing a course
of exposure therapy, this study also included a component of therapy that specifically
Agoraphobia 955
focused on the development of communication skills in the relationship. Couples’

communication skills training emphasized the modification of interactions that may
play a role in maintaining agoraphobic symptoms. In this study, female agoraphobia
patients received exposure plus couples relaxation training or exposure plus couples
communication skills training. All participants first received 4 weeks of exposure to
feared situations. Exposure was delivered in a group format that included the partici-
pation of partners. Couples were then assigned to receive 8 weeks of either relaxation
training or communication skills training. The relaxation group served as a comparison
group with similar situational exposure, partner involvement, and overall therapy time.
Participants who received exposure plus communication skills training demonstrated
more improvement in relationship communication skills and better posttreatment
outcomes on behavioral and self-report measures of agoraphobia. Further, the superi-
ority of the communication skills group was maintained, with no significant differences
found on outcome measures between posttreatment and 8-month follow-up. It is
noteworthy that both studies providing support for the involvement of spouses
included communication skills development either as a primary focus of therapy
(Arnow et al., 1985) or as a component of therapy (Barlow et al., 1984). Future
research should further examine the role of improved relationship communication
skills in enhancing outcomes of exposure-based therapy for agoraphobia.
Fading of Safety Behaviors

Human beings are hardwired to engage in protective actions when faced with
perceived threats. Examples of such actions include wearing seat belts while driving,
wearing warm clothing when venturing outside on a winter’s day, and using condoms
with a sexual partner. However, engaging in such protective actions when no real
threat exists appears to actually contribute to the development of new forms of
pathological anxiety (Olatunji, Etzel, Tomarken, Ciesielski, & Deacon, 2011) or
maintain pathological anxiety that already exists. Several putative causal pathways
through which safety behaviors exert their anxiety-maintaining effects are discussed
elsewhere (see Telch & Lancaster, 2012).
In the case of agoraphobia, Kamphuis and Telch (1998) factor analyzed safety
behavior data from 105 panic disorder patients (with or without agoraphobia)
recruited from the community. Based on their analyses of the 50 items of the Texas
Safety Maneuver Scale (TSMS; Kamphuis & Telch, 1998), five interpretable factors
emerged. These five factors were named (a) classic agoraphobic avoidance—such as
avoidance of crowded stores, and avoidance of public transportation; (b) relaxation
techniques—such as meditation or yoga to relieve anxiety; (c) avoidance of stressful
encounters—such as arguments with loved ones or stress at work; (d) avoidance of
somatic perturbations—such as avoidance of caffeine or rigorous exercise; and (e)
use of distraction techniques—such as listening to music, or staying busy in order to
avoid anxiety or panic symptoms.
The first empirical evidence supporting the utility of fading safety behaviors dur-
ing exposure therapy with agoraphobia patients was reported by Salkovskis, Clark,
Hackmann, Wells, and Gelder (1999). They randomized participants with panic
disorder and moderate to severe avoidance to receive 15 minutes of in vivo expo-

sure therapy, with or without instructions to reduce safety behaviors. Though
both treatment groups reported similar anxiety levels during exposure, the group
instructed to reduce safety behaviors had superior outcomes. More recently, this
same group (Salkovskis, Hackmann, Wells, Gelder, & Clark, 2006) replicated their
earlier finding. In this study, agoraphobia patients underwent 3.25 hours of exposure
therapy with a habituation rationale, or exposure therapy with a threat disconfirma-
tion rationale and the fading of safety behaviors. At the conclusion of treatment,
patients assigned to the exposure plus safety behavior fading arm showed markedly
greater improvement (between-group effect sizes [Cohen’s d] ranging from 1.7 to
2.7) on self-report measures of anxiety and situational avoidance, and completed
significantly more steps on a standardized behavioral approach test. These data
are consistent with findings from a recent review showing that out of eight con-
trolled trials investigating safety behavior fading in anxiety disorders, all eight have
shown significant enhancement effects (see Telch & Lancaster, 2012). Accordingly,
there is compelling evidence suggesting that clinicians should assist their agora-
phobic patients in eliminating safety behaviors when encountering fear-provoking
situations.
Intensive Treatment Programs for Agoraphobia
The development of more efficient interventions, including high-density and brief

exposure-based treatments, has been a tradition in clinical research, with successful
applications to the treatment of agoraphobia. For instance, Hahlweg, Fiegenbaum,
Frank, Schroeder, and von Witzleben (2001) provided high-density exposure to a
large community health center-based sample (N = 416) of patients all meeting DSM-
III-R- criteria for panic disorder with agoraphobia. Treatment consisted of 4 to 10
days of in vivo exposure with each session lasting several hours per day. At 6-week
and 1-year follow-ups, patients showed significant reductions in measures of anxiety,
depression, general symptomatology, and agoraphobic avoidance. Within-group effect
sizes (Cohen’s d) ranged from 0.93 to 1.82 (mean = 1.23) at posttreatment, and
ranged from 0.92 to 1.7 (mean = 1.24) at follow-up. Despite several limitations (i.e.,
reliance on self-report measures and a lack of treatment integrity data), this study
offers evidence that high-density exposure can be successfully translated from research
to applied settings.
An intensive eight-session treatment program for patients presenting with moderate
to severe agoraphobia was developed in David Barlow’s Center at Boston Univer-
sity. Coined Sensation-Focused Intensive Treatment (SFIT; Morissette, Spiegel, &
Heinrichs, 2006), this approach incorporates cognitive restructuring and massed
interoceptive and situational exposure. During Days 1 to 3, patients receive standard
CBT components including psychoeducation, interoceptive exposure, and cognitive
restructuring. On Days 4 and 5, patients receive two full days of ungraded, massed
therapist-accompanied exposure to their most fear-provoking situations. This is fol-
lowed by two full days of unaccompanied intensive self-exposure, and a final session
Agoraphobia 957
focusing on maintenance of treatment gains and relapse prevention. A small proof-

of-concept study (Bitran, Morissette, Spiegel, & Barlow, 2008) with 40 patients all
meeting criteria for panic disorder with moderate to severe agoraphobia revealed that
the program led to large pre-to-post improvements in panic, agoraphobic avoidance,
anxiety sensitivity, and self-efficacy. Gains were maintained at follow-up (1 to 6
months posttreatment) on all measures, and further gains emerged for measures of
anxiety sensitivity and agoraphobic avoidance.
Innovative Agoraphobia Treatment Delivery Systems
In the last decade, a number of new treatments for panic disorder and agorapho-
bia have emerged, prompted by barriers to dissemination, as well as a need to
augment existing treatments and boost their economic appeal. With a foundation
rooted in established cognitive behavioral techniques and driven by technological
innovations, these treatments reflect two major movements in the extant research.
The first movement aims to improve patient access through efficacy and effectiveness
trials of teletherapy and Internet-based treatments. The second movement, driven by
advances in virtual reality (VR) technologies, aims to enhance exposure-based treat-
ments through incorporating VR components in the therapist’s arsenal of effective
techniques. Here we review these innovative and emerging treatments, which have
shown promising preliminary results.
Teletherapy and Internet-Based Treatments

Both the isolative nature of agoraphobia and advances in telecommunication technol-
ogy have prompted a number of investigators to examine the efficacy of teletherapy
and Internet-based variants of established cognitive behavioral treatments. The obvi-
ous benefit of these techniques addresses significant barriers to treatment; namely,
that patients suffering from agoraphobia often do not have access to evidence-based
treatments either because of prominent avoidance behaviors or because of a lack of
access to clinicians skilled in their implementation.
Prior to the advent of videoconferencing capabilities, the question of whether
anxiety disorders, generally, were amenable to telephone-delivered therapies was
being explored; however, very few studies examined applying distance-therapies to the
treatment of agoraphobia, despite its obvious appeal. One early study by McNamee,
O’Sullivan, Lelliott, and Marks (1989) investigated the efficacy of exposure versus
relaxation techniques administered via telephone to 23 patients with panic disorder
with agoraphobia, 14 of whom were assessed at 32 weeks posttreatment. While
psychotherapeutic contact was very brief relative to standard CBT protocols (i.e.,
patients spent just 2 hours dispersed over 12 weeks consulting with therapists), the
exposure-based intervention was found to be significantly more effective than the
relaxation-based intervention in improving phobia and social functioning.
Another seminal study by Swinson, Fergus, Cox, and Wickwire (1995) investigated
the effectiveness of an 8-week course of telephone-delivered, exposure-based behavior
therapy administered to 42 patients with panic disorder with agoraphobia relative to
a wait-list control. Results revealed significant reductions in phobic avoidance, fear,

and anticipatory anxiety; furthermore, treatment gains were maintained at 3- and
6-month follow-ups.
It has been noted that videoconferencing is qualitatively different from telephone-
based treatments (e.g., Bouchard et al., 2004), and so results based on telephone-
delivered therapies may not generalize to videoconferencing treatments. For instance,
teletherapy may not have the same potential for establishing a strong therapeutic
alliance if one considers the importance of face-to-face contact in patient–therapist
interactions; further, teletherapy may limit the capacity to clinically monitor symptoms
and the integrity of therapist-assisted, self-administered interventions.
In an early pilot investigation, Bouchard et al. (2000) examined the efficacy of
administering 12 sessions of CBT via videoconferencing to 8 adults suffering from
panic disorder with agoraphobia. Despite having a very small sample, significant results
were found for all outcome measures (with large within-group effect sizes [r] ranging
from 0.71 to 0.89), including panic frequency and apprehension, self-efficacy, and
global measures of panic and agoraphobia, anxiety, and disability. Bouchard’s group
later extended these results experimentally by comparing CBT administered either
face-to-face or via videoconferencing to a sample of 21 patients with panic disorder
with agoraphobia (Bouchard et al., 2004). The two modalities were comparable
in effectiveness; for both groups, clinically significant reductions were found on
all measures, with no significant differences between conditions. Furthermore,
therapeutic alliances were readily established in the videoconferencing group, a
finding that refutes a common criticism of teletherapy, namely, that rapport and
working alliance may be diminished relative to that achieved in face-to-face therapies.
Internet-Based Self-Help Treatments

In addition to increasing access and affordability of treatment through the use and
development of teletherapy, other avenues have been pursued, including evidence-
based self-help programs administered via the Internet. Derived from the tradition
of bibliotherapy and aided by the increased capabilities of dissemination afforded by
the World Wide Web, research suggests that these programs are at least marginally
effective. While the evidence is scant in regards to applying such programs to the
treatment of agoraphobia, considering the potential benefits of increased accessibility,
their continued use and empirical development is warranted.
Contributing to this line of research, Carlbring, Ekselius, and Andersson (2003)
investigated the efficacy of Internet-based self-help treatment with minimal therapist
contact for panic disorder in a sample of 22 patients (of whom over 90% met
criteria for agoraphobia). Participants were randomized to either applied relaxation
or a multicomponent treatment based on CBT. Although both groups improved,
counter to expectations, participants receiving applied relaxation showed a greater
clinical response than those receiving CBT. The authors note that one possible factor
accounting for the observed advantage shown for the applied relaxation treatment
was the fact that this group had materials they could take home to use (i.e., a CD
with relaxation instructions), and they perhaps enjoyed more frequent rewards as they
progressed through shorter modules. Importantly, a major limitation of this study,
Agoraphobia 959
and perhaps a potential pitfall of Internet-administered therapies generally, is that only

56% of the treatment materials were completed. The authors provide some possible
explanations for such low engagement, including that participants complained the
treatment was too impersonal, and that treatment credibility was lower relative to
previous studies. Importantly, the authors report they have had greater success in
terms of homework completion in previous studies (i.e., up to 90%).
In a similar study with minimal therapist contact, Wims, Titov, Andrews, and Choi
(2010) assessed the efficacy of clinician-assisted, Internet-based CBT administered
to patients with panic disorder with and without agoraphobia. While controlling for
pretreatment symptom severity, those assigned to the Internet CBT group (n = 32)
exhibited significantly less posttreatment symptoms of panic, fear of body sensations,
and agoraphobic cognitions relative to controls (n = 27). Furthermore, remission rates
were 31% and 8% for the treated versus control groups, respectively. Note however,
that, posttreatment measures targeting symptoms of phobic avoidance revealed no
group differences. Overall, these results suggest that Internet-based CBT for panic
disorder achieves about half the level of improvement on panic disorder severity
relative to therapist-delivered CBT interventions, but does not exert an appreciable
effect on agoraphobia symptoms specifically.
Virtual Reality Exposure Therapy

Another developing, innovative therapy bolstered by the advancement of technology
is virtual reality exposure therapy (VRET), which has been lauded as an alterna-
tive to in vivo and imaginal exposure (Krijn, Emmelkamp, Olafsson, & Biemond,
2004). Certainly, the ability to sensorially immerse a patient in a virtual environment
has enormous appeal in the treatment of anxiety disorders. Among the many con-
ceivable benefits are increased acceptability (especially for severely phobic patients),
greater control over graduated exposures, improved cost-effectiveness, the ability
to tailor treatment precisely to the individual patient, and the possibility of repeat-
ing exposures as frequently as desired. In the early 1990s, the first conceptions
and investigations of applying VR exposure to anxiety disorders were underway
(e.g., North, North, & Coble, 1998), despite the fact that the technology was in
its infancy. Technological advances, improved virtual environments, and the ability
to manipulate those environments and to integrate multiple sensory inputs have
allowed the construction of more convincing virtual worlds. This important feat,
in turn, has afforded a greater sense of “presence” in patients immersed in vir-
tual environments, which has been identified as an important variable in creating
viable, evocative stimuli (Jang, Ku, Shin, Choi, & Kim, 2000), and in invoking
emotion in VR exposures (Krijn et al., 2004). Moreover, invoking emotion dur-
ing exposure (e.g., activation of fear structures) is held as a theoretically important
mechanism underlying the effectiveness of exposure therapies (Foa & Kozak, 1986).
To date, research on VR exposure for anxiety disorders supports the use of this
technology for fear of heights and fear of flying (see Krijn et al., 2004, for a
review); however, findings for its efficacy in treating other anxiety disorders are
inconclusive, and there is a paucity of clinical studies applying this technique to
agoraphobia.
In an early study investigating the use of VRET with 60 university students

who expressed the presence of agoraphobic symptoms on a general measure of
agoraphobic attitudes, North, North, and Coble (1996) demonstrated significant
reductions in subjective distress across eight (or fewer) sessions of exposure to
anxiety-provoking, interactive virtual environments, and significant reductions on
a (nonvalidated) measure of agoraphobia administered posttreatment. While these
results suggest an effective therapeutic manipulation when considering the significant
habituation observed across sessions, the results do not speak to the ecological validity
of this technique; that is, the question remains as to whether results would generalize
outside laboratory settings to truly clinical populations.
Another notable investigation by Jang et al. (2000) demonstrated the importance
of the design of virtual environments, and the environmental conditions under which
such manipulations are administered. A sample of 45 patients diagnosed with panic
disorder with agoraphobia, all of whom identified the same scene as most distressing
(i.e., being in a traffic-jammed tunnel), were later subjected to this scene using
a VR head-mounted display. Due to insufficient patient immersion in the virtual
environment, the authors discontinued use of VRET with patients after just two
sessions, and no viable data were obtained. They cite a number of issues that may
have prevented proper immersion in the virtual scene, including having a burdensome
apparatus with a limited field of view (i.e., 50 degrees), having multiple physiological
sensors, having the therapist present and actively reassuring distressed patients, and
having the external environment interfere with engagement with the virtual scenes
(e.g., bright light flooding in through the crevice of the head-mounted display). The
authors note the importance of creating realistic virtual scenes; however, they suggest
that preparing the environmental conditions under which patients will engage with
these scenes may be a more prominent factor in eliciting patients’ presence in virtual
scenes.
With a more refined protocol, more promising results were achieved by Vincelli
et al. (2003), who developed and tested a new treatment called experiential-cognitive
therapy (ECT), which combines VR exposure and traditional cognitive behavioral
techniques. Twelve patients with panic disorder with agoraphobia were assigned
to receive either eight sessions of ECT or 12 sessions of standard CBT, or to a
wait-list control group. Results revealed significant improvement in the number of
panic attacks, the level of depression, and state and trait anxiety, but no significant
differences were found between the two treatment groups. While this suggests
comparable efficacy, the authors interpret this finding as indicative that ECT can
produce its effects in 33% fewer sessions (i.e., eight vs. 12 sessions) relative to standard
CBT, boosting its economic appeal and justifying the addition of VR techniques to
established treatment protocols.
In a sample of 40 patients with panic disorder with agoraphobia, Choi et al. (2005)
showed similar effectiveness of ECT, compared to a more established panic control
program (PCP). Both groups showed significant improvement with no differences
in high end-state functioning and medication discontinuation at posttreatment, but
more patients discontinued medication in the PCP group at 6-month follow-up,
which the authors take as evidence that ECT may be relatively less effective in the
long term.
Agoraphobia 961
Botella et al. (2007) compared nine weekly sessions of VRET, in vivo exposure, or
a wait-list control administered to 37 patients with panic disorder with agoraphobia
(82.9% of the sample) or without agoraphobia (17.1% of the sample). At posttreatment
and 9-month follow-up, VRET showed similar efficacy relative to the in vivo exposure
treatment, with no significant differences on any outcome measures, whereas both
active treatments were significantly superior to the wait-list control condition on all
outcome measures (with effect sizes [partial eta squared] ranging from 0.35 to 0.8,
and most measures obtaining medium to large pre-to-post effects).
Treating a sample of 29 panic disorder patients with or without agoraphobia,
Perez-Ara et al. (2010) compared the efficacy of virtual reality interoceptive exposure
(VRIE), in which patients were simultaneously exposed to arousal-inducing audio and
visual effects in virtual agoraphobic situations, to a traditional interoceptive exposure
(IE) treatment. Results revealed significant reductions in primary outcome measures
at posttreatment which were maintained or even improved at 3-month follow-up, but
no differences were found between treatment conditions. While these data suggest
that VRIE is comparable to traditional, gold standard IE in the absence of VR
components, the authors argue that VR may be more palatable for some patients, and
conclude that the incorporation of multisensory stimulation in VR may enhance the
ecological validity of exposure situations.
In a recent study, Pelissolo et al. (2012) compared the effects of 12, hour-long
sessions of VRET, CBT, and a wait-list control, administered to 92 patients with
panic disorder with agoraphobia. Results revealed no significant differences between
groups, providing evidence that VRET is at least as effective as traditional CBT.
Despite a lack of statistical difference between groups (and curiously, this study did
not show significant differences between the active treatment groups and wait-list
groups, perhaps due to relatively high rates of attrition), treatment effects were
impressive, with a mean reduction of around 50% in measures of agoraphobia and
panic at 9 months posttreatment.
In sum, the evidence supporting the use of VR exposure for the treatment of
agoraphobia is inconclusive. Some authors suggest that its use is as effective (Botella
et al., 2007; Pelissolo et al., 2012; Perez-Ara et al., 2010) or more efficient (Vincelli
et al., 2003) compared to traditional CBT, while others demonstrate that traditional
techniques are superior (e.g., Choi et al., 2005). Still, considering the potential
benefits of applying VR technology to the treatment of agoraphobia, and notable
advances in the technology and refined protocols that may directly boost treatment
effects, continued empirical development appears warranted.
Alternatives to Cognitive Behavioral Therapy: Other

Psychosocial Treatments for Agoraphobia
Though CBT is currently the gold standard treatment for agoraphobia, several
alternative approaches are available for patients seeking treatment. It is vital to the
well-being of agoraphobia patients that researchers actively investigate alternative
treatments being employed in the field, and that practitioners, in turn, consider
research outcomes when selecting treatment approaches. Therefore, this section will
provide a brief review of literature related to three alternative approaches to treating

panic disorder with agoraphobia: psychodynamic approaches, interpersonal therapy,
and acceptance and commitment therapy.
Psychodynamic Treatment Approaches

Psychodynamic therapy has been tested as a possible approach for the treatment
of agoraphobia (Hoffart & Matinsen, 1990). This approach assumes that intrapsy-
chic conflicts from childhood, reactivated by adult stressors, play an important
role in the pathogenesis of agoraphobia. The principal therapeutic goals are to
assist the patient in developing autonomy by addressing suppressed inner conflicts,
guided by experiences that arise during exposure. Hoffart and Matinsen (1990)
compared the effectiveness of psychodynamic therapy alone with a program that
integrated psychodynamic therapy with exposure therapy administered to an inpa-
tient agoraphobic sample. The exposure component included graduated in vivo
exposure combined with cognitive restructuring. At 1-year follow-up, results demon-
strated superior outcomes for the integrated treatment group on assessments of
ability to approach agoraphobic-related situations alone, agoraphobic-related cog-
nitions, and several other measures of anxiety. Although the group receiving
psychodynamic treatment alone demonstrated posttreatment improvements, gains
were not maintained through 1-year follow-up. Overall, results of this study sug-
gest that psychodynamic therapy alone has little therapeutic benefit, whereas there
is preliminary support for combining psychodynamic therapy and exposure treat-
ment. However, conclusions should be interpreted with caution given notable
weaknesses in study design (e.g., no random assignment, and the clinician-rated
assessments were conducted by the therapist for most patients in the study).
Furthermore, the integrated treatment should be compared with a control group
(i.e., psychological placebo or wait-list control) and the gold standard treatment
(i.e., CBT) before drawing conclusions about its effectiveness in the treatment of
agoraphobia.
Milrod and her colleagues (Milrod et al., 2001; Milrod et al., 2007) have developed
and tested a 24-session manualized panic-focused psychodynamic treatment for panic
disorder with and without agoraphobia. The treatment consists of three distinct
phases: (a) initial evaluation and early treatment, (b) panic vulnerability, and (c)
termination (see Milrod et al., 2007, for a detailed overview of the clinical strategies
used in each of the phases). To examine the effectiveness of this approach, a well-
executed small-scale comparative study was conducted in which 49 patients with panic
disorder with and without agoraphobia (the proportion of those with agoraphobia
was not specified) were randomized to either psychodynamic treatment or applied
relaxation. Intent-to-treat clinical response rates in the two treatments based on a
40% reduction in the total score on the Panic Disorder Severity Scale (Shear et al.,
1997) were 73% for psychodynamic therapy versus 39% for applied relaxation. Subject
attrition in the applied relaxation condition was significantly higher (34%) than in
the psychodynamic treatment (7%) which speaks to the favorable tolerability of the
treatment. Nevertheless, the differential dropout rates make interpretation of the
Agoraphobia 963
between-group differences problematic, and, unfortunately, specific outcome indices

for agoraphobic avoidance were not reported.
Interpersonal Psychotherapy
Given data suggesting that interpersonal stressors may contribute to the onset and
maintenance of panic and agoraphobia (Faravelli & Pallanti, 1989), it is reasonable to
expect that psychotherapy aimed at correcting interpersonal problems may confer sig-
nificant benefits to patients presenting with agoraphobia. Interpersonal psychotherapy
(IPT) is a time-limited, manualized, structured treatment originally developed for the
treatment of depression (Klerman, Weissman, Rounsaville, & Chevron, 1984), which
has been adapted and shown to be efficacious for a range of problems including major
depression, bipolar disorder, bulimia, and substance use disorders (see Markowitz &
Weissman, 2012, for a review). Encouraging preliminary findings were reported from
an open pilot trial of IPT in 12 patients meeting DSM-IV criteria for panic disorder
(Lipsitz et al., 2006).
More recently, Vos, Huibers, Diels, and Arntz (2012) completed an RCT com-
paring IPT and CBT in 91 patients meeting DSM-IV criteria for panic disorder
with moderate to severe agoraphobia. The major treatment components included
in the IPT protocol were (a) characterizing panic disorder in terms of the medical
model, (b) determining the focus of treatment (e.g., role conflict, transition, grief,
or skills deficit), (c) exploration and improvement of interpersonal problems, and (d)
treatment termination. CBT included cognitive therapy, interoceptive exposure, and
in vivo exposure. Relative to IPT, CBT produced significantly greater improvement in
panic attack frequency (i.e., from baseline to 1-month follow-up, within-group effect
sizes [Cohen’s d] were 0.74 and 0.51 for the CBT and IPT groups, respectively), but
more importantly, CBT was also superior on multiple measures of agoraphobic dys-
function (i.e., from baseline to 1-month follow-up, effect sizes based on a composite
agoraphobia score were 1.05 and 0.58 for the CBT and IPT groups, respectively).
The authors concluded that IPT appears to have limited value in the treatment of
moderate to severe agoraphobia.

While conventional forms of CBT conceptualize the goal of therapy as changing
maladaptive behavior and cognitions, acceptance and commitment therapy (ACT)
was designed to promote a balance of acceptance and change. One might concep-
tualize CBT as a therapy that promotes judging certain cognitions and emotions
as in need of elimination. In contrast, ACT suggests that clients should accept the
experience of cognitions or emotions without judging them, and commit to act in
a way that is consistent with their values. The literature regarding the treatment of
agoraphobia with ACT is still in its infancy, with only a few case studies currently
available.
For example, Carrascoso López (2000) reported the case study of an individual
diagnosed with panic disorder with agoraphobia treated with ACT. Though therapy
incorporated some techniques employed in CBT, such as in vivo exposure homework
and interoceptive exposure, these techniques were framed in terms of ACT goals and
objectives (e.g., learning to abandon the attempt to control bodily sensations, rather
than striving to habituate fear response to bodily sensations). A comparison of baseline
to posttreatment scores revealed a significant decrease in panic and agoraphobia
symptoms. The patient also exhibited a reduction in escape and avoidance behaviors
observed during the session and in self-reported agoraphobic symptoms. However,
the inclusion of exposure treatment for this case precludes drawing conclusions about
the specific contribution of ACT.
Codd, Twohig, Crosby, and Enno (2011) reported the outcome of another case
in which panic disorder with agoraphobia was treated with ACT. In contrast to
Carrascoso López (2000), the authors specifically avoided conducting any in-session
exposure therapy to reduce the overlap of ACT with previously established treatments
for panic and agoraphobia. At posttreatment, the patient demonstrated a clinically
significant decrease in clinician-rated symptoms of panic disorder and no longer met
diagnostic criteria for panic disorder with agoraphobia. Furthermore, self-reported
reductions in daily ratings of avoidance behaviors were noted after the first couple
of sessions and maintained through the end of treatment. Interestingly, while the
client’s diagnostic status and avoidance behaviors changed, her mean anxiety level
remained somewhat constant throughout therapy. The authors note that this pattern
of findings suggests that the change process in ACT alters the function of anxiety in
one’s life, rather than altering the severity of anxiety experienced.
The case studies reviewed herein provide preliminary support for the feasibility
of ACT as a treatment for panic disorder with agoraphobia; however, additional
empirical support is needed before conclusions can be drawn regarding the efficacy of
ACT in treating panic with agoraphobia. RCTs are needed to determine the efficacy
of ACT relative to CBT. Furthermore, research exploring predictors of treatment
outcome may help identify subsets of patients most amenable to this approach.
Predictors of Treatment Outcome
Research aimed at identifying factors that influence agoraphobia patients’ response to

treatment has important implications for clinical management. As more data emerge
on patient and treatment variables that impact treatment outcome, clinicians are in a
better position to prescribe more individualized treatment regimens for their patients.
Despite such clear advantages, identifying prognostic factors has been traditionally
less prominent as an investigational aim relative to establishing, comparing, and
augmenting treatment efficacy. Furthermore, only recently have the sample sizes
in panic/agoraphobia treatment studies been large enough to provide sufficient
statistical power to investigate the relationship between various patient prognostic
factors and response to cognitive behavioral treatment. Methodologies have also
generally improved; for example, while many of the early studies relied solely on
self-report measures as indices of outcome, more modern studies have utilized
clinician-based assessments, and other more objective assessments, the sensitivity of
which allows evidence of predictors to emerge more reliably from the data. In this
Agoraphobia 965
section, we review those studies that examine one or more patient prognostic factors
on measures of agoraphobia treatment outcome.
Psychiatric Comorbidity Predicting Treatment Outcome

Patients with agoraphobia often present with one or more co-occurring psychiatric
conditions such as depression, other anxiety disorders, and substance use disorders
(Kessler et al., 2006). The fact that psychiatric comorbidity is more the rule than
the exception raises the important question: How does the presence of a comorbid
psychiatric condition impact patients’ response to cognitive behavioral treatment?
Probably the best data available on the impact of comorbid anxiety and depression
on patients’ level of improvement in agoraphobia symptoms during cognitive
behavioral treatment come from a recent report by Allen et al. (2010) using data
from a large multisite treatment study of panic disorder and agoraphobia (Aaronson
et al., 2008). The investigators tested whether the presence of a comorbid anxiety
disorder, comorbid depression, or comorbid anxiety and depression resulted in less
improvement in panic and agoraphobia symptoms, relative to patients without any
comorbid diagnoses. The results of this study are presented in Figure 40.1. Consistent
with early reports (Brown, Antony, & Barlow, 1995; McLean, Woody, Taylor, &
Koch, 1998), patients presenting with comorbid anxiety and depression diagnoses
at baseline showed greater severity of panic disorder and agoraphobia at baseline.
The only baseline comorbid condition associated with a poorer treatment response
was adult separation anxiety disorder. The good news, however, is that with the
20
No comorbidity
18 Only anxiety
Only depression
16 Both anxiety and depression
14
PDSS-IE score
12
10
8
6
4
2
0
Pre Post
Assessment
Figure 40.1 PDSS-IE scores (with standard errors) across treatment for participants with
no comorbidity, only anxiety comorbidity, only depression comorbidity, and both anxiety
and depression comorbidity. PDSS-IE Panic Disorder Severity Scale—Independent Evalu-
ator Version, Pre pretreatment, Post posttreatment. With kind permission from Springer
Science+Business Media: Laura B. Allen (2009), Cognitive-behavior therapy (CBT) for panic
disorder: Relationship of anxiety and depression comorbidity with treatment outcome, Journal
of Psychopathology and Behavioral Assessment, 32, 185–192.
exception of adult separation anxiety disorder, patients who have panic disorder with
agoraphobia and comorbid anxiety and depression seem to benefit just as much from
CBT as those without comorbid conditions. This latter finding is generally consistent
with earlier reports (Brown et al., 1995; Tsao, Mystkowski, Zucker, & Craske, 2005).
The other positive finding is that patients also showed significant reductions in
comorbid conditions, which is consistent both with earlier reports (e.g., Brown et al.,
1995) and with a more recent naturalistic study of changes in comorbid conditions
following CBT treatment for anxiety disorders (Davis, Barlow, & Smith, 2010).
Axis II Comorbidity Predicting Treatment Outcome

Personality disorder comorbidity is frequently cited as a factor implicated in poor treat-
ment response to both pharmacotherapy (Slaap & den Boer, 2001) and psychosocial
treatments (Reich & Green, 1991). Although not studied systematically, personality
dysfunction may negatively affect agoraphobia treatment outcome through its poten-
tial influence on other moderators of treatment outcome such as patient dropout
(Grilo et al., 1998), compliance with treatment regimens (Schmidt & Woolaway-
Bickel, 2000), the therapeutic alliance, or motivation for treatment (Persons, Burns,
& Perloff, 1988).
Despite claims that agoraphobia patients displaying comorbid Axis II pathology
respond less favorably to cognitive behavioral treatment (Mennin & Heimberg, 2000),
evidence from controlled prospective studies is inconclusive due to the small number
of prospective studies and the methodological limitations of the existing studies (i.e.,
small sample size, use of questionnaires to assess personality dysfunction, and failure
to control for baseline severity of Axis I pathology; Dreessen, Arntz, Luttels, &
Sallaerts, 1994). In the largest study to date to examine whether personality disorders
interfere with patients’ responses to treatment, Telch, Kamphuis, and Schmidt (2011)
investigated the influence of personality pathology assessed both dimensionally and
categorically on acute clinical response to cognitive behavioral treatment in a sample of
173 outpatients diagnosed with panic disorder with or without agoraphobia. Results
revealed that approximately one-third of the sample met criteria for one or more
personality disorders, with the majority meeting criteria for an “Anxious or Fearful”
Cluster C diagnosis. Consistent with earlier reports (Friedman, Shear, & Frances,
1987; Reich & Chaudry, 1987), patients presenting with personality disorders were
significantly more likely to show extensive agoraphobia relative to patients without
personality disorders. Without controlling for pretreatment panic severity, patients
presenting with one or more personality disorders showed greater posttreatment
symptoms on the continuous panic outcome measures and were significantly less
likely (39% vs. 65% for patients with and without personality disorders, respectively)
to achieve clinically meaningful change at posttreatment. However, after controlling
for pretreatment panic/agoraphobia severity, the results showed that the presence
of personality disturbance, whether assessed via dimensional or categorical indices,
conferred a very modest, albeit statistically significant, deleterious effect on treatment
outcome (see Figure 40.2).
Agoraphobia 967
30
% Variance explained in
25
improvement status
20
15
10
5
0
Pretreatment Cluster A Pers-D Cluster B Pers-D Cluster C Pers-D
panic/agoraphobia
severity
Figure 40.2 Proportion of variance in clinically significant change explained by pretreatment

panic disorder/agoraphobia severity, and the presence of Cluster A, B, and C personality
disorders (pers-d).
Cognitive and Family Relationship Variables Predicting Agoraphobia

Treatment Outcome
Cognitive variables as well as relationship variables have each been posited as potential
mediators of change in behavioral and cognitive behavioral treatments for agorapho-
bia. Using structural equation modeling, Renshaw, Chambless, and Steketee (2003)
examined the relationship between perceived criticism in the family and treatment
outcome in 67 patients with either obsessive compulsive disorder or panic disor-
der with agoraphobia. Results indicated that pretreatment levels of perceived family
criticism significantly predicted posttreatment symptom severity while controlling
for pretreatment symptom severity. Although subanalyses by disorder were not pre-
sented, their findings hint at the importance of perceived family criticism as a negative
prognostic factor in behavioral treatment of obsessive compulsive disorder and panic
disorder with agoraphobia.
Using mediational analyses outlined by Baron and Kenny (1986), Smits, Powers,
Cho, and Telch (2004) examined whether changes in fear of fear (FOF) mediate
improvement in CBT treatment of panic disorder with agoraphobia. Although
treatment effects were quite large and statistically significant across all symptom
facets (i.e., global disability, anxiety, agoraphobic avoidance, and panic attacks), CBT
accounted for greater symptom change on measures of panic-related anxiety and
agoraphobia than for panic attacks. Mediational analyses revealed that change in
FOF, as assessed by a composite of two widely used FOF indices (i.e., the Body
Sensations Questionnaire and the Anxiety Sensitivity Index), met Baron and Kenny
criteria for treatment mediation across each of the four symptom facets of panic
disorder with agoraphobia. However, the strength of mediation also varied as a
function of symptom facet; full mediation for FOF was demonstrated for change in
global disability, whereas partial mediation effects of FOF were found for measures of
agoraphobia, anxiety, and panic frequency.
Cho, Smits, Powers, and Telch (2007) examined pre- to posttreatment change in
three panic appraisal dimensions (anticipated panic, panic consequences, and panic
coping) in predicting panic disorder with agoraphobia patients’ clinical status at

a 6-month follow-up. Patients (N = 120) undergoing group-administered CBT
were administered the Panic Appraisal Inventory (PAI; Telch, Brouillard, Telch,
Agras, & Taylor, 1989) at three time points (pre, post, and 6-month follow-up),
along with a standard outcome assessment battery indexing panic-related anxiety,
agoraphobic avoidance, panic attack frequency, and global impairment. When entered
together, pre- to posttreatment changes in the three panic appraisal dimensions
accounted for 28% of the variance in agoraphobia severity at follow-up. Perceived panic
consequences emerged as the most consistent predictor of anxiety, global impairment,
and agoraphobic avoidance at 6-month follow-up. Change in anticipated panic also
uniquely predicted anxiety and agoraphobic avoidance but not global impairment.
Van Apeldoorn et al. (2010) compared the long-term effectiveness of CBT, selective
serotonin reuptake inhibitor medication, or a combination of the two for 150 patients
with panic disorder with or without agoraphobia. For the entire mixed sample (i.e.,
patients with and without agoraphobia), results demonstrated slight superiority of
the combined treatment over either individual treatment alone at posttreatment, but
these differences were not maintained at 6- and 12-month follow-up. Consistent with
findings reported earlier by Telch et al. (1989), the more severely agoraphobic patients
endorsed less confidence in their ability to cope with future panicogenic situations
relative to their less agoraphobic counterparts. Unfortunately, formal mediational
analyses were not conducted to test whether changes in patients’ panic appraisals
mediated change over the course of treatment.
Utilizing a large sample of patients with agoraphobia (with or without panic
disorder; N = 427) and a sample of patients with social phobia (N = 98), Vögele et al.
(2010) conducted mediational analyses of cognitive change on clinical improvement
following a course of high-density exposure in a community-based treatment setting.
Results demonstrated strong, significant, and maintained clinical improvement in
both groups. Cognitive mediation was demonstrated differentially for the two groups.
Cognitive change related to physical catastrophes mediated outcome only for patients
with agoraphobia, whereas changes in cognitions related to control mediated outcome
for both groups. Changes in relationship satisfaction were not found to mediate
outcome in either group. Based on these results, the authors conclude that cognitive
change is an important mechanism, even in purely exposure-based interventions.
In a recent study investigating the differential effectiveness of guided mastery
alone, interoceptive exposure alone, or their combination in the treatment of panic
disorder with agoraphobia, Reilly, Gill, Dattilio, and McCormick (2005) found that
all three treatments were equally effective for both panic and agoraphobia. Further, in
predictive analysis, they found that changes in FOF, anticipated panic, panic coping
efficacy, and agoraphobic self-efficacy all predicted improvement in panic frequency,
whereas only changes in agoraphobia self-efficacy and anticipated panic predicted
improvement in agoraphobia.
Predicting Long-Term Outcome

Using survival analysis on a relatively large sample (N = 200) meeting DSM-III-R and
DSM-IV-TR criteria for panic disorder with agoraphobia, Fava et al. (2001) examined
Agoraphobia 969
long-term outcome up to 14 years posttreatment with a standard protocol that empha-

sized regular, non-therapist-assisted situational exposure. The probability of remitting
was found to increase with younger age, but lessen with the presence of a personality
disorder, high levels of pretreatment depression, persisting agoraphobic avoidance at
posttreatment, and concurrent use of antidepressants and benzodiazepines. Impor-
tantly, patients who entirely overcame agoraphobic behaviors at posttreatment
exhibited better outcomes, indicating that a primary aim of treatment should be
the elimination of agoraphobic avoidance and not simply the elimination of panic.
Future Directions
In this final section we provide some recommendations for advancing research and
treatment for agoraphobia.
First, there is a need for research on the nature and treatment of individuals pre-
senting with pervasive situational avoidance (agoraphobia) without a history of panic
disorder/panic attacks. Evidence from epidemiological studies suggests that almost
50% of adults meeting diagnostic criteria for agoraphobia have no history of panic
disorder or panic attacks that predate the onset of their agoraphobia (Wittchen et al.,
2010). Unfortunately, with the exception of large-scale epidemiological studies, vir-
tually all agoraphobia research studies (intervention and nonintervention) conducted
over the past 25 years have restricted their samples to adults with agoraphobia and
panic disorder/panic attacks. This state of affairs has created a tremendous knowledge
gap in our understanding of the nature and treatment of individuals disabled by
pervasive situational avoidance without panic disorder/panic attacks.
Second, there is a need for treatment matching research aimed at identifying factors
that predict differential treatment response to pharmacological, exposure, cognitive,
and combined therapies. Our review of the research studies examining predictors of
agoraphobia treatment outcome suggests that we have yet to identify specific patient
factors that predict differential clinical response to one treatment modality relative to
another. To meet this objective, we need a large-scale multisite trial with the following
features: (a) a sufficient number of treatment arms to accommodate the treatment
matching objective, (b) a thoughtfully selected battery of putative moderator variables,
and (c) recruitment of research participants who display pervasive situational avoidance
with and without a history of panic disorder/panic attacks.
Third, research should test new strategies for increasing compliance with exposure
therapy regimens. Despite its established clinical efficacy, a sizeable minority of
patients make only minimal progress or show significant return of fear due to poor
compliance with exposure treatment prescriptions, and continued use of subtle forms
of avoidance such as excessive use of safety aids during exposure outings. We also
know that compliance with exposure homework predicts treatment outcome in PDA
patients (Schmidt & Woolaway-Bickel, 2000).
The possible causes of poor compliance with exposure therapy are numerous
but usually fall into one of three major classes: (a) strategic errors on the part of
the therapist—examples include poor choice of exposure target, inadequate patient
training in the execution of exposure, and insufficient monitoring of patients’ exposure
homework; (b) patient factors—these may include comorbid health problems, low
distress tolerance, high anxiety sensitivity, and faulty assumptions about exposure
therapy, and (c) environmental stressors, including relationship, family, or work
stressors.
Given the prominent status of exposure to fear-eliciting targets as a central thera-
peutic element in the treatment of agoraphobia (not to mention most other anxiety
disorders), research aimed at improving our understanding of exposure noncompli-
ance and strategies for its amelioration should be given high research priority.
Conclusions
Based on our qualitative review of the literature spanning the past 35 years, the
following conclusions can be drawn with a reasonable degree of confidence:
1. Exposure techniques, whether administered alone or in combination with panic-

focused education, cognitive restructuring, and relaxation/breathing retraining
techniques, provide the most consistent evidence for clinical efficacy.
2. Agoraphobia patients achieve greater improvement from in vivo exposure when
therapists accompany patients into the field for at least some of their exposure
outings.
3. More cost-effective CBT delivery systems including group treatments, brief
treatments, and computer/Internet-based treatments outperform no treatment
or attentional control interventions and thus appear promising for delivering
CBT to a broader range of agoraphobia sufferers.
4. Agoraphobia patients presenting with significant Axis I or Axis II comorbidity
show greater baseline severity of their agoraphobia and panic symptoms but
appear to benefit as much from CBT as those without significant psychiatric
comorbidity.
5. Research on change mechanisms governing symptom improvement among ago-
raphobia patients receiving CBT has provided the most consistent support for
cognitive change variables including coping self-efficacy, panic appraisal, and
anxiety sensitivity.
References
Aaronson, C. J., Shear, M. K., Goetz, R. R., Allen, L. B., Barlow, D. H., White, K. S., …
Gorman, J. M. (2008). Predictors and time course of response among panic disorder
patients treated with cognitive-behavioral therapy. Journal of Clinical Psychiatry, 69,
418–424. doi:10.4088/JCP.v69n0312
Adler, L. A., Spencer, T., Faraone, S. V., Kessler, R. C., Howes, M. J., Biederman, J., &
Secnik, K. (2006). Validity of pilot Adult ADHD Self-Report Scale (ASRS) to rate
adult ADHD symptoms. Annals of Clinical Psychiatry, 18, 145–148. doi:10.1080/
10401230600801077
Agras, S., Leitenberg, H., & Barlow, D. H. (1968). Social reinforcement in the modification
of agoraphobia. Archives of General Psychiatry, 19, 423–427.
Agoraphobia 971
Agras, S., Sylvester, D., & Oliveau, D. (1969). The epidemiology of common fears and phobia.
Allen, L. B., White, K. S., Barlow, D. H., Shear, M. K., Gorman, J. M., & Woods, S. W.
(2010). Cognitive-behavior therapy (CBT) for panic disorder: Relationship of anxiety
and depression comorbidity with treatment outcome. Journal of Psychopathology and
Behavioral Assessment, 32, 185–192. doi:10.1007/s10862-009-9151-3
Arnow, B. A., Taylor, C. B., Agras, W. S., & Telch, M. J. (1985). Enhancing agoraphobia
treatment outcome by changing couple communication patterns. Behavior Therapy, 16,
452–467.
Bandelow, B. (1995). Assessing the efficacy of treatments for panic disorder and agoraphobia.
II: The Panic and Agoraphobia Scale. International Clinical Psychopharmacology, 10,
73–81.
Bandura, A., Adams, N. E., Hardy, A. B., & Howells, G. N. (1980). Tests of the generality of
self-efficacy theory. Cognitive Therapy and Research, 4, 39–66.
Bandura, A., Jeffery, R. W., & Gajdos, E. (1975). Generalizing change through participant
modeling with self-directed mastery. Behaviour Research and Therapy, 13, 141–152.
Bandura, A., Jeffery, R. W., & Wright, C. L. (1974). Efficacy of participant modeling as a
function of response induction aids. Journal of Abnormal Psychology, 83, 56–64.
panic disorder. Behavior Therapy, 20, 261–282.
Barlow, D. H., O’Brien, G. T., & Last, C. G. (1984). Couples treatment of agoraphobia.
Baron, R. M., & Kenny, D. A. (1986). The moderator–mediator variable distinction in social
psychological research: Conceptual, strategic, and statistical considerations. Journal of
Personality and Social Psychology, 51, 1173–1182.
Bitran, S., Morissette, S. B., Spiegel, D. A., & Barlow, D. H. (2008). A pilot study of sensation-
focused intensive treatment for panic disorder with moderate to severe agoraphobia:
Preliminary outcome and benchmarking data. Behavior Modification, 32, 196–214.
Bonn, J. A., Readhead, C. P., & Timmons, B. H. (1984). Enhanced adaptive behavioural
response in agoraphobic patients pretreated with breathing retraining. Lancet, 324,
665–669.
Botella, C., Garc ı́a-Palacios, A., Villa, H., Baños, R. M., Quero, S., Alcañiz, M., & Riva, G.
(2007). Virtual reality exposure in the treatment of panic disorder and agoraphobia: A con-
trolled study. Clinical Psychology and Psychotherapy, 14, 164–175. doi:10.1002/cpp.524
Bouchard, S., Paquin, B., Payeur, R., Allard, M., Rivard, V., Fournier, T., … Lapierre,
J. (2004). Delivering cognitive-behavior therapy for panic disorder with agorapho-
bia in videoconference. Telemedicine Journal and e-Health, 10, 13–25. doi:10.1089/
153056204773644535
Bouchard, S., Payeur, R., Rivard, V., Allard, M., Paquin, B., Renaud, P., & Goyer, L. (2000).
Cognitive behavior therapy for panic disorder with agoraphobia in videoconference:
Preliminary results. CyberPsychology and Behavior, 3, 999–1007.
Boulougouris, J. C., Marks, I. M., & Marset, P. (1971). Superiority of flooding (implosion) to
desensitisation for reducing pathological fear. Behaviour Research and Therapy, 9, 7–16.
Brown, T. A., Antony, M. M., & Barlow, D. H. (1995). Diagnostic comorbidity in panic
disorder: Effect on treatment outcome and course of comorbid diagnoses following
Byrne, M., Carr, A., & Clark, M. (2004). The efficacy of couples-based interventions for panic
disorder with agoraphobia. Journal of Family Therapy, 26, 105–125.
Carlbring, P., Ekselius, L., & Andersson, G. (2003). Treatment of panic disorder via the
Internet: A randomized trial of CBT vs. applied relaxation. Journal of Behavior Therapy
Carrascoso López, F. J. (2000). Acceptance and commitment therapy (ACT) in panic disorder
with agoraphobia: A case study. Psychology in Spain, 4, 120–128.
Cerny, J. A., Barlow, D. H., Craske, M. G., & Himadi, W. G. (1987). Couples treatment of
agoraphobia: A two-year follow-up. Behavior Therapy, 18, 401–415.
Chambless, D. L. (1990). Spacing of exposure sessions in treatment of agoraphobia and simple
phobia. Behavior Therapy, 21, 217–229.
Chambless, D. L., Foa, E. B., Groves, G. A., & Goldstein, A. J. (1979). Flooding with Brevital
in the treatment of agoraphobia: Countereffective? Behaviour Research and Therapy, 17 ,
243–251.
Cho, Y., Smits, J. A. J., Powers, M. B., & Telch, M. J. (2007). Do changes in panic appraisal
predict improvement in clinical status following cognitive-behavioral treatment of panic
disorder? Cognitive Therapy and Research, 31, 695–707.
Choi, Y.-H., Vincelli, F., Riva, G., Wiederhold, B. K., Lee, J.-H., & Park, K.-H. (2005).
Effects of group experiential cognitive therapy for the treatment of panic disorder with
agoraphobia. CyberPsychology and Behavior, 8, 387–393.
Clark, D. M., Salkovskis, P. M., Hackmann, A., Middleton, H., Anastasiades, P., & Gelder,
M. (1994). A comparison of cognitive therapy, applied relaxation and imipramine in the
treatment of panic disorder. British Journal of Psychiatry, 164, 759–769.
Clark, D. M., Salkovskis, P. M., Hackmann, A., Wells, A., Ludgate, J., & Gelder, M. (1999).
Brief cognitive therapy for panic disorder: A randomized controlled trial. Journal of
Consulting and Clinical Psychology, 67 , 583–589.
Cobb, J. P., Mathews, A. M., Childs-Clarke, A., & Blowers, C. M. (1984). The spouse as
co-therapist in the treatment of agoraphobia. British Journal of Psychiatry, 144, 282–287.
Codd, R. T., Twohig, M. P., Crosby, J. M., & Enno, A. (2011). Treatment of three anxiety
disorder cases with acceptance and commitment therapy in a private practice. Journal of
Côté, G., Gauthier, J. G., Laberge, B., Cormier, H. J., & Plamondon, J. (1994). Reduced
therapist contact in the cognitive behavioral treatment of panic disorder. Behavior Therapy,
25, 123–145.
Craske, M. G., DeCola, J. P., Sachs, A. D., & Pontillo, D. C. (2003). Panic control treatment
for agoraphobia. Journal of Anxiety Disorders, 17 , 321–333. doi:10.1016/S0887-
6185(02)00203-7
Craske, M. G., Golinelli, D., Stein, M. B., Roy-Byrne, P., Bystritsky, A., & Sherbourne,
C. (2005). Does the addition of cognitive behavioral therapy improve panic disorder
treatment outcome relative to medication alone in the primary-care setting? Psychological
Medicine, 35, 1645–1654.
Craske, M. G., Maidenberg, E., & Bystritsky, A. (1995). Brief cognitive-behavioral versus
nondirective therapy for panic disorder. Journal of Behavior Therapy and Experimental
Agoraphobia 973
versus breathing retraining within cognitive-behavioural therapy for panic disorder with
Crowe, M. J., Marks, I. M., Agras, W. S., & Leitenberg, H. (1972). Time-limited desensiti-
sation, implosion and shaping for phobic patients: A crossover study. Behaviour Research
Davis, L., Barlow, D. H., & Smith, L. (2010). Comorbidity and the treatment of principal
anxiety disorders in a naturalistic sample. Behavior Therapy, 41, 296–305.
Dreessen, L., Arntz, A., Luttels, C., & Sallaerts, S. (1994). Personality disorders do not
influence the results of cognitive behavior therapies for anxiety disorders. Comprehensive
Eaton, W. W., Kessler, R. C., Wittchen, H. U., & Magee, W. J. (1994). Panic and panic
disorder in the United States. American Journal of Psychiatry, 151, 413–420.
Emmelkamp, P. M. (1974). Self-observation versus flooding in the treatment of agoraphobia.
Emmelkamp, P. M., & Emmelkamp-Benner, A. (1975). Effects of historically portrayed
modeling and group treatment on self-observation: A comparison with agoraphobics.
Emmelkamp, P. M., van Dyck, R., Bitter, M., Heins, R., Onstein, E. J., & Eisen, B. (1992).
Spouse-aided therapy with agoraphobics. British Journal of Psychiatry, 160, 51–56.
Everaerd, W. T., Rijken, H. M., & Emmelkamp, P. M. (1973). A comparison of “flooding”
and “successive approximation” in the treatment of agoraphobia. Behaviour Research and
Therapy, 11, 105–117.
Faravelli, C., & Pallanti, S. (1989). Recent life events and panic disorder. American Journal of
Fava, G. A., Rafanelli, C., Grandi, S., Conti, S., Ruini, C., Mangelli, L., & Belluardo, P. (2001).
Long-term outcome of panic disorder with agoraphobia treated by exposure. Psychological
Medicine, 31, 891–898.
Friedman, C. J., Shear, M. K., & Frances, A. (1987). DSM-III personality disorders in panic
patients. Journal of Personality Disorders, 1, 132–135.
Gelder, M. G., Bancroft, J. H., Gath, D. H., Johnston, D. W., Mathews, A. M., & Shaw,
P. M. (1973). Specific and non-specific factors in behaviour therapy. British Journal of
Gelder, M. G., & Marks, I. M. (1966). Severe agoraphobia: A controlled prospective trial of
behaviour therapy. British Journal of Psychiatry, 112, 309–319.
Gelder, M. G., Marks, I. M., & Wolff, H. H. (1967). Desensitization and psychotherapy in
the treatment of phobic states: A controlled inquiry. British Journal of Psychiatry, 113,
53–81.
Gillan, P., & Rachman, S. (1974). An experimental investigation of desensitization in phobic
patients. British Journal of Psychiatry, 124, 392–401.
Gloster, A. T., Wittchen, H. U., Einsle, F., Lang, T., Helbig-Lang, S., Fydrich, T., … Arolt,
V. (2011). Psychological treatment for panic disorder with agoraphobia: A randomized
controlled trial to examine the role of therapist-guided exposure in situ in CBT. Journal
of Consulting and Clinical Psychology, 79, 406–420. doi:10.1037/a0023584
Goisman, R. M., Warshaw, M. G., Peterson, L. G.,Rogers, M. P., Cuneo … (1987). Self-
directed exposure for agoraphobia: A controlled trial. Behavior Therapy, 18, 3–16.
Gould, R. A., Clum, G. A., & Shapiro, D. (1993). The use of bibliotherapy in the treatment
of panic: A preliminary investigation. Behavior Therapy, 24, 241–252.
Greist, J., Marks, I., Berlin, F., Gournay, K., & Noshirvani, H. (1980). Avoidance versus
confrontation of fear. Behavior Therapy, 11, 1–14.
Grilo, C. M., Money, R., Barlow, D. H., Goddard, A. W., Gorman, J. M., Hofmann, S. G., …
Woods, S. W. (1998). Pretreatment patient factors predicting attrition from a multicenter
randomized controlled treatment study for panic disorder. Comprehensive Psychiatry, 39,
323–332.
Hahlweg, K., Fiegenbaum, W., Frank, M., Schroeder, B., & von Witzleben, I. (2001). Short-
and long-term effectiveness of an empirically supported treatment for agoraphobia. Journal
of Consulting and Clinical Psychology, 69, 375–382. doi:10.1037//0022-006x.69.3.375
Hand, I., Lamontagne, Y., & Marks, I. M. (1974). Group exposure (flooding) in vivo for
agoraphobics. British Journal of Psychiatry, 124, 588–602.
Hecker, J. E., Losee, M. C., Fritzler, B. K., & Fink, C. M. (1996). Self-directed versus
therapist-directed cognitive behavioral treatment for panic disorder. Journal of Anxiety
Disorders, 10, 253–265.
Hibbert, G. A., & Chan, M. (1989). Respiratory control: Its contribution to the treatment of
panic attacks. A controlled study. British Journal of Psychiatry, 154, 232–236.
Hoffart, A. (1995). A comparison of cognitive and guided mastery therapy of agoraphobia.
Hoffart, A. (1998). Cognitive and guided mastery therapy of agoraphobia: Long-term outcome
and mechanisms of change. Cognitive Therapy and Research, 22, 195–207.
Hoffart, A., & Matinsen, E. W. (1990). Exposure-based integrated vs. pure psychodynamic
treatment of agoraphobic inpatients. Psychotherapy, 27 , 210–218.
Hussain, M. Z., & Nolan, G. (1971). Exposure treatment for phobias. British Medical Journal,
2, 46–47.
Jang, D. P., Ku, J. H., Shin, M. B., Choi, Y. H., & Kim, S. I. (2000). Objective validation of the
effectiveness of virtual reality psychotherapy. CyberPsychology and Behavior, 3, 369–374.
Jannoun, L., Munby, M., Catalan, J., & Gelder, M. (1980). A home-based treatment program
for agoraphobia: Replication and controlled evaluation. Behavior Therapy, 11, 294–305.
Kamphuis, J. H., & Telch, M. J. (1998). Assessment of strategies to manage or avoid perceived
threats among panic disorder patients: The Texas Safety Maneuver Scale (TSMS). Clinical
Psychology & Psychotherapy, 5, 177–186.
Kessler, R. C., Chiu, W. T., Jin, R., Ruscio, A. M., Shear, K., & Walters, E. E. (2006). The
epidemiology of panic attacks, panic disorder, and agoraphobia in the National Comor-
bidity Survey Replication. Archives of General Psychiatry, 63, 415–424. doi:10.1001/
archpsyc.63.4.415
Klein, D. F. (1993). False suffocation alarms, spontaneous panics, and related conditions. An
integrative hypothesis. Archives of General Psychiatry, 50, 306–317.
Klerman, G. L., Weissman, M. M., Rounsaville, B. J., & Chevron, E. (1984). Interpersonal
psychotherapy of depression. New York, NY: Basic Books.
Krijn, M., Emmelkamp, P. M. G., Olafsson, R. P., & Biemond, R. (2004). Virtual reality
exposure therapy of anxiety disorders: A review. Clinical Psychology Review, 24, 259–281.
Ley, R. (1985). Agoraphobia, the panic attack and the hyperventilation syndrome. Behaviour
Lipsitz, J. D., Gur, M., Miller, N. L., Forand, N., Vermes, D., & Fyer, A. J. (2006). An
open pilot study of interpersonal psychotherapy for panic disorder (IPT-PD). Journal of
Nervous and Mental Disease, 194, 440–445.
Marchand, A., Roberge, P., Primiano, S., & Germain, V. (2009). A randomized, controlled
clinical trial of standard, group and brief cognitive-behavioral therapy for panic disorder
Agoraphobia 975
with agoraphobia: A two-year follow-up. Journal of Anxiety Disorders, 23, 1139–1147.

doi:10.1016/j.janxdis.2009.07.019
Margraf, J., Barlow, D. H., Clark, D. M., & Telch, M. J. (1993). Psychological treatment
of panic: Work in progress on outcome, active ingredients, and follow-up. Behaviour
Markowitz, J. C., & Weissman, M. M. (2012). Interpersonal psychotherapy: Past, present and
future. Clinical Psychology and Psychotherapy, 19, 99–105. doi:10.1002/cpp.1774
Marks, I. M. (1978). Living with fear: Understanding and coping with anxiety. New York, NY:
McGraw-Hill.
Marks, I., Boulougouris, J., & Marset, P. (1971). Flooding versus desensitization in the
treatment of phobic patients: A crossover study. British Journal of Psychiatry, 119,
353–375.
Mathews, A. M., Johnston, D. W., Lancashire, M., Munby, M., Shaw, P. M., & Gelder, M.
G. (1976). Imaginal flooding and exposure to real phobic situations: Treatment outcome
with agoraphobic patients. British Journal of Psychiatry, 129, 361–371.
Mathews, A., Teasdale, J., Munby, M., Johnston, D., & Shaw, P. (1977). A home-based
treatment program for agoraphobia. Behavior Therapy, 8, 915–924.
McDonald, R., Sartory, G., Grey, S., Cobb, J., Stern, R., & Marks, I. (1979). The effects of
self-exposure instructions on agoraphobic outpatients. Behaviour Research and Therapy,
17 , 83–85.
McLean, P. D., Woody, S., Taylor, S., & Koch, W. J. (1998). Comorbid panic disorder and
major depression: Implications for cognitive-behavioral therapy. Journal of Consulting
McNamee, G., O’Sullivan, G., Lelliott, P., & Marks, I. (1989). Telephone-guided treatment
for housebound agoraphobics with panic disorder: Exposure vs. relaxation. Behavior
Therapy, 20, 491–497.
Mennin, D. S., & Heimberg, R. G. (2000). The impact of comorbid mood and personality
disorders in the cognitive-behavioral treatment of panic disorder. Clinical Psychology
Review, 20, 339–357.
Meuret, A. E., Wolitzky-Taylor, K. B., Twohig, M. P., & Craske, M. G. (2012). Coping
skills and exposure therapy in panic disorder and agoraphobia: Latest advances and future
directions. Behavior Therapy, 43, 271–284. doi:10.1016/j.beth.2011.08.002
Michelson, L. K., Marchione, K. E., Greenwald, M., Testa, S., & Marchione, N. J. (1996).
A comparative outcome and follow-up investigation of panic disorder with agoraphobia:
The relative and combined efficacy of cognitive therapy, relaxation training, and therapist-
assisted exposure. Journal of Anxiety Disorders, 10, 297–330.
Milrod, B., Busch, F., Leon, A. C., Aronson, A., Roiphe, J., Rudden, M., … Shear, M.
K. (2001). A pilot open trial of brief psychodynamic psychotherapy for panic disorder.
Journal of Psychotherapy Practice and Research, 10, 239–245.
Milrod, B., Leon, A. C., Busch, F., Rudden, M., Schwalberg, M., Clarkin, J., … Shear, M. K.
(2007). A randomized controlled clinical trial of psychoanalytic psychotherapy for panic
disorder. American Journal of Psychiatry, 164, 265–272.
Morissette, S. B., Spiegel, D. A., & Heinrichs, N. (2006). Sensation-focused intensive treatment
for panic disorder with moderate to severe agoraphobia. Cognitive and Behavioral Practice,
12, 17–29.
North, M. M., North, S. M., & Coble, J. R. (1996). Effectiveness of virtual environment
desensitization in the treatment of agoraphobia. Presence, 5, 346–352.
North, M. M., North, S. M., & Coble, J. R. (1998). Virtual reality therapy: An effective
treatment for phobias. Studies in Health Technology and Informatics, 58, 112–119.
Oatley, K., & Hodgson, D. (1987). Influence of husbands on the outcome of their agoraphobic
wives’ therapy. British Journal of Psychiatry, 150, 380–386.
Olatunji, B. O., Etzel, E. N., Tomarken, A. J., Ciesielski, B. G., & Deacon, B. (2011). The
effects of safety behaviors on health anxiety: An experimental investigation. Behaviour
Research and Therapy. doi:10.1016/j.brat.2011.07.008
controlled studies. Behaviour Research and Therapy, 25, 397–409.
Öst, L.-G. (1988). Applied relaxation vs. progressive relaxation in the treatment of panic
disorder. Behaviour Research and Therapy, 26, 13–22.
Öst, L.-G., Thulin, U., & Ramnero, J. (2004). Cognitive behavior therapy vs. exposure in vivo
in the treatment of panic disorder with agoraphobia. Behaviour Research and Therapy, 42,
1105–1127. doi:10.1016/j.brat.2003.07.004
Öst, L.-G., Westling, B. E., & Hellstrom, K. (1993). Applied relaxation, exposure in vivo
and cognitive methods in the treatment of panic disorder with agoraphobia. Behaviour
Pelissolo, A., Zaoui, M., Aguayo, G., Yao, S. N., Roche, S., Ecochard, R., … Jouvent, R. (2012).
Virtual reality therapy versus cognitive-behavior therapy for panic disorder with agora-
phobia: A randomized comparison study. Journal of Cybertherapy and Rehabilitation, 5,
35–43.
Pérez-Ara, M. A., Quero, S., Botella, C., Baños, R., Andreu-Mateu, S., Garcia-Palacios, A., &
Bretón-López, J. (2010). Virtual reality interoceptive exposure for the treatment of panic
disorder and agoraphobia. Studies in Health Technology and Informatics, 154, 77–81.
Persons, J. B., Burns, D. D., & Perloff, J. M. (1988). Predictors of dropout and outcome
in cognitive therapy for depression in a private practice setting. Cognitive Therapy and
Research, 12, 557–575.
Reich, J. H., & Chaudry, D. (1987). Personality of panic disorder alcohol abusers. Journal of
Reich, J. H., & Green, A. I. (1991). Effect of personality disorders on outcome of treatment.
Journal of Nervous and Mental Disease, 179, 74–82.
Reilly, K. P., Gill, M. J., Dattilio, F. M., & McCormick, A. (2005). Panic and agoraphobia:
Do treatments targeted for one problem also improve the other? A pilot study. Archives
of Psychiatry and Psychotherapy, 7 , 11–28.
Renshaw, K. D., Chambless, D. L., & Steketee, G. (2003). Perceived criticism predicts severity
of anxiety symptoms after behavioral treatment in patients with obsessive-compulsive
disorder and panic disorder with agoraphobia. Journal of Clinical Psychology, 59, 411–421.
doi:10.1002/jclp.10048
Roberge, P., Marchand, A., Reinharz, D., & Savard, P. (2008). Cognitive-behavioral treatment
for panic disorder with agoraphobia: A randomized, controlled trial and cost-effectiveness
analysis. Behavior Modification, 32, 333–351.
Salkovskis, P. M., Clark, D. M., Hackmann, A., Wells, A., & Gelder, M. G. (1999). An
experimental investigation of the role of safety-seeking behaviours in the maintenance of
panic disorder with agoraphobia. Behaviour Research and Therapy, 37 , 559–574.
Salkovskis, P. M., Hackmann, A., Wells, A., Gelder, M. G., & Clark, D. M. (2006). Belief
disconfirmation versus habituation approaches to situational exposure in panic disor-
der with agoraphobia: A pilot study. Behaviour Research and Therapy, 45, 877–885.
doi:10.1016/J.Brat.2006.02.008
Schmidt, N. B., & Woolaway-Bickel, K. (2000). The effects of treatment compliance on
outcome in cognitive-behavioral therapy for panic disorder: Quality versus quantity.
Agoraphobia 977
Schmidt, N. B., Woolaway-Bickel, K., Trakowski, J., Santiago, H., Storey, J., Koselka, M.,
& Cook, J. (2000). Dismantling cognitive-behavioral treatment for panic disorder:
Questioning the utility of breathing retraining. Journal of Consulting and Clinical
Sharp, D. M., Power, K. G., & Swanson, V. (2004). A comparison of the efficacy and
acceptability of group versus individual cognitive behaviour therapy in the treatment of
panic disorder and agoraphobia in primary care. Clinical Psychology & Psychotherapy, 11,
73–82.
Shear, M. K., Brown, T. A., Barlow, D. H., Money, R., Sholomskas, D. E., Woods, S. W., …
Papp, L. A. (1997). Multicenter collaborative Panic Disorder Severity Scale. American
Slaap, B. R., & den Boer, J. A. (2001). The prediction of nonresponse to pharmacotherapy in
panic disorder: A review. Depression and Anxiety, 14, 112–122.
Smits, J. A., Powers, M. B., Cho, Y., & Telch, M. J. (2004). Mechanism of change
in cognitive-behavioral treatment of panic disorder: Evidence for the fear of fear
mediational hypothesis. Journal of Consulting and Clinical Psychology, 72, 646–652.
doi:10.1037/0022-006X.72.4.646
Stern, R., & Marks, I. (1973). Brief and prolonged flooding. A comparison in agoraphobic
patients. Archives of General Psychiatry, 28, 270–276.
Swinson, R. P., Fergus, K. D., Cox, B. J., & Wickwire, K. (1995). Efficacy of telephone-
administered behavioral therapy for panic disorder with agoraphobia. Behaviour Research
Teasdale, J. D., Walsh, P. A., Lancashire, M., & Mathews, A. M. (1977). Group exposure for
agoraphobics: A replication study. British Journal of Psychiatry, 130, 186–193.
Telch, M. J., Agras, W. S., Taylor, C. B., Roth, W. T., & Gallen, C. C. (1985). Combined
pharmacological and behavioral treatment for agoraphobia. Behaviour Research and
Therapy, 23, 325–335.
Telch, M. J., Brouillard, M., Telch, C. F., Agras, W. S., & Taylor, C. B. (1989). Role
of cognitive appraisal in panic-related avoidance. Behaviour Research and Therapy, 27 ,
373–383.
Telch, M. J., Kamphuis, J. H., & Schmidt, N. B. (2011). The effects of comorbid personality
disorders on cognitive behavioral treatment for panic disorder. Journal of Psychiatric
Research, 45, 469–474. doi:10.1016/J.Jpsychires.2010.08.008
Telch, M. J., & Lancaster, C. L. (2012). Is there room for safety behaviors in exposure
therapy for anxiety disorders? In P. Neudeck & H. U. Wittchen (Eds.), Exposure therapy:
Rethinking the model: Refining the method (pp. 313–334). New York, NY: Springer.
Telch, M. J., Lucas, J. A., Schmidt, N. B., Hanna, H. H., LaNae Jaimez, T., & Lucas, R. A.
(1993). Group cognitive-behavioral treatment of panic disorder. Behaviour Research and
Therapy, 31, 279–287.
Telch, M. J., Schmidt, N. B., Jaimez, T. L., Jacquin, K. M., & Harrington, P. J. (1995). Impact
of cognitive-behavioral treatment on quality of life in panic disorder patients. Journal of
Tsao, J. C., Mystkowski, J. L., Zucker, B. G., & Craske, M. G. (2005). Impact of
cognitive-behavioral therapy for panic disorder on comorbidity: A controlled investigation.
van Apeldoorn, F. J., Timmerman, M. E., Mersch, P. P., van Hout, W. J., Visser, S., van
Dyck, R., & den Boer, J. A. (2010). A randomized trial of cognitive-behavioral therapy
or selective serotonin reuptake inhibitor or both combined for panic disorder with or
without agoraphobia: Treatment results through 1-year follow-up. Journal of Clinical
Psychiatry, 71, 574–586. doi:10.4088/JCP.08m04681blu
van den Hout, M., Arntz, A., & Hoekstra, R. (1994). Exposure reduced agoraphobia but not
panic, and cognitive therapy reduced panic but not agoraphobia. Behaviour Research and
Therapy, 32, 447–451.
Vincelli, F., Anolli, L., Bouchard, S., Wiederhold, B. K., Zurloni, V., & Riva, G. (2003). Experi-
ential cognitive therapy in the treatment of panic disorders with agoraphobia: A controlled
study. Cyberpsychology & Behavior, 6, 321–328. doi:10.1089/109493103322011632
Vögele, C., Ehlers, A., Meyer, A. H., Frank, M., Hahlweg, K., & Margraf, J. (2010). Cognitive
mediation of clinical improvement after intensive exposure therapy of agoraphobia and
social phobia. Depression and Anxiety, 27 , 294–301. doi:10.1002/da.20651
Vos, S. P., Huibers, M. J., Diels, L., & Arntz, A. (2012). A randomized clinical trial of cognitive
behavioral therapy and interpersonal psychotherapy for panic disorder with agoraphobia.
Psychological Medicine, 42, 1–12. doi:10.1017/S0033291712000876
Watson, J. P., Gaind, R., & Marks, I. M. (1971). Prolonged exposure: A rapid treatment for
phobias. British Medical Journal, 1, 13–15.
Watson, J. P., Mullett, G. E., & Pillay, H. (1973). The effects of prolonged exposure to phobic
situations upon agoraphobic patients treated in groups. Behaviour Research and Therapy,
11, 531–545.
Westphal, C. (1871). Eline neuropathische Erscheinung. Archiv fur Psychiatrie und
Nervenkrankheiten, 3, 138–161.
Williams, S. L. (1990). Guided mastery treatment of agoraphobia: Beyond stimulus exposure.
Progress in Behavior Modification, 26, 89–121.
Williams, S. L., Dooseman, G., & Kleifield, E. (1984). Comparative effectiveness of guided
mastery and exposure treatments for intractable phobias. Journal of Consulting and
Williams, S. L., & Falbo, J. (1996). Cognitive and performance-based treatments for panic
attacks in people with varying degrees of agoraphobic disability. Behaviour Research and
Therapy, 34, 253–264.
Williams, S. L., & Zane, G. (1989). Guided mastery and stimulus exposure treatments for severe
performance anxiety in agoraphobics. Behaviour Research and Therapy, 27 , 237–245.
Wims, E., Titov, N., Andrews, G., & Choi, I. (2010). Clinician-assisted Internet-based
treatment is effective for panic: A randomized controlled trial. Australian and New
Zealand Journal of Psychiatry, 44, 599–607. doi:10.3109/00048671003614171
Wittchen, H.-U., & Essau, C. A. (1991). The epidemiology of panic attacks, panic disorder,
and agoraphobia. In J. R. Walker, G. R. Norton, & C. A. Ross (Eds.), Panic disorder and
agoraphobia: A comprehensive guide for the practitioner (pp. 103–149). Pacific Grove, CA:
Brooks/Cole.
Wittchen, H.-U., Gloster, A. T., Beesdo-Baum, K., Fava, G. A., & Craske, M. G. (2010).
Agoraphobia: A review of the diagnostic classificatory position and criteria. Depression and
Anxiety, 27 , 113–133. doi:10.1002/da.20646
Wolpe, J. (1974). The practice of behaviour therapy. New York, NY: Pergamon Press.
World Health Organization. (1992). International statistical classification of diseases and related
health problems (10th rev.). Geneva, Switzerland: Author.
41
Specific Phobia
Matilda E. Nowakowski, Jenny Rogojanski,
and Martin M. Antony
Ryerson University, Canada
Introduction
According to the current edition of the Diagnostic and Statistical Manual of Mental
Disorders (DSM-IV-TR; American Psychiatric Association, 2000), a specific phobia is
characterized by clinically significant fear or anxiety in response to a specific object
or situation. Exposure to the feared object or situation consistently provokes an
immediate fear or anxiety response, the intensity of which varies as a function of one’s
proximity to the object and the degree to which escape is possible. A diagnosis of
specific phobia requires that the individual recognize his or her response as being
exaggerated or in excess of what is reasonable given the actual danger posed by the
object or situation. Individuals typically exhibit significant anticipatory anxiety prior
to encountering the object of their fear, engage in active avoidance of the feared
object or situation, or endure the phobic stimulus with severe anxiety or distress.
A diagnosis of specific phobia also requires that the individual’s fear or anxiety be
associated with significant interference with his or her typical routine, occupational
or academic functioning, or social activities and relationships, or that the individual is
significantly distressed about having the fear. Lastly, the DSM-IV-TR stipulates that
the fear, anxiety, and avoidance associated with the feared object or situation are not
better accounted for by another mental disorder (American Psychiatric Association,
2000).
The DSM-IV-TR categorizes specific phobias into five types: animal type (e.g., fears
of dogs, spiders, snakes), natural environment type (e.g., fears of heights, storms, being
near water), blood-injection-injury type (e.g., fears of receiving an injection, seeing
blood, dental procedures, undergoing surgery, or other invasive medical procedures),
situational type (e.g., fears of flying, closed spaces, driving), and other type (e.g., fears
of loud noises, vomiting, choking, costumed characters such as clowns). Regardless

DOI: 10.1002/9781118528563.wbcbt41
of the type of phobia, most individuals’ fear or anxiety is focused around the
idea that some aspect of the feared object or situation will cause them harm. In
addition, research indicates that strong feelings of disgust, concerns about panicking,
experiencing anxious arousal, losing control, or fainting during an encounter with the
feared object or situation may also motivate individuals to avoid particular objects or
situations (e.g., Ehlers, Hofmann, Herda, & Roth, 1994; Öst, 1992; Sawchuk, Lohr,
Tolin, Lee, & Kleinknecht, 2000; Teghtsoonian & Frost, 1982). It is not uncommon
for individuals to experience a panic attack prior to or upon confronting a feared
stimulus, and fainting is common among people with phobias of blood or injections
(Öst, 1992).
In the present chapter, we first provide a brief overview of the epidemiology and
etiology of specific phobias, followed by a detailed overview of the assessment and
treatment of specific phobias. We conclude with a case example of a patient with a
specific phobia of elevators.
Epidemiology
Specific phobias are among the most common psychiatric disorders in the general
population, with lifetime prevalence estimates ranging between 9.4% and 12.8%
(Becker et al., 2007; Kessler, Berglund, Demler, Jin, & Walters, 2005; Stinson
et al., 2007). Interestingly, prospective prevalence rates tend to exceed rates collected
retrospectively, with estimates as high as 18.8% (Moffitt et al., 2010). Research
indicates that the prevalence rates of specific fears vary according to phobia type, with
animal and height phobias being the most commonly reported (Becker et al., 2007;
LeBeau et al., 2010; Stinson et al., 2007). Furthermore, subclinical fears that do not
meet full diagnostic criteria for specific phobia are even more common (Antony et al.,
1994; Curtis, Magee, Eaton, Wittchen, & Kessler, 1998).
The initial symptoms of a specific phobia typically emerge in childhood or early
adolescence, with the mean age of onset varying according to phobia type (Stinson
et al., 2007). However, the fear of an object or situation must cause significant distress
for the individual or impairment in his or her life before it can be considered a specific
phobia, and one study found an average lapse of 9 years between the onset of fear and
the point at which the fear was impairing enough to warrant the label phobia (Antony,
Brown, & Barlow, 1997). Notably, situational phobias tend to be more prevalent
among older individuals (Fredrikson, Annas, Fischer, & Wik, 1996) and have a
significantly later age of onset than animal and blood-injection-injury phobias (Depla,
ten Have, van Balkom, & de Graaf, 2008; Lipsitz, Barlow, Mannuzza, Hofmann, &
Fyer, 2002). Without intervention, specific phobias typically persist over time.
Research suggests that there are ethnic and sex differences associated with the
diagnosis of specific phobia. Epidemiological data indicate that specific phobias are
more common among Caucasian than Asian and Hispanic adults (Stinson et al.,
2007), the reasons for which have not yet been determined. Furthermore, specific
phobias of animals and heights, and situational phobias, tend to be more prevalent
among women than men, whereas findings regarding blood-injection-injury phobias
are mixed such that some studies suggest greater prevalence among women (Beesdo,
Specific Phobia 981
Knappe, & Pine, 2009; Bienvenu & Eaton, 1998), whereas others find similar
prevalence rates across genders (Fredrikson et al., 1996). These findings may be
partially explained by men’s tendency to underreport their levels of fear (Pierce &
Kirkpatrick, 1992), as well as findings suggesting that women in Western countries
tend to present for treatment more readily than do men, which may also contribute to
the sex differences found in studies of individuals presenting for treatment in clinical
settings versus those in epidemiological studies (Rowa, McCabe, & Antony, 2006).
When specific phobia is the principal diagnosis, rates of comorbidity with other
Axis I disorders are generally lower than those associated with principal diagnoses of
other anxiety and mood disorders (Brown, Campbell, Lehman, Grisham, & Mancill,
2001). However, it has been found that most individuals with a specific phobia
experience multiple phobias during their lifetime, particularly of the same type (Curtis
et al., 1998; Wittchen, Lecrubier, Beesdo, & Nocon, 2003). Specific phobias also
frequently co-occur with other DSM-IV-TR disorders as an additional diagnosis,
particularly when the principal diagnosis is an anxiety or mood disorder (Brown
et al., 2001; Stinson et al., 2007). Among these disorders, rates of comorbidity
are highest for panic disorder with agoraphobia and bipolar II disorder, respectively
(Stinson et al., 2007). While some research suggests that specific phobias tend to co-
occur less frequently with major depressive disorder (Schatzberg, Samson, Rothschild,
Bond, & Regier, 1998; Stinson et al., 2007), bulimia nervosa (Schwalberg, Barlow,
Alger, & Howard, 1992), and alcohol use disorders (Lehman, Patterson, Brown, &
Barlow, 1998), studies have found that situational and blood-injection-injury phobias
are frequently comorbid with depression and substance use disorders (Becker et al.,
2007; Depla et al., 2008), particularly marijuana use (Bienvenu & Eaton, 1998).
Etiology of Specific Phobias
Mowrer’s (1939) two-stage model proposes that the development and maintenance
of specific phobias occur in two sequential stages involving classical conditioning
and operant conditioning, respectively. During the first phase, a neutral stimulus
is paired with an aversive event, thus resulting in the neutral stimulus becoming a
trigger for fear (e.g., being bitten by a dog triggers a fear of dogs). The second
phase of Mowrer’s two-stage model suggests that the avoidance of the feared object
is negatively reinforced as it reduces feelings of fear and distress, thus maintaining the
specific phobia. Although Mowrer’s two-stage model is parsimonious in explaining
the development of specific phobias, it is limited by the fact that (a) not all individuals
with specific phobias can recall an aversive event related to the development of their
specific phobia (e.g., Graham & Gaffan, 1997; Ollendick & King, 1991), and (b)
many individuals who do recall experiencing an aversive event related to a particular
stimulus do not go on to develop a specific phobia (e.g., Poulton & Menzies,
2002a, 2002b).
Accordingly, Rachman (1978) suggested that fear acquisition occurred through
three pathways: one direct and two indirect. The direct pathway involved aversive
classical conditioning, as described by Mowrer’s (1939) model, while the two indirect
pathways included (a) vicarious learning (i.e., learning through observing another
individual’s reaction to an object, event, or situation), and (b) negative information

transmission (i.e., learning that a stimulus or situation is dangerous through informa-
tion transmitted from sources such as a parental figure, television, or the newspaper).
There is a large body of research using both animal models and humans that has
supported these three pathways to fear acquisition (e.g., Broeren, Lester, Muris, &
Field, 2011; Cook & Mineka, 1989; Egliston & Rapee, 2007; Field, Lawson, &
Banerjee, 2008; Gerull & Rapee, 2002; Mineka & Cook, 1986; Muris & Field,
2010; see also Askew & Field, 2008, and Coelho & Purkis, 2009, for comprehensive
reviews).
It is important to note, however, that many individuals with specific phobias
report that they have always had the fear and are unable to recall a particular
direct or indirect pathway for its development (e.g., Menzies & Clarke, 1993;
Merckelbach, Muris, & Schouten, 1996). These observations have led to the
suggestion that for evolutionary-relevant stimuli (e.g., snakes), fears may develop
without any conditioning or learning experiences (Poulton & Menzies, 2002a;
Stein & Bouwer, 1997), whereas for evolutionary-irrelevant stimuli (e.g., dentists,
etc.), conditioning and/or learning experiences are necessary for the development of
fear. Accordingly, Menzies and Clarke (1993) added a fourth nonassociative pathway
to Rachman’s model to account for fears that are not developed or maintained
through conditioning processes or learning.
Efficacy and Effectiveness of Treatments
Exposure, which involves patients gradually facing the feared object or situation, is the
most widely studied treatment for specific phobias and is viewed as the most efficacious
(Choy, Fyer, & Lipsitz, 2007; Wolitzky-Taylor, Horowitz, Powers, & Telch, 2008).
Across studies, exposure has resulted in significantly greater reductions in fear, as
assessed by self-report and behavioral measures, compared to wait-list, placebo, and
non-exposure-based treatments such as relaxation (see Barlow, Moscovitch, & Micco,
2004; Choy et al., 2007; Wolitzky-Taylor et al., 2008, for reviews). In their 2008
meta-analysis of randomized controlled trials, Wolitzky-Taylor and colleagues found
that the effect sizes in these studies ranged from medium to large and, in general,
were maintained at follow-up intervals ranging from 6 to 14 months. For instance, the
effect sizes (as measured by Cohen’s d) when comparing exposure to non-exposure-
based treatments and wait-list were 0.51 and 1.15, respectively. In some studies,
it has even been found that the treatment effects have increased posttreatment,
especially if patients continue to engage in regular exposure practices (see Choy et al.,
2007; Wolitzky-Taylor et al., 2008). For instance, the effect size for exposure-based
treatments compared to placebo treatments was 0.48 at posttreatment but increased
to 0.80 at follow-up (Wolitzky-Taylor et al., 2008).
Although single-session exposure treatments lead to clinically significant improve-
ments in specific phobias (Zlomke & Davis, 2008), there is evidence that multisession
exposure treatments lead to significantly greater improvements, especially at follow-
up (Cohen’s d = 0.35; Wolitzky-Taylor et al., 2008). It has been suggested that
individuals who complete a multisession treatment protocol are more likely to
Specific Phobia 983
continue to engage in exposure posttreatment compared to individuals who com-

plete a single-session treatment protocol, thus explaining the enhanced reduction in
fear.
In addition to in vivo or real-life exposure, the past 10 years have seen an increase
in the application of virtual reality to the treatment of specific phobias. During virtual
reality exposure, patients are exposed to a virtual environment that involves the feared
object or situation (e.g., flying, thunderstorms). Virtual reality exposure can be used
when repeated in vivo exposure is costly (e.g., flying) or when the occurrence of
the feared situation is unpredictable (e.g., weather-related events), thus making the
planning of exposure practices difficult. Most of the studies to date on virtual reality
exposure have focused on height phobia and flying phobia. In general, these studies
have suggested that virtual reality exposure is as efficacious as in vivo exposure (see
Meyerbroker & Emmelkamp, 2010; Parsons & Rizzo, 2008; Powers & Emmelkamp,
2008, for reviews), although there is a need for more controlled studies with larger
sample sizes as well as more studies investigating specific phobias other than flying
and heights.
In general, there is little evidence for the efficacy of psychotropic medications,
either in isolation or in combination with exposure, for the treatment of specific
phobias (Antony & Barlow, 2002; Choy et al., 2007). However, recent studies using
animal models and humans have shown that D-cycloserine (DCS), a partial agonist
at the glutamatergic N-Methyl-D-aspartate (NMDA) receptor, significantly enhances
fear extinction when combined with exposure (Davis, 2002; Davis, Walker, & Myers,
2003; Deveney, McHugh, Tolin, Pollack, & Otto, 2009; Hofmann, Pollack, & Otto,
2006; Norberg, Krystal, & Tolin, 2008; Ressler et al., 2004). For instance, Ressler
et al. (2004) found that patients with a fear of heights who received either 50 or 500
mg of DCS 2 to 4 hours before exposure to high places (using virtual reality) evidenced
significantly greater reductions in fear following exposure, as assessed through self-
report, behavioral, and physiological measures, compared to patients who received a
placebo and exposure treatment. Furthermore, the differences between groups were
maintained at 3-month follow-up. Thus, the addition of DCS to exposure may be
promising in increasing the effectiveness of treatment. It should be noted, however,
that the research on DCS in humans is preliminary and there is little knowledge about
the mechanisms of action, dosage, frequency of use, and long-term effects of taking
DCS in humans, if any.
Most of the treatment outcome studies to date have based their analyses on
treatment completers. Thus, there is a lack of research using intent-to-treat samples.
This is an important area for future research to better understand the effectiveness of
exposure in the treatment of specific phobias and to suggest possible modifications
and strategies that can be implemented to assist those who drop out of treatment.
Assessment
A comprehensive assessment of a patient’s symptoms is important for (a) diagnosis,

(b) case conceptualization and treatment planning, and (c) treatment monitoring
and evaluation. There are two main semistructured interviews that are widely used
for the diagnosis of anxiety disorders, including specific phobias: the Structured
Clinical Interview for DSM-IV Axis I Disorders (SCID I/P; First, Spitzer, Gibbon, &
Williams, 1996) and the Anxiety Disorders Interview Schedule for DSM-IV (ADIS-IV;
Di Nardo, Brown, & Barlow, 1994). In addition to these semistructured interviews,
there are a number of psychometrically sound self-report questionnaires that patients
can complete to provide more information about their specific fears (see Antony, 2001;
McCabe, Ashbaugh, & Antony, 2010, for comprehensive reviews). Most of these
questionnaires focus on a particular fear (e.g., spiders, dental procedures, dogs, etc.).
It is also important for the clinician to obtain information about the physiological
reactions (e.g., racing heart, sweating, difficulty in breathing), anxiety-provoking
thoughts (e.g., “The other cars are going to hit me,” or “This dog is going to
bite me”), and overt and covert behavioral reactions that patients experience when
anticipating or exposed to the feared stimulus or situation. When assessing behavioral
reactions, in addition to asking about overt avoidance, it is also important to note
any safety behaviors or subtle avoidance strategies (e.g., looking away when receiving
a needle, listening to music while driving, holding on to the railing when on a
balcony, etc.) used by the patient. Given that behavioral exposures are an essential
component of treatment for specific phobias, the clinician should obtain information
about factors that influence levels of fear (e.g., the size of a dog/spider, whether
alone or with someone else while driving, etc.) as this information will assist in the
development of the fear hierarchy (described later). It is also important to assess
any past treatment experiences and their outcomes as well as the suitability of the
patient for cognitive behavioral therapy (CBT). When assessing the outcome of past
treatments, the clinician should make note of any potential obstacles to treatment
(e.g., early termination, inability to complete homework) as well as what was effective
in the past, to obtain a better idea of what may work best for the patient (e.g.,
emphasizing the planning and completion of between-session homework for a patient
with previous difficulties completing homework).
In addition to the information obtained through self-report, it is also useful to
conduct a behavioral assessment. The most commonly used behavioral assessment
for specific phobias is the Behavioral Approach Task (BAT). During this assessment
procedure, the patient is asked to complete a series of tasks that progress from easiest
to hardest and require the patient to approach the feared stimulus or situation. For
instance, for a patient with a fear of spiders, the first task may involve looking at
pictures of spiders while the last task may involve touching a real spider. Patients are
asked to rate the intensity of their fears on a 100-point rating scale. The number
of tasks that patients are able to complete, the length of time they can stay in the
presence of the feared object or situation, as well as their reported level of fear, provide
information about the intensity of the fear.
Depending on the focus of fear, it may also be important for clinicians to assess any
skills deficits related to the feared situation or object. For instance, for an individual
with a fear of driving, it would be important to inquire about driving skills. Similarly,
for an individual with a fear of water, it may be helpful to inquire whether the patient
can swim. The clinician can then work with the patient to determine the importance
of improving relevant skills (e.g., taking a driving course) prior to or during the
completion of behavioral exposures.
Specific Phobia 985
In summary, a comprehensive assessment is necessary before beginning treatment

in order to clarify diagnostic considerations, understand the nature of the patient’s
symptoms, and ensure the development of an appropriate and acceptable treatment
plan. The assessment should not be limited to the first one or two sessions of
treatment. Rather, assessments such as the completion of specific questionnaires or
the completion of the BAT should be conducted regularly throughout treatment to
provide an evaluation of treatment progress as well as to highlight any new factors
that should be considered and incorporated into the treatment plan.
Exposure-Based Strategies
Types of Exposure
In vivo exposure. In vivo exposure involves confronting a feared stimulus, object, or

event in real life, and is the best supported approach for treating specific phobias.
In vivo exposure has been found to be more effective than exposure in imagination
(Emmelkamp & Wessels, 1975; Stern & Marks, 1973), although imaginal exposure
may be useful in situations where repeated exposure is not practical (e.g., flying
phobia). As well, some patients may experience such high levels of anxiety that they
refuse to partake in real-life exposure. In such situations, it may be helpful to begin
with imaginal exposure and then to move on to in vivo exposure when the patient
has experienced a decrease in anxiety.
Imaginal exposure. Imaginal exposure involves confronting the feared stimulus,

object, or event in imagination. The patient may provide a verbal or written account
of the feared stimulus, object, or event or may listen while the clinician describes the
feared stimulus, object, or event. Imaginal exposure is most likely to be effective when
a vivid and detailed image is generated. The clinician can ask a number of questions to
help the patient develop a detailed image of the feared object or situation, including:
“What are you feeling?” “What are you thinking?” “Are you experiencing any physical
reactions?” “What are you seeing/smelling/doing right now?” (Foa & Rothbaum,
1998).
Interoceptive exposure. Interoceptive exposure involves confronting feared physical

sensations (e.g., racing heart, shortness of breath, dizziness, etc.). During interoceptive
exposure, patients complete a variety of exercises that have been shown to produce
particular physical arousal sensations (e.g., spinning to get dizzy, running on the spot
to experience increased heart rate, hyperventilation to experience lightheadedness).
Although interoceptive exposure is best studied in patients with panic disorder
(Antony, Ledley, Liss, & Swinson, 2006; Antony & Swinson, 2000), individuals with
specific phobias may also benefit from interoceptive exposure if they fear physical
arousal sensations, particularly in the context of their feared stimulus, object, or event.
For instance, patients with a fear of heights who fear feeling dizzy when standing on a
balcony may benefit from exposure to dizziness (e.g., by spinning) while standing on
a balcony, though research on the use of interoceptive exposure for specific phobias
is limited.
Virtual reality exposure. Virtual reality exposure involves the patient confronting the
feared stimulus, object, or event in a computer-generated, virtual environment. Virtual
reality exposure is especially relevant for confronting situations for which repeated
exposure may not be practical (e.g., fear of flying) or for which the occurrence of
the feared stimulus or event may be unpredictable and uncontrollable (e.g., fear of
storms).
Conducting Exposure
When introducing exposure, it is important that the clinician provide the client with
a rationale for how exposure works. The effectiveness of exposure can be explained
through a behavioral or a cognitive conceptualization. Behaviorally, the clinician can
explain that during exposure the conditioned stimulus (e.g., a dog) is being presented
without the conditioned response (e.g., being bitten by a dog). Thus, repeated
exposure to the conditioned stimulus without the conditioned response decreases the
strength of the association between the conditioned stimulus and the conditioned
response, resulting in decreased fear. A cognitive rationale for exposure might explain
that the process of exposure provides information that disconfirms the patient’s
fearful predictions. As a result, exposure provides patients with new experiences that
are inconsistent with their fearful beliefs.
Development of a fear hierarchy. Once the process and rationale for exposure is
discussed and the patient has consented to engaging in exposure, the clinician and
patient work collaboratively on developing a fear hierarchy. This is a list of typically
between 10 and 15 situations that the individual fears or avoids. Each item can be
ranked on a scale from 0 to 100, reflecting fear and/or avoidance, where 0 indicates
no fear or avoidance and 100 indicates maximum fear or avoidance. The items are then
rank-ordered from lowest fear/avoidance at the bottom to highest fear/avoidance
at the top. The patient and therapist should attempt to generate a variety of items
that range in difficulty from low to high, including a number of items in the middle
to enable a gradual progression toward facing the feared stimulus or situation. It is
important that the items on the fear hierarchy are specific and detailed to enable
the patient and clinician to reliably evaluate the patient’s fear and avoidance of each
hierarchy item.
Guidelines for Exposure

It is common for patients to question the utility of exposure, given that they will likely
have faced the feared stimuli, objects, and events in the past, with no reduction in
fear. There are a number of ways in which therapeutic exposure differs from everyday
exposure, and it is often helpful for the clinician to highlight these with the patient.
This section describes guidelines for maximizing the effectiveness of therapeutic
exposure.
Specific Phobia 987
Planning, monitoring, and evaluating. The details of each exposure (i.e., what the
patient will do, when and where it will be completed, who will be involved) should
be established before the patient undertakes the exposure. As well, any potential
obstacles for completing the exposure should be identified and solutions should be
brainstormed. It is often also a good idea to plan a back-up exposure in case the
patient is not able to complete the original exposure due to logistic constraints (e.g.,
someone who is supposed to be involved in the exposure is not available). During
the exposure, the patient should regularly rate his or her fear using a scale of 0 (no
fear) to 100 (extreme fear). Following the exposure, the patient should evaluate the
outcome. The patient should be encouraged to evaluate the outcome of the practice
based on what he or she did, rather than what he or she felt (it is perfectly normal to
feel anxious during an exposure practice).
Length of exposure. The patient should continue the exposure until one of two things
happens: (a) the patient experiences a significant decrease in fear, or (b) the patient
learns that the feared consequence is unlikely to occur or that the consequence can be
coped with (Craske & Mystkowski, 2006). In general, longer exposures are associated
with better outcomes (Stern & Marks, 1973). For situations that are inherently brief
(e.g., driving over a bridge), the patient should complete the practice repeatedly until
the situation is manageable.
Control and predictability. Ensuring that exposure practices are both predictable and
under the patient’s control will generally lead to better outcomes (Rose, McGlynn, &
Lazarte, 1995). Patients should know what will happen during an exposure practice
and when it will happen. As well, patients should have control over what happens
during the practice, especially in the early stages of treatment. Patients should never
be forced or tricked into doing something they did not agree to do. In some cases,
control and predictability may be difficult to guarantee (e.g., one cannot always
predict how an animal will react or how others will drive on the road). In such
situations, it may be helpful to talk with the patient about possible outcomes and
to brainstorm ways in which the patient can cope with each possible outcome. As
patients progress in treatment, the predictability of exposure can be decreased in a
gradual manner.
Elimination of safety behaviors. Safety behaviors are subtle avoidance strategies that
patients may use to decrease their fear or protect themselves from possible harm when
facing a feared object or situation. Examples include looking away when getting a
needle, driving only when someone else is in the car, and wearing long pants to keep
spiders off one’s legs. It is important to monitor and reduce the use of safety behaviors
over the course of treatment, though the use of these strategies early in treatment
may help patients to approach and stay longer in feared situations, particularly if their
fear is otherwise very high (Rachman, Radomsky, & Shafran, 2008).
Frequency of exposure practices. Exposure should be conducted at least a few times per
week in between treatment sessions. Research has shown that the more frequent the
exposure, the better the therapeutic outcome. For instance, in one study, individuals
who engaged in daily exposure had a significantly greater reduction of fear compared
to individuals who engaged in weekly exposure, despite completing the same total
number of exposures (Foa, Jameson, Turner, & Payne, 1980). Some studies have also
suggested that different frequencies of exposure have different effects such that massed
exposure (i.e., completing an exposure four times per day) is more effective for short-
term symptom reduction (Foa et al., 1980; Stern & Marks, 1973) whereas spaced
exposure (i.e., completing four exposure practices per week) is best for long-term
treatment outcome (Rowe & Craske, 1998; Tsao & Craske, 2000). It is important to
note, however, that the definition of massed exposure in these studies is not reflective
of real clinical practice, as most clinicians would not ask their patients to complete
the same exposure practice four times per day but would rather encourage patients to
complete exposure practices daily or at least several times per week. Further research is
needed to provide more clarity about the most effective exposure schedule. However,
based on the research to date (e.g., Foa et al., 1980), daily exposure practices are
recommended.
Involving helpers. In many cases, the patient may need to find a helper who can assist
with the completion of exposure between sessions, especially during the early stages
of treatment. The helper can assist with such tasks as locating and collecting the
materials (e.g., pictures of spiders) necessary for exposure, controlling certain aspects
of the exposure (e.g., holding a dog on a leash), as well as modeling exposure for the
patient. When considering involving a helper, it is important that the patient chooses
someone who is likely to be supportive, and who is comfortable with the feared object
or event. At the same time, the helper should be able to tolerate the patient’s distress
and encourage the patient to stay in the situation so that exposure is not terminated
prematurely. If the patient provides consent, it is often helpful to have the helper
observe one or two clinician-administered treatment sessions.
Other Treatment Strategies
Psychoeducation
Psychoeducation is often included in the behavioral treatment of specific phobias,
particularly early in treatment, and may include discussion regarding (a) the nature of
fear and anxiety (e.g., the survival value of these emotions), (b) the components of fear
and anxiety (e.g., physical sensations, cognitions, behavioral responses), (c) how pho-
bias develop, (d) correction of myths or misconceptions regarding the feared object or
situation, (e) the costs and benefits of engaging in exposure therapy, (f) guidelines for
maximizing the effectiveness of exposure, and (g) strategies for maintaining gains (e.g.,
continuing to engage in occasional exposure practices after treatment has ended).
Cognitive Strategies
Distorted or irrational beliefs, such as an unrealistic fear of danger from a stimulus
or situation, have been shown to play a role in specific phobia (Thorpe & Salkovskis,
Specific Phobia 989
1995). Consequently, a small number of studies have examined the use of cognitive
strategies in the treatment of specific phobia. These strategies involve evaluating the
evidence regarding negative beliefs about feared situations, and modifying biased
thinking through cognitive restructuring. Research has yielded evidence supporting
the use of cognitive strategies for the treatment of claustrophobia, either as a stand-
alone treatment or in conjunction with in vivo exposure (Booth & Rachman, 1992;
Craske, Mohlman, Yi, Glover, & Valeri, 1995; Öst, Alm, Brandberg, & Breitholtz,
2001). Additionally, several studies support the use of cognitive strategies for the
treatment of dental phobia (e.g., de Jongh et al., 1995; Willumsen, Vassend, &
Hoffart, 2001) and flying phobia (Capafons, Sosa, & Vina, 1999). In two investi-
gations, Hunt and colleagues (Hunt et al., 2006; Hunt & Fenton, 2007) examined
the impact of directly modifying fear imagery on fear of snakes and found that the
modification of these images via cognitive strategies led to a significant reduction in
behavioral avoidance of snakes. However, it has been found that cognitive strategies
do not generally add much incremental benefit to in vivo exposure for flying and
animal phobias (Koch, Spates, & Himle, 2004; Van Gerwen, Spinhoven, Diekstra, &
Van Dyck, 2002).
Systematic desensitization (Wolpe, 1958) is one of the earliest treatments for specific
phobias, and involves combining graduated imaginal exposure with progressive muscle
relaxation (PMR). PMR uses a series of exercises that involve tensing and relaxing
muscle groups in the legs, arms, abdomen, chest, and head in a sequential order, in
an effort to suppress anxiety through deep muscle relaxation. The use of PMR during
imaginal exposure sessions is based on the principle of reciprocal inhibition (Wolpe,
1958), the notion that fear associations can be weakened through the repeated pairing
of mental images of anxiety-provoking stimuli with a response that is incompatible
with anxiety (i.e., relaxation). Although studies have been conducted to examine
the efficacy of systematic desensitization for specific phobias (for a review, see Choy
et al., 2007), it is seldom recommended in current practice. This is largely due
to the fact that there has been little empirical support for the notion that anxiety
can be counterconditioned through the use of systematic desensitization (Marshall,
1975), and the effectiveness of systematic desensitization is largely dependent upon
an individual’s ability to generate vivid and concrete mental images of his or her
feared object or situation (Lazarus, 1964), which is an ability that not everyone has.
Applied Tension
For individuals with blood and needle phobias who have a history of fainting,
exposure treatment should be combined with applied tension (Öst, Fellenius, &
Sterner, 1991). During applied tension, patients learn to tense their muscles while
engaging in exposure to the feared stimuli in order to create a temporary increase in
blood pressure to prevent fainting. Controlled investigations of the efficacy of applied
muscle tension for blood phobia suggest that it is more efficacious than in vivo
exposure alone (Choy et al., 2007). A more detailed description of this procedure is
provided elsewhere (Antony & Watling, 2006).
Managing Treatment Challenges
This section provides a brief overview of common obstacles that may be encountered
during treatment, and ways to overcome them. For a more comprehensive overview
the reader is directed to Antony and Swinson (2000).
Homework Noncompliance
In general, homework compliance has been found to be related to outcome in
CBT for anxiety disorders. For instance, Edelman and Chambless (1993) found
that greater homework compliance was associated with a greater reduction in fear
and avoidance behaviors in a group of agoraphobic patients. Moreover, Westra,
Dozois, and Marcus (2007) found that the relation between expectancy for change
and early symptom reduction was mediated by homework completion in patients
with anxiety disorders. However, ensuring compliance with homework is often a
challenge in practice. There are a number of factors that may contribute to homework
noncompliance, including a lack of understanding by the patient regarding the
content or relevance of the homework task, ambivalence about overcoming the
problem, high levels of anxiety that prevent homework completion, and competing
demands (e.g., life stresses, overly full schedule). Before one can intervene to improve
compliance, it is essential to determine which factors are interfering with homework
completion in the first place. Depending on the reasons for noncompliance, a number
of approaches have been proposed for increasing homework completion (Antony
& Swinson, 2000), including (a) planning homework collaboratively and practicing
therapist-assisted exposure before trying exposure for homework, (b) implementing
strategies for resolving ambivalence (e.g., motivational interviewing) for clients who
are ambivalent about overcoming their fear (Westra & Dozois, 2008), (c) ensuring
that the level of difficulty of assigned homework is appropriate and manageable, (d)
scheduling telephone contact between sessions to discuss homework practices, and
(e) using problem-solving strategies to manage life stresses or scheduling challenges
that interfere with homework compliance.
Lack of Fear Reduction during Exposure

If a patient’s fear does not decrease over the course of exposure treatment, the clinician
should check to see whether the patient is engaging in any subtle avoidance strategies
or using substances while conducting the exposure, as these may minimize patients’
learning from exposure (Salkovskis, Clark, Hackmann, Wells, & Gelder, 1999; Sloan
& Telch, 2002; but see Milosevic & Radomsky, 2008). As well, the clinician should
assess the patient’s cognitions during the exposure practices. If patients are engaging
in catastrophic thinking or minimizing the outcome of exposure (i.e., believing that
they were lucky the dog did not bite them), it may be necessary to target the
Specific Phobia 991
patient’s anxious thinking more directly through cognitive restructuring or behavioral

experiments. Lastly, the clinician should inquire about the frequency and duration
of exposure to ensure that the patient remains in the feared situation long enough
to experience a reduction in fear and that exposure practices are scheduled in close
proximity to one another.
Refusal to Complete Exposures

If the patient is too fearful to complete an exposure practice, a first step is to identify
a practice that he or she will complete. For example, if a patient with a driving phobia
refuses to drive on a particular day, the clinician can ask whether the patient might
be willing to sit in the car with the engine running. After a few minutes, the patient
might then be willing to try driving a short distance if he or she has experienced some
reduction in fear. Other strategies (e.g., imaginal exposure, cognitive strategies, slow
diaphragmatic breathing) may also be useful to bring the patient’s anxiety to a level
at which he or she is willing to try the exposure practice.
Case Example: Specific Phobia of Elevators
Julie was a 35-year-old business professional who had been afraid of riding elevators
all of her life. Although Julie was not able to trace the onset of her fear to a particular
event, she did recall that her mother was afraid of riding elevators as well and would
often tell Julie that elevators were unsafe and likely to get stuck. As a result of her
fear of elevators, Julie always used the stairs, even if it meant climbing 15 flights.
When Julie was looking for a job five years ago, she made sure that all the offices that
she applied to were located on a low floor (e.g., second or third floor) and were in
low-rise buildings (i.e., no more than eight floors). Julie often phoned in sick to work
when her company had meetings with other companies in high-rise buildings because
she knew that she would not be able to get to the meeting. Julie also made sure that
if she was traveling, which she currently did at least four or five times per year for her
work, she stayed at a low-rise hotel or she requested that her room be on one of the
lower floors of the hotel. A number of Julie’s friends lived in high-rise condominiums
and Julie always turned down their invitations to parties or get-togethers because she
was unable to get to their apartments. Most recently, Julie had been offered a position
to work for a business company as a junior manager. However, the office was located
on the 20th floor of a 30-floor building. Julie felt that this was a great opportunity
in her career and she did not want to have to turn it down. However, she knew that
she could not manage working on the 20th floor with her fear of riding elevators.
Therefore, Julie decided to seek treatment.
During the initial session, a thorough clinical assessment was conducted. The
ADIS-IV was administered and full diagnostic criteria were met for a specific phobia
of elevators. Julie also identified more general fears about being in enclosed places
where escape might be difficult, such as tunnels and subways. It was decided, however,
to focus on Julie’s specific fear of elevators as this was her main concern. Julie did
not endorse any other anxiety disorders or depression. During the clinical assessment,
Julie reported the following physiological reactions when she thought about riding an
elevator: sweating, racing heart, shakiness, dizziness, and nausea. Julie identified the
following thoughts regarding riding elevators: “The elevator is going to break down
and I will not be able to get out,” “If the elevator breaks down I will be stuck in it for
many hours without any food or water,” and “If the elevator breaks down I will panic
and not know what to do.” During the BAT, Julie experienced mild anxiety while
standing in front of the elevator and pressing the button to summon it. She was able
to step into the elevator for 30 seconds while her therapist was in the elevator and held
the door open but reported her anxiety as very high in this situation. She was unable
to stay in the elevator for longer than 30 seconds and was not able to ride it to the next
floor. Following her assessment, Julie received two 120-minute treatment sessions.
Treatment Session 1
Psychoeducation about anxiety was presented, including the cognitive behavioral
model for specific phobias. Julie was also given some psychoeducation about elevators
and their safety. The rationale and procedure for exposure was described and Julie
agreed to engage in exposure during treatment. Julie and her therapist then worked
collaboratively on developing a fear hierarchy that enabled Julie to break down the
task of riding an elevator into various steps that caused mild, moderate, and severe
levels of fear (see Table 41.1).
Julie then worked with her therapist on riding the elevator. Julie rated her fear at
40 out of 100 when she pressed the button and waited for the elevator. When Julie
walked into the elevator while the clinician was holding the door open, she initially
Table 41.1 Sample Exposure Hierarchy for a Fear of Riding Elevators
Item Description Fear rating Avoidance rating

(0 to 100) (0 to 100)
1 Ride an elevator to the 30th floor alone. 100 100

5 Ride an elevator to the 8th floor with a helper. 75 70
6 Ride an elevator for 3 floors alone. 70 70
7 Ride an elevator 1 floor alone. 65 60
8 Ride an elevator 1 floor with a helper. 60 55
9 Enter an elevator for 2 minutes alone while 55 50
holding the door open.
10 Enter an elevator for 30 seconds alone while 50 45
11 Enter an elevator for 30 seconds while a helper is 45 40
12 Press button to summon an elevator and wait for 40 40
it to arrive.
Specific Phobia 993
rated her fear at 75. However, after five minutes of standing in the elevator, Julie
rated her fear at 40 and was able to have her therapist close the door and ride down
one floor. Julie initially rated her fear at 85 when riding one floor with her therapist
in the elevator, but after trying it eight more times, her fear had decreased to 55.
With Julie’s consent, her therapist then brought Andrew, Julie’s boyfriend, into
the office to discuss in vivo exposure practice between sessions. Julie’s therapist spoke
with Andrew about the rationale and procedure for exposure practice. Julie and her
therapist then worked on deciding what Julie would work on for homework. Julie
decided that she would continue to practice riding the elevator one floor at a time
with Andrew, and would then proceed to do it alone. Her therapist encouraged Julie
to ride different elevators in various buildings to enhance the generalization of her
learning.
Treatment Session 2
When Julie came in for her next session, she reported that she was successful in
practicing riding the elevator by herself one floor. Julie said that her fear was a 90
when she first rode the elevator by herself one floor but that it had decreased to 40.
Julie and her therapist then worked on increasing the number of floors that Julie
rode the elevator, first with her therapist, and then by herself. By the end of the
second treatment session, Julie was able to ride the elevator nine floors by herself
with minimal discomfort. With the clinician’s encouragement, Julie agreed that over
the next few weeks she would work on riding the elevators in various buildings and
would continue to increase the number of floors that she was able to ride.
Follow-up Visit
A 30-minute follow-up assessment was conducted one month after Julie’s second
visit. Julie said that she had continued to practice riding elevators both with Andrew
and by herself and that she was now able to ride elevators up to the 25th floor with
minimal fear. A final BAT was conducted and Julie was able to ride the elevator by
herself from the first floor to the 20th floor of the hospital with a fear rating of 10.
The ADIS-IV was readministered and Julie’s symptoms no longer met the diagnostic
criteria for a specific phobia of elevators. Julie told the clinician that she had accepted
the position at the new company and was able to ride the elevator up to her office
with minimal anxiety.
Conclusion
In summary, specific phobias are the most common anxiety disorders and there is
an extensive body of research examining their etiology, maintenance, and treatment.
Exposure is the first line of treatment for specific phobias and there is a robust
body of literature illustrating its effectiveness. It is important to note, however, that
there is individual variability in treatment outcome (albeit less than for other anxiety
disorders), and not all patients experience treatment success. There is a need for
more research that examines predictors of treatment outcome as this will enable us to
further enhance our current treatments and increase our knowledge of how to adapt
treatments to patient and environmental characteristics.
References
Antony, M. M. (2001). Measures for specific phobia. In M. M. Antony, S. M. Orsillo, &
L. Roemer (Eds.), Practitioner’s guide to empirically-based measures of anxiety (pp.
133–158). New York, NY: Springer.
Antony, M. M., & Barlow, D. H. (2002). Specific phobias. In D. H. Barlow (Ed.), Anxiety
and its disorders: The nature and treatment of anxiety and panic (2nd ed., pp. 380–417).
Antony, M. M., Brown, T. A., & Barlow, D. H. (1997). Heterogeneity among specific phobia
types in DSM-IV. Behaviour Research and Therapy, 35, 1089–1100. doi:10.1016/S0005-
7967(97)80003-4
Antony, M. M., Ledley, D. R., Liss, A., & Swinson, R. P. (2006). Responses to symptom
induction exercises in panic disorder. Behaviour Research and Therapy, 44, 85–98.
doi:10.1016/j.brat.2004.12.005
Antony, M. M., Moras, K., Meadows, E. A., Nardo, P. A., Utech, J. E., & Barlow, D. H.
(1994). The diagnostic significance of the functional impairment and subjective distress
criterion: An illustration with the DSM-III-R anxiety disorders. Journal of Psychopathology
and Behavioral Assessment, 16, 253–263. doi:10.1007/BF02229212
Antony, M. M., & Swinson, R. P. (2000). Phobic disorders and panic in adults: A guide to
assessment and treatment. Washington, DC: American Psychological Association.
Antony, M. M., & Watling, M. A. (2006). Overcoming medical phobias: How to conquer fear of
blood, needles, doctors, and dentists. Oakland, CA: New Harbinger Publications.
Askew, C., & Field, A. P. (2008). The vicarious learning pathway to fear 40 years on. Clinical
Barlow, D. H., Moscovitch, D. A., & Micco, J. A. (2004). Psychotherapeutic interventions
for phobias: A review. In M. Maj, H. S. Akistal, J. J. Lopez-Ibor, & A. Okasha (Eds.),
Phobias, 7, 179–210.
Becker, E. S., Rinck, M., Türk, V., Kause, P., Goodwin, R., Neumer, S., & Margraf, J. (2007).
Epidemiology of specific phobia subtypes: Findings from the Dresden mental health study.
European Psychiatry, 22, 69–74. doi:10.1016/j.eurpsy.2006.09.006
Beesdo, K., Knappe, S., & Pine, D. S. (2009). Anxiety and anxiety disorders in children
and adolescents: Developmental issues and implications for DSM-V. Psychiatric Clinics of
North America, 32, 483–524. doi:10.1016/j.psc.2009.06.002
Bienvenu, O., & Eaton, W. (1998). The epidemiology of blood/injection/injury phobia.
Booth, R., & Rachman, S. (1992). The reduction of claustrophobia–I. Behaviour Research
and Therapy, 30, 207–221. doi:10.1016/0005-7967(92)90067-Q
Broeren, S., Lester, K. J., Muris, P., & Field, A. P. (2011). They are afraid of the animal, so
therefore I am too: Influence of peer modeling on fear beliefs and approach-avoidance
behaviors towards animals in typically developing children. Behaviour Research and
Brown, T. A., Campbell, L. A., Lehman, C. L., Grisham, J. R., & Mancill, R. B. (2001).
Current and lifetime comorbidity of the DSM-IV anxiety and mood disorders in a
Specific Phobia 995
large clinical sample. Journal of Abnormal Psychology, 110, 585–599. doi:10.1037/0021-

843X.110.4.585
Capafons, J. I., Sosa, C. D., & Vina, C. M. (1999). A reattributional training program as
a therapeutic strategy for fear of flying. Journal of Behavior Therapy and Experimental
Psychiatry, 30, 259–272. doi:10.1016/S0005-7916(99)00028-2
Choy, Y., Fyer, A. J., & Lipsitz, J. D. (2007). Treatment of specific phobia in adults. Clinical
Psychology Review, 27 , 266–286. doi:10.1016/j.cpr.2006.10.002
Coelho, C. M., & Purkis, H. (2009). The origins of specific phobias: Influential theories and
current perspectives. Review of General Psychology, 13, 335–348. doi:10.1037/a0017759
Cook, M., & Mineka, S. (1989). Observational conditioning of fear-relevant versus fear-
irrelevant stimuli in rhesus monkeys. Journal of Abnormal Psychology, 98, 448–459.
doi:10.1037/0021-843X.98.4.448
Craske, M. G., Mohlman, J., Yi, J., Glover, D., & Valeri, S. (1995). Treatment of claustropho-
bias and snake/spider phobias: Fear of arousal and fear of context. Behaviour Research
and Therapy, 33, 197–203. doi:10.1016/0005-7967(94)P4441-V
Craske, M. G., & Mystkowski, J. L. (2006). Exposure therapy and extinction: Clinical studies.
In M. G. Craske, D. Hermans, & D. Vansteenwegen (Eds.), Fear and learning: From basic
processes to clinical implications (pp. 217–233). Washington, DC: American Psychological
Association.
Curtis, G. C., Magee, W. J., Eaton, W. W., Wittchen, H.-U., & Kessler, R. C. (1998). Specific
fears and phobias: Epidemiology and classification. British Journal of Psychiatry, 173,
212–217. doi:10.1192/bjp.173.3.212
Davis, M. (2002). Role of NMDA receptors and MAP kinase in the amygdala in extinction
of fear: Clinical implications for exposure therapy. European Journal of Neuroscience, 16,
395–398. doi:10.1046/j.1460-9568.2002.02138.x
Davis, M., Walker, D., & Myers, K. (2003). Role of the amygdala in fear extinction measured
with potential startle. Annals of the New York Academy of Science, 985, 218–232.
doi:10.1111/j.1749-6632.2003.tb07084.x
Depla, M., ten Have, M., van Balkom, A., & de Graaf, R. (2008). Specific fears and phobias in
the general population: Results from the Netherlands Mental Health Survey and Incidence
Study. Social Psychiatry and Psychiatric Epidemiology, 42, 200–208. doi:10.1007/s00127-
007-0291-z
Deveney, C. M., McHugh, K. R., Tolin, D. F., Pollack, M. H., & Otto, M. W. (2009).
Combining D-cycloserine and exposure-based CBT for the anxiety disorders. Clinical
Neuropsychiatry, 6, 75–82.
de Jongh, A., Muris, P., Horst, G. T., van Zuuren, F., Schoenmakers, N., & Makkes, P. (1995).
One-session cognitive treatment of dental phobia: Preparing dental phobics for treatment
by restructuring negative cognitions. Behaviour Research and Therapy, 33, 947–954.
doi:10.1016/0005-7967(95)00027-U
Di Nardo, P., Brown, T. A., & Barlow, D. H. (1994). Anxiety Disorders Interview Schedule for
DSM-IV . New York, NY: Oxford University Press.
Edelman, R. E., & Chambless, D. L. (1993). Compliance during sessions and homework in
exposure based treatment of agoraphobia. Behaviour Research and Therapy, 31, 767–773.
doi:10.1016/0005-7967(93)90007-H
Egliston, K. A., & Rapee, R. (2007). Inhibition of fear acquisition in toddlers follow-
ing modeling by their mothers. Behaviour Research and Therapy, 45, 1871–1882.
doi:10.1016/j.brat.2007.02.007
Ehlers, A., Hofmann, S. G., Herda, C. A., & Roth, W. T. (1994). Clinical characteristics
of driving phobia. Journal of Anxiety Disorders, 8, 323–339. doi:10.1016/0887-
6185(94)00021-2
Emmelkamp, P. M. G., & Wessels, H. (1975). Flooding in imagination vs. flooding in

vivo: A comparison with agoraphobics. Behaviour Research and Therapy, 13, 7–15.
doi:10.1016/0005-7967(75)90047-9
Field, A. P., Lawson, J., & Banerjee, R. (2008). The verbal threat information pathway to
fear in children: The longitudinal effects on fear cognitions and the immediate effects on
avoidance behavior. Journal of Abnormal Psychology, 117 , 214–224. doi:10.1037/0021-
843X.117.1.214
First, M. B., Spitzer, R. L., Gibbon, M. M., & Williams, J. B. W. (1996). Structured Clinical
Interview for DSM-IV Axis I Disorder: Patient Edition (SCID-I/P Version 2.0). New York,
NY: Biometrics Research Department, New York State Psychiatric Institute.
doi:10.1016/0005-7967(80)90092-3
Foa, E. B., & Rothbaum, B. O. (1998). Treating the trauma of rape: Cognitive behavioral
therapy for PTSD. New York, NY: Guilford Press.
Fredrikson, M., Annas, P., Fischer, H., & Wik, G. (1996). Gender and age differences in the
prevalence of specific fears and phobias. Behaviour Research and Therapy, 34, 33–39.
doi:10.1016/0005-7967(95)00048-3
Gerull, F. C., & Rapee, R. M. (2002). Mother knows best: Effects of maternal modeling on the
acquisition of fear and avoidance behaviour in toddlers. Behaviour Research and Therapy,
40, 279–287. doi:10.1016/S0005-7967(01)00013-4
Graham, J., & Gaffan, E. A. (1997). Fear of water in children and adults: Etiology and
familial effects. Behaviour Research and Therapy, 35, 91–108. doi:10.1016/S0005-
7967(96)00086-1
Hofmann, S. G., Pollack, M. H., & Otto, M. W. (2006). Augmentation treatment of
psychotherapy for anxiety disorders with D-cycloserine. CNS Drug Review, 12, 208–217.
doi:10.1111/j.1527-3458.2006.00208.x
Hunt, M., Bylsma, L., Brock, J., Fenton, M., Goldberg, A., Miller, R., … Urgelles, J. (2006).
The role of imagery in the maintenance and treatment of snake fear. Journal of Behavior
Therapy and Experimental Psychiatry, 37 , 283–298. doi:10.1016/j.jbtep.2005.12.002
Hunt, M., & Fenton, M. (2007). Imagery rescripting versus in vivo exposure in the treatment
of snake fear. Journal of Behavior Therapy and Experimental Psychiatry, 38, 329–344.
doi:10.1016/j.jbtep.2007.09.001
Kessler, R. C., Berglund, P., Demler, O., Jin, R., & Walters, E. E. (2005). Lifetime prevalence
and age-of-onset distributions of DSM-IV disorders in the National Comorbidity Survey
Replication. Archives of General Psychiatry, 62, 593–602.
Koch, E., Spates, R., & Himle, J. (2004). Comparison of behavioral and cognitive-behavioral
one-session exposure treatments for small animal phobias. Behaviour Research and Ther-
apy, 42, 1483–1504. doi:10.1016/j.brat.2003.10.005
Lazarus, A. A. (1964). Crucial procedural factors in desensitization therapy. Behaviour Research
and Therapy, 2, 63–70. doi:10.1016/0005-7967(64)90057-9
LeBeau, R. T., Glenn, D., Liao, B., Wittchen, H.-U., Beesdo-Baum, K., Ollendick, T., &
Craske, M. G. (2010). Specific phobia: A review of DSM-IV specific phobia and prelimi-
nary recommendations for DSM-V. Depression and Anxiety, 27 , 148–167. doi:10.1002/
da.20655
Specific Phobia 997
Lehman, C. L., Patterson, M. D., Brown, T. A., & Barlow, D. H. (1998, November). Lifetime
alcohol use disorders in patients with anxiety and mood disorders. Paper presented at the
meeting of the Association for the Advancement of Behavior Therapy, Washington, DC.
Lipsitz, J. D., Barlow, D. H., Mannuzza, S., Hofmann, S. G., & Fyer, A. J. (2002). Clinical
features of four DSM-IV-specific phobia subtypes. Journal of Nervous and Mental Disease,
190, 471–478. doi:10.1097/00005053-200207000-00009
Marshall, W. L. (1975). An examination of reciprocal inhibition and counterconditioning
explanations of desensitization therapy. European Journal of Behavioural Analysis and
Modification, 1, 74–86.
McCabe, R. E., Ashbaugh, A. R., & Antony, M. M. (2010). Specific and social phobias. In
M. M. Antony & D. H. Barlow (Eds.), Handbook of assessment and treatment planning
for psychological disorders (2nd ed., pp. 186–223). New York, NY: Guilford Press.
Menzies, R. G., & Clarke, J. C. (1993). The etiology of childhood water phobia. Behaviour
Research and Therapy, 31, 499–501. doi:10.1016/0005-7967(93)90131-D
Merckelbach, H., Muris, P., & Schouten, E. (1996). Pathways to fear in spider phobic children.
Behaviour Research and Therapy, 34, 935–938. doi:10.1016/S0005-7967(96)00052-6
Meyerbroker, K., & Emmelkamp, P. M. G. (2010). Virtual reality exposure therapy in anxiety
27 , 933–944. doi:10.1002/da.20734
Milosevic, I., & Radomsky, A. S. (2008). Safety behaviour does not necessarily interfere with
exposure therapy. Behaviour Research and Therapy, 46, 1111–1118.
Mineka, S., & Cook, M. (1986). Immunization against the observational conditioning
of snake fear in rhesus monkeys. Journal of Abnormal Psychology, 95, 307–318.
doi:10.1037//0021-843X.95.4.307
Moffitt, T. E., Caspi, A., Taylor, A., Kokaua, J., Milne, B. J., Polanczyk, G., & Poulton, R.
(2010). How common are common mental disorders? Evidence that lifetime prevalence
rates are doubled by prospective versus retrospective ascertainment. Psychological Medicine,
40, 899–909. doi:10.1017/S0033291709991036
Mowrer, O. H. (1939). Stimulus response theory of anxiety. Psychological Review, 46, 553–565.
Muris, P., & Field, A. P. (2010). The role of verbal threat information in the development of
childhood fear: “Beware the Jabberwock!” Clinical Child and Family Psychology Review,
13, 129–150. doi:10.1007/s10567-010-0064-1
Norberg, M. M., Krystal, J. H., & Tolin, D. F. (2008). A meta-analysis of D-cycloserine and the
facilitation of fear extinction and exposure therapy. Biological Psychiatry, 63, 1118–1126.
doi:10.1016/j.biopsych.2008.01.012
Ollendick, T. H., & King, N. J. (1991). Origins of childhood fears: An evaluation of
Rachman’s theory of fear acquisition. Behaviour Research and Therapy, 29, 117–123.
doi:10.1016/0005-7967(91)90039-6
Öst, L.-G. (1992). Blood and injection phobia: Background and cognitive, physiological and
behavioral variables. Journal of Abnormal Psychology, 101, 68–74. doi:10.1037/0021-
843X.101.1.68
Öst, L.-G., Alm, T., Brandberg, M., & Breitholtz, E. (2001). One vs. five sessions of exposure
and five sessions of cognitive therapy in the treatment of claustrophobia. Behaviour
Research and Therapy, 39, 167–183. doi:10.1016/S0005-7967(99)00176-X
Öst, L.-G., Fellenius, J., & Sterner, U. (1991). Applied tension, exposure in vivo, and tension-
only in the treatment of blood phobia. Behaviour Research and Therapy, 29, 561–574.
doi:10.1016/0005-7967(91)90006-O
Parsons, T. D., & Rizzo, A. A. (2008). Affective outcomes for virtual reality exposure
therapy for anxiety and specific phobias: A meta-analysis. Journal of Behavior Therapy and
Experimental Psychology, 39, 250–261. doi:10.1016/j.jbtep.2007.07.007
Pierce, K. A., & Kirkpatrick, D. R. (1992). Do men lie on fear surveys? Behaviour Research and
Therapy, 30, 415–418. doi:10.1016/0005-7967(92)90055-L
Poulton, R., & Menzies, R. G. (2002a). Fears born and bred: Toward a more inclusive theory
of fear acquisition. Behaviour Research and Therapy, 40, 197–208. doi:10.1016/S0005-
7967(01)00052-3
Poulton, R., & Menzies, R. G. (2002b). Non-associative fear acquisition: A review of the
evidence from retrospective and longitudinal research. Behaviour Research and Therapy,
40, 127–149. doi:10.1016/S0005-7967(01)00045-6
Powers, M. B., & Emmelkamp, P. M. G. (2008). Virtual reality exposure therapy
for anxiety disorders: A meta-analysis. Journal of Anxiety Disorders, 22, 561–569.
doi:10.1016/j.janxdis.2007.04.006
Rachman, S. (1978). Fear and courage. San Francisco, CA: Freeman.
Rachman, S., Radomsky, A. S., & Shafran, R. (2008). Safety behaviour: A reconsideration.
Davis, M. (2004). Cognitive enhancers as adjuncts to psychotherapy: Use of D-cycloserine
in phobics to facilitate extinction of fear. Archives of General Psychiatry, 61, 1136–1144.
doi:10.1001/archpsyc.61.11.1136
Rose, M. P., McGlynn, F. D., & Lazarte, A. (1995). Control and attention influence snake
phobics’ arousal and fear during laboratory confrontation with a caged snake. Journal of
Anxiety Disorders, 9, 293–302. doi:10.1016/0887-6185(95)00010-L
Rowa, K., McCabe, R. E., & Antony, M. M. (2006). Specific phobias. In F. Andrasik (Ed.),
Comprehensive handbook of personality and psychopathology, vol. 2: Adult psychopathology
Rowe, M. K., & Craske, M. G. (1998). Effects of an expanding-spaced vs. massed exposure
schedule on fear reduction and return of fear. Behaviour Research and Therapy, 36,
701–717. doi:10.1016/S0005-7967(97)10016-X
Salkovskis, P. M., Clark, D., Hackmann, A., Wells, A., & Gelder, M. (1999). An experimental
investigation of the role of safety-seeking behaviors in the maintenance of panic disorder
with agoraphobia. Behaviour Research and Therapy, 37 , 559–574. doi:10.1016/S0005-
7967(98)00153-3
Sawchuk, C. N., Lohr, J. M., Tolin, D. F., Lee, T. C., & Kleinknecht, R. A. (2000). Disgust
sensitivity and contamination fears in spider and blood-injection-injury phobias. Behaviour
Research and Therapy, 38, 753–762. doi:10.1016/S0005-7967(99)00093-5
Schatzberg, A. F., Samson, J. A., Rothschild, A. J., Bond, T. C., & Regier, D. A. (1998).
McLean Hospital depression research facility: Early-onset phobic disorders and adult-onset
major depression. British Journal of Psychiatry, 34, 29–34.
Schwalberg, M. D., Barlow, D. H., Alger, S. A., & Howard, L. J. (1992). Comparison
of bulimics, obese binge eaters, social phobics and individuals with panic disorder on
comorbidity across the DSM-III-R anxiety disorders. Journal of Abnormal Psychology,
101, 675–681. doi:10.1037/0021-843X.101.4.675
Sloan, T., & Telch, M. J. (2002). The effects of safety-seeking behavior and guided threat
reappraisal on fear reduction during exposure: An experimental investigation. Behaviour
Research and Therapy, 40, 235–251. doi:10.1016/S0005-7967(01)00007-9
Stein, D. J., & Bouwer, C. (1997). A neuro-evolutionary approach to the anxiety disorders.
Journal of Anxiety Disorders, 11, 409–429. doi:10.1016/S0887-6185(97)00019-4
Stern, R., & Marks, I. (1973). Brief and prolonged flooding: A comparison in agorapho-
bic patients. Archives of General Psychiatry, 28, 270–276. doi:10.1001/archpsyc.1973.
01750320098015
Specific Phobia 999
Stinson, F. S., Dawson, D. A., Chou, S. P., Smith, S., Goldstein, R. B., Ruan, W. J., & Grant,
B. F. (2007). The epidemiology of DSM-IV specific phobia in the USA: Results from the
national epidemiological survey on alcohol and related conditions. Psychological Medicine,
37 , 1047–1059. doi:10.1017/S0033291707000086
Teghtsoonian, R., & Frost, R. O. (1982). The effects of viewing distance on fear of snakes. Jour-
nal of Behavior Therapy and Experimental Psychiatry, 13, 181–190. doi:10.1016/0005-
7916(82)90002-7
Thorpe, S. J., & Salkovskis, P. M. (1995). Phobic beliefs: Do cognitive factors play a role
in specific phobias? Behaviour Research and Therapy, 33, 805–816. doi:10.1016/0005-
7967(95)00022-P
Tsao, J. C. I., & Craske, M. G. (2000). Timing of treatment and return of fear: Effects
of massed, uniform-, and expanding-spaced exposure schedules. Behavior Therapy, 31,
479–497. doi:10.1016/S0005-7894(00)80026-X
Van Gerwen, L. J., Spinhoven, P., Diekstra, R. F., & Van Dyck, R. (2002). Multicomponent
standardized treatment program for fear of flying: Description and effectiveness. Cognitive
and Behavioral Practice, 9, 138–149. doi:10.1016/S1077-7229(02)80007-4
Westra, H. A., & Dozois, D. J. A. (2008). Integrating motivational interviewing in the
treatment of anxiety. In H. Arkowitz, H. A. Westra, W. R. Miller, & S. Rollnick (Eds.),
Motivational interviewing in the treatment of psychological problems (pp. 26–56). New
Willumsen, T., Vassend, O., & Hoffart, A. (2001). A comparison of cognitive therapy, applied
relaxation, and nitrous oxide sedation in the treatment of dental fear. Acta Odontologica
Scandinavica, 59, 290–296. doi:10.1080/000163501750541156
Wittchen, H.-U., Lecrubier, Y., Beesdo, K., & Nocon, A. (2003). Relationships among anxiety
disorders: Patterns and implications. In D. J. Nutt & J. C. Ballenger (Eds.), Anxiety
disorders (pp. 25–37). Oxford, England: Wiley Blackwell.
Wolitzky-Taylor, K. B., Horowitz, J. D., Powers, M. B., & Telch, M. J. (2008). Psychological
approaches in the treatment of specific phobias: A meta-analysis. Clinical Psychology
Review, 28, 1021–1037. doi:10.1016/j.cpr.2008.02.007
Press.
Zlomke, K., & Davis, T. E. (2008). One-session treatment of specific phobias: A
detailed description and review of treatment efficacy. Behavior Therapy, 39, 207–233.
doi:10.1016/j.beth.2007.07.003
42
Lauren E. Szkodny and Michelle G. Newman
Pennsylvania State University, United States
Therapists and clinical scientists involved in the study, assessment, and treatment of
generalized anxiety disorder (GAD) undoubtedly encounter individuals preoccupied
with intense and pervasive worry and anxiety. Whereas worry is a universal experience,
common in both nonpathological and anxious populations, individuals with GAD
stand apart, as their worry is more pervasive and less controllable, thereby engendering
greater distress and life interference. Typically describing themselves as lifelong
worriers, these individuals perceive their worrisome thinking and associated anxiety as
facets of their personality, enduring traits rather than phenomena prone to fluctuations
that can be monitored, targeted, and effectively changed. In fact, worry may be viewed
as such a central part of life, a primary coping strategy used to avoid perceived threat
and changes in emotional reactivity, that treatment may not even be considered
(Newman, Crits-Christoph, & Szkodny, in press).
GAD has been referred to as the “basic” anxiety disorder (Brown, Barlow, &
Liebowitz, 1994), an appellation that suggests understanding the development and
maintenance of GAD is important for understanding all anxiety disorders. Given
GAD’s course and documented resistance to change, research has centered not
only on elucidating the nature and etiology of this disorder, but also on developing
treatments that improve upon standard versions of cognitive behavioral therapy
(CBT). This has been most critical since worry is a means to avoid anticipated threats,
as opposed to tangible, anxiety-provoking stimuli, and thus is not as easily addressed
with exposure interventions commonly executed in the treatment of other anxiety
disorders (Newman & Borkovec, 2002). The principal objective of this chapter is to
present an overview of CBT for GAD. First, the symptomatology of GAD is discussed,
followed by a presentation of the cognitive behavioral treatment rationale and CBT
techniques. Additionally, empirical evidence supporting the efficacy of CBT for GAD

DOI: 10.1002/9781118528563.wbcbt42
is reviewed. This chapter also discusses the limitations of CBT methods and presents
a number of integrative techniques that have been incorporated into CBT for GAD.
Phenomenology of Generalized Anxiety Disorder
The Diagnostic and Statistical Manual of Mental Disorders (5th ed.; DSM-5; American
Psychiatric Association [APA], 2013) indicates that excessive and uncontrollable
worry, defined as apprehensive expectation, is the core feature of GAD. To meet
criteria, individuals must experience worry more days than not for at least 6 months
about a number of events or activities. Additionally, their worry and anxiety is
generally associated with at least three of the following six physical symptoms: (a)
restlessness or feeling keyed up or on edge, (b) being easily fatigued, (c) difficulty
concentrating or mind going blank, (d) irritability, (e) muscle tension, and (f) sleep
disturbance characterized by difficulty falling or staying asleep, or restless, unsatisfying
sleep. Finally, their worry and anxiety must (a) not be confined to features of an
Axis I disorder (e.g., worry about having a panic attack [panic disorder] or being
embarrassed in public [social phobia]), (b) cause clinically significant distress or
impairment in important domains of functioning, and (c) not be due to the direct
physiological effects of a substance or a general medical condition.
GAD symptoms have undergone extensive empirical revision since its inception in
the DSM-III (APA, 1980) 3rd edn. as a residual category (Brown et al., 1994). In
the DSM-III-R (APA, 1987) 3rd edn. revised, the pervasiveness and uncontrollability
of worry were emphasized, but the unrealistic nature of worry was dropped from the
definition.
Following an investigation of the reliability and frequency of the endorsement of
the 18 associated features (somatic symptoms) delineated in the DSM-III-R (Marten
et al., 1993), autonomic hyperactivity symptoms (e.g., sweating, dry mouth) were
identified as the least reliable and least frequently endorsed among individuals with
GAD. The six symptoms indicated in the DSM-IV-TR (APA, 2000) 4th edn. text
review, were identified as the symptoms that significantly discriminated patients with
GAD from individuals diagnosed with other anxiety disorders (Brown, Marten, & Bar-
low, 1995). Members of the GAD work group for the DSM-5 originally proposed to
remove the criterion related to the difficulty of controlling worry given its overlap with
the excessiveness criterion, to reduce GAD’s threshold to 3 months (as opposed to 6
months), to change the number of physical symptoms required from three to one, and
to add a criterion that tapped into situational avoidance, excessive effort toward prepa-
ration, procrastination, and reassurance seeking. However, these proposed revisions
to the GAD diagnostic criteria have not been included in the DSM-5.
Contrary to the notion that GAD is a reflection of a highly functioning diagnostic
group (e.g., the worried well), or that GAD is only impairing as a result of its high
degree of comorbidity with other disorders, the degree of disability in persons with
pure GAD (without comorbidity) is as severe as pure major depressive disorder (MDD)
and other mood disorders (Hoffman, Dukes, & Wittchen, 2008). Also, incapacity
as a result of GAD is analogous to that seen in chronic medical illnesses (Ansseau
et al., 2008; Fifer et al., 1994; Stein, 2001). GAD is also more debilitating than pure
Generalized Anxiety Disorder 1003
alcohol and drug use disorders, nicotine dependence, other anxiety disorders, and
personality disorders even when controlling for sociodemographic factors and all other
co-occurring conditions (Grant et al., 2005). Persons with GAD are among the most
frequent consumers of primary care, specialty clinic, and emergency room services,
incurring significant nonpsychiatric cost (Fogarty, Sharma, Chetty, & Culpepper,
2008; Mehl-Madrona, 2008). GAD is also a major risk factor for coronary heart
disease independent of depression (Barger & Sydeman, 2005; Todaro, Shen, Raffa,
Tilkemeier, & Niaura, 2007). The direct excess yearly cost of GAD has been estimated
to be as high as $20,184 per case (Olfson & Gameroff, 2007). Therefore, untreated
GAD is very costly in terms of distress, disability, lost work productivity, quality of
life, and medical problems (Newman, 2000).
Worry has been defined as “a chain of thoughts and images, negatively affect-
laden and relatively uncontrollable; it represents an attempt to engage in mental
problem-solving on an issue whose outcome is uncertain but contains the possibility
of one or more negative outcomes; consequently, worry relates closely to the fear
process” (Borkovec, Robinson, Pruzinsky, & DePree, 1983, p. 10). Individuals with
GAD are generally apprehensive about the occurrence of negative future outcomes
related to major life issues (e.g., family and interpersonal relationships, finances,
health, occupational and academic pursuits) and minor concerns (e.g., household
repairs or chores) (Borkovec, Ray, & Stober, 1998). Pathological worry comprises
a spiraling chain of cognitive, behavioral, and physiological events (Newman &
Borkovec, 2002) triggered by a perceived stressor, especially one characterized by
ambiguity or uncertainty. To illustrate, in response to an ambiguous comment made
by a romantic partner, an individual with GAD would likely experience an anxious
thought (e.g., “He is angry with me”) and associated physiological response (e.g.,
increased tension, which may interfere with falling asleep), to be followed by another
worrisome thought (e.g., “He is going to break up with me”) and elicited negative
emotion (e.g., anxiety, despair), which might activate more anxious thoughts related
to a core negative belief (e.g., “I’m unlovable and will be alone forever”). This cycle
is often difficult to break as one worry leads to another and so on to the point that
it becomes disabling and is a source of extreme emotional discomfort, so cognitive
behavioral techniques are implemented to teach clients to identify initial anxiety cues
to reduce the intensity of the worry/anxiety spiral (Newman & Borkovec, 2002).
Additionally, individuals with GAD exhibit an information processing bias; they
scan their surrounding environment for potential danger, and negatively interpret
ambiguous or neutral stimuli, thereby detecting threat in them (Mathews, 1990;
Mathews & MacLeod, 1994). In perceiving the world as a dangerous place, their
anticipation of negative outcomes or worst-case scenarios seemingly enhances
their sense of control, such that worry represents mental attempts at avoidance of
threat or preparation for its occurrence if it cannot be avoided (Borkovec et al.,
1998; Borkovec, Alcaine, & Behar, 2004). Nevertheless, worry’s avoidant function
precludes repeated exposure to those stimuli necessary for extinction, thus preserving
anxious meaning associated with the threat (Newman & Llera, 2011). Specifically,
it diminishes initial cardiovascular response to threatening images and reduces the
likelihood of additional affective reactivity subsequent to an anxiety-provoking event
or situation (Borkovec & Hu, 1990; Llera & Newman, 2010; Newman & Llera,
2011), which impedes emotional processing of aversive stimuli.
Although worry is associated with increased anxiety and distress, it is maintained by
positive beliefs regarding its functionality. For instance, individuals with GAD have
indicated that worry helps them to determine ways to avoid negative events, prepare
for the occurrence of negative outcomes, problem solve, and retain motivation
(Borkovec & Roemer, 1995). Likewise, worry is inherently reinforcing since the
feared negative outcomes rarely, if ever, occur (Borkovec, Hazlett-Stevens, & Diaz,
1999). Over time, worry, the nonoccurrence of the feared event, and subsequent
reduction in anxiety become inextricably linked, in the absence of intervention.
Therefore, treatment for GAD has involved identification of those factors maintaining
worry, especially since positive perceived benefits of worrisome thinking can interfere
with individuals’ willingness to commit to treatment and engage in interventions
designed to reduce their worry.
GAD is a prevalent and highly comorbid and chronic psychiatric disorder that is
associated with fluctuations in symptom severity and impairment (Wittchen, Lieb,
Pfister, & Schuster, 2000; Yonkers, Warshaw, Massion, & Keller, 1996) that are
not necessarily indicative of recovery (Newman et al., in press). Epidemiological
studies revealed lifetime prevalence of DSM-III-R GAD from 3.6 to 5.1% (Wittchen,
Zhao, Kessler, & Eaton, 1994) and 5.7% for DSM-IV GAD (Kessler et al., 2005).
GAD comorbidity rates are high in both clinical and community samples; major
depressive disorder, followed by panic disorder, social phobia, and dysthymia, are
the four most common comorbid Axis I anxiety and mood disorders, respectively
(Brown & Barlow, 1992; Massion, Warshaw, & Keller, 1993). Additionally, avoidant
and dependent personality disorders have been found to be the two most common
comorbid Axis II diagnoses for GAD (Sanderson & Wetzler, 1991; Sanderson,
Wetzler, Beck, & Betz, 1994). The gravity of this disorder is not only captured by its
extensive comorbidity, but by its course as well. GAD is a chronic illness characterized
by a later onset than other anxiety disorders (Berger et al., 2011; Kessler et al., 2005),
low probability of recovery, and high likelihood of recurrence (Newman et al., in
press). Naturalistic prospective studies of psychiatric and primary care patients found
a 32–58% probability of recovery in GAD over a 2- to 12-year period, and a 45–52%
recurrence in individuals who did not recover (Rodriguez et al., 2006; Yonkers, Dyck,
Warshaw, & Keller, 2000).
Cognitive Behavioral Therapy for

The uncontrollability and pervasiveness of worry central to GAD, its degree of comor-
bidity and chronic course, and its associated psychosocial impairment underscore the
need for highly effective GAD treatments. GAD symptoms have been conceptu-
alized as an interaction between the cognitive, affective, imaginal, behavioral, and
somatic responses to perceived future threat (Holmes & Newman, 2006; Newman
& Borkovec, 2002). Thus, CBT packages attempt to target each of those response
systems. Traditional cognitive behavioral interventions include self-monitoring, relax-

ation techniques, stimulus control, self-control desensitization, and cognitive therapy,
and reflect five principles of change: (a) challenging misconceptions, (b) actively test-
ing the validity of erroneous beliefs, (c) using repeated exposure methods, (d) reducing
avoidance behaviors, and (e) improving skills (Newman, Stiles, Janeck, & Woody,
2006). The efficacy of these methods has been documented in a series of randomized
controlled trials (RCTs); however, GAD symptoms do not appear to remit at the same
rate as those of other anxiety disorders (Yonkers, Bruce, Dyck, & Keller, 2003), so
research centered on enhancing understanding of the etiology, maintenance, and treat-
ment of GAD has continued. Therapeutic advancement for GAD has been made in the
areas of interpersonal and emotional processing therapy, emotional contrast exposure
therapy, metacognitive therapy, treatment of intolerance of uncertainty, integration of
acceptance and mindfulness techniques with CBT, and emotion regulation therapy.
A Cognitive Behavioral Approach to Psychopathology and Treatment

Cognitive behavioral theory posits that forms of psychopathology are due to mal-
adaptive patterns of thoughts and behaviors (e.g., Beck, 2005). Symptoms arise from
modeling negative coping behaviors, classical and operant conditioning processes,
and core beliefs that influence maladaptive responses to stressful events. Individuals
with emotional disorders have biased schemata, perceiving situations in terms of
loss, danger, or other types of threat to the self. Specifically, individuals with GAD
interpret ambiguous or neutral information in a negative light. They are convinced
that by anticipating the worst-case scenario, they will be prepared in the event of
a negative outcome. Their worry becomes such a consuming, cyclical process that
they are unable to incorporate all information available in their environment to func-
tion effectively. Instead, they are biased toward negative information and/or distort
situations to fit their beliefs, which interferes with adaptively coping with stressful
situations (Borkovec, 2002).
In anxiety-provoking and perceived threatening situations, the instinctive maneuver
is to attempt to prepare for a threatening outcome via worry, which may serve a self-
sustaining function, until it becomes habitual. Individuals’ life functioning becomes
more restricted; they do fewer things and see fewer people, all in the interest
of circumventing potential threat (Wittchen, 2002). Therefore, CBT targets this
process, and encourages individuals to confront and challenge their fears. The goal
of therapy is not to eliminate worry and anxiety altogether, but to reduce them in
manageable increments while enhancing individuals’ ability to cope and function in
spite of some anxiety. A cognitive behavioral treatment framework focuses on the
acquisition of skills to manage worry and anxiety. Clients learn to slow down their
breathing, reduce chronic bodily tension, and challenge and change their negative
thinking patterns. As with most CBT, these skills are developed through the use of
in- and between-session practices. Ultimately, CBT emphasizes identification of early
anxiety triggers, the disruption of factors maintaining worry, and the development of
more adaptive ways of thinking and behaving in the face of ambiguous situations.
Psychoeducation. Initial therapy sessions center on teaching clients about the nature
of their worry and anxiety, as well as factors that can contribute to the maintenance of
GAD. An overview of treatment components and rationale is also typically provided.
Self-monitoring/early cue detection. As indicated, an objective of CBT is to interrupt

factors maintaining worry and anxiety. Before therapist and client can intervene,
it is important to know what those factors are and when and where they occur.
Such identification is facilitated by ongoing daily self-monitoring, which helps to
increase patients’ awareness of maladaptive and habitual cognitive, behavioral, and
physiological patterns of responding. The more adept clients become at identifying
early automatic processes or triggers for their symptoms, the more efficient they
can become in engaging adaptive and strategic behaviors to overcome maladaptive
response biases. The primary functions of self-monitoring are to increase clients’
awareness of their early worry and anxiety triggers and how they behave in response
to those triggers and enhance recognition of shifts in their internal state (Borkovec,
2006). By learning to detect worry cues as soon as they occur, clients will be able
to intervene by deploying coping strategies early on in the worry/anxiety spiral. This
process is considered crucial to successful treatment.
Furthermore, self-monitoring also enables individuals with GAD to focus on the
present moment. Since they are preoccupied with the anticipation of negative events
or the future implications of past stressors, their anxiety is predominantly generated
by their biased thoughts and images (Borkovec, 2006). Thus, individuals with GAD
tend to be distracted from what is happening in the moment and instead tend to live
their lives in the future. Monitoring internal and external anxiety triggers encourages
clients to become more grounded in the present moment and to make use of all
information available to them in their environment. Through monitoring, clients learn
to draw in-the-moment connections between their anxious responses and negatively
biased interpretations, thereby creating opportunities for intervention and application
of more flexible, present-focused thinking.
Self-monitoring is practiced both in and out of session through the use of several
tracking techniques. Clients typically engage in this process by first keeping a daily
record of their anxiety levels and associated thoughts, feelings, and behaviors at
regular intervals throughout the day (e.g., morning, afternoon, evening, before going
to bed). Clients may also monitor their anxiety on an hourly basis or with every
change in activity (Newman & Borkovec, 2002). This repeated monitoring may help
them better understand the mechanisms that are operating to trigger their worry.
Additionally, they learn to identify different manifestations of their anxiety, such as
their thoughts, behaviors, and affect, that interact to exacerbate their distress and
impair functioning. As distorted and biased cognitions are likely to contribute to
anticipatory anxiety, ongoing self-monitoring facilitates more accurate assessment
and interpretation of worry and anxiety. Daily records also allow for observing and
tracking changes in anxious thoughts, feelings, and bodily sensations, as well as other
negative emotions, such as depression, anger, and shame (Newman & Borkovec,
2002) over time. These diaries may be used to monitor intraindividual variation in
symptoms (Fisher, Newman, & Molenaar, 2011) and functioning and therapeutic
progress, and evaluate clients’ degree of success in applying more effective coping
strategies. Therapist and client may also use them to generate dialogue about the
causal relationships between internal and external cue, symptom, and distress.
Additionally, the therapist may have clients imagine themselves in (or describe past
instances of) stressful, worrisome, or anxiety-provoking situations with the aim of
focusing on their thought processes, behaviors, and emotions. Having clients silently
engage in a period of worry and describe their sequence of cognitive, affective, and
somatic reactions, as their anxiety and worry processes develop, may also facilitate
observation of worry and anxiety. During this exercise, the therapist also monitors
shifts in clients’ verbal and nonverbal behaviors that signal anxiety, and halts clients’
worry episodes to inquire whether they noticed their reaction and can identify the
internal cues that may have triggered the nonverbal behavior (Borkovec, 2006;
Newman & Borkovec, 2002). Between session, clients may also be instructed to
track their worry episodes, including information on initial cues, worry content
including feared outcome, amount of time spent worrying, highest anxiety level,
actual outcome, and how well they coped with the outcome (Newman & Borkovec,
2002). The ultimate goal of self-monitoring is to learn to identify early triggers for
and signs of worry, before such worry becomes too intense to intervene. The sooner
the client intervenes in response to a worry trigger, the more effective the intervention
is theorized to be. If clients wait until their worry has become more intense or until
later in the worry cycle, it is virtually impossible to cut it off successfully. Thus, clients
are asked to objectively observe earlier and earlier shifts in anxiety and associated
internal and external responses, and immediately apply effective coping strategies to
remediate patterns of habitual and maladaptive functioning.
Relaxation training. Individuals with GAD exhibit a distinctive psychophysiological

profile relative to other anxiety disorders. GAD has been associated with chronic
vigilance to threat and scanning, and, in some individuals, excessive muscle tension
(Hoehn-Saric & McLeod, 1988; Lyonfields, Borkovec, & Thayer, 1995). Individuals
with GAD do not demonstrate typical cardiac reactivity in response to threat observed
in those diagnosed with other anxiety disorders. Rather, they show a reduction in the
range of heart rate variability, or vagal tone, indicative of autonomic rigidity (e.g.,
lack of autonomic reactivity) (Hoehn-Saric & McLeod, 1988; Thayer, Friedman, &
Borkovec, 1996). Experimental studies have demonstrated that inducing worry states
reduces vagal tone (Llera & Newman, 2010; Thayer & Borkovec, 1995), suggesting
that pervasive worry is related to the vagal deficit and autonomic rigidity found in GAD
(Holmes & Newman, 2006). Such a vagal deficit is indicative of high chronic heart
rate and sustained chronic levels of negative emotionality (Newman & Llera, 2011).
Accordingly, various relaxation techniques have been incorporated in the treatment
of GAD to increase autonomic flexibility. Relaxation methods include diaphragmatic
breathing, progressive muscle relaxation, pleasant imagery, meditation, and applied
relaxation. These strategies assist clients in slowing down their breathing, differentiat-
ing between feelings of tension and relaxation, and enhancing flexibility of responding.
Slowed, paced diaphragmatic breathing is a relaxation technique that induces a
rapid relaxation response (Newman & Borkovec, 2002). Clients are first taught
that anxiety is associated with rapid breathing originating in the chest rather than
the diaphragm. Whereas chest breathing activates the sympathetic nervous system,
which is implicated in the fight-or-flight response to perceived threat, diaphragmatic

breathing stimulates the parasympathetic nervous system, which is responsible for
“rest and digest” activities. Clients learn to distinguish between these two types of
breathing by first simulating rapid chest breathing until they induce anxiety, and
then engaging in slow-paced, diaphragmatic breathing to reduce their anxiety. The
therapist should encourage clients to practice this slowed breathing exercise during
and between sessions, and apply it in response to anxiety cues. In sum, clients learn
about how their breathing affects how they feel and monitor and alter their breathing
habits with the goal of gaining more control over their physiological and emotional
responding (Newman & Borkovec, 2002).
Progressive muscle relaxation (PMR; Bernstein, Borkovec, & Hazlett-Stevens,
2000) is another useful relaxation method that can benefit individuals with GAD.
PMR involves the systematic tensing and releasing of different groups of muscles of the
body, as well as focusing on subsequent relaxing bodily sensations. In our approach,
relaxation practice occurs as a component of virtually every therapy session. Clients
begin by tensing and releasing 16 separate muscle groups, including the right hand and
forearm, right biceps, left hand and forearm, left biceps, forehead (upper face), eyes
and nose (central face), mouth, jaws, and cheeks (lower face), neck, chest, shoulders
and upper back, abdomen, right thigh, right calf, right foot, left thigh, left calf, and left
foot. As sessions progress, muscle groups are combined to enhance the efficiency of
the method (e.g., producing a more relaxed state in less time) (Borkovec, 2006). Over
time, clients are effectively able to engage in “relaxation by recall,” or relax their mus-
cles in the absence of tensing them. This is achieved through remembering the feeling
produced by repeated tension and release of their muscles (Borkovec, 2006; Newman
& Borkovec, 2002). During this procedure, clients learn to pair PMR with the “letting
go” of their anxiety and troublesome emotions. They are taught to release their wor-
risome thoughts and images, and instead focus on their breathing and sensations of
relaxation. Eventually, clients are taught “recall and counting,” a technique where they
sequentially focus on various muscle groups and relax away tension while counting to
10. Ultimately, clients learn to relax by counting alone. They engage in these relax-
ation exercises while simultaneously attempting regular applied relaxation wherein
they regularly scan their bodies and in the moment attempt to release any tension.
Diaphragmatic breathing and PMR may be supplemented through the use of
pleasant imagery or meditation techniques. Imagery relaxation involves vividly creating
a scene that is associated with feelings of relaxation, peace, comfort, and tranquility.
Guided pleasant imagery, a method in which the therapist and client collaborate in
constructing a peaceful mental scenario, can be used in therapy to achieve deeper states
of relaxation. A useful associated meditational technique involves the incorporation of
a specific cue, such as repeating the word “calm” to oneself. Clients can use this device
to refocus their attention when they notice their minds wandering or infiltration of
cognitive intrusions (Borkovec, 2006; Newman & Borkovec, 2002). Likewise, clients
are taught to engage in applied relaxation (Öst, 1987). In other words, they are
encouraged to utilize their relaxation skills in response to internal and external signs
of anxiety or shifts in emotional and/or physiological responding identified during
self-monitoring in order to release their tension.
Overall, relaxation techniques are used in the context of therapy for GAD to
enhance clients’ focus on the present moment, eliminate unnecessary bodily tension,
and decrease the frequency of worry episodes. This enables them to incorporate new
information from their environment to facilitate adaptive learning and behavior. The
availability of different relaxation techniques can be especially beneficial for clients who
experience relaxation-induced anxiety (RIA; Heide & Borkovec, 1984). Although
they may experience increased discomfort or a fear of losing control in response to
the enhanced awareness of emotional responding attributed to a specific relaxation
technique, continued relaxation practice helps them overcome this feeling (Heide &
Borkovec, 1983; Newman & Borkovec, 2002). Thus, relaxation training aims to help
clients gain control over their worry and anxiety.
Imaginal rehearsal of coping skills. The treatment of GAD less frequently incorporates
the use of traditional exposure methods often used in targeting phobias since the fear
resides in the mind of the individual with GAD. Conversely, imaginal rehearsal of the
execution of coping skills allows for repeated practice of adaptive coping strategies
and enhanced self-efficacy. Specifically, self-control desensitization (Goldfried, 1971)
makes use of imagery after the induction of a deeply relaxed state through the use of
PMR. Initially, a client creates a hierarchy of worry triggers that are graded from least
to most anxiety-provoking. Then the therapist selects a trigger from the hierarchy
and works with the client to come up with a prototypical scenario wherein the
trigger might occur for him or her. Next the client undergoes progressive muscle
relaxation. Once relaxed, the therapist presents an image that comprises both internal
and external anxiety cues relevant to the client’s daily emotional experience. The
client imagines him- or herself in the scene and signals to the therapist with his or
her finger once anxiety is experienced. The client then applies relaxation techniques
and practices replacing anxiety-provoking thoughts with more adaptive, accurate
perspectives formed during the cognitive therapy portions of therapy (Borkovec,
2006). The client then indicates when there is a decrease in his or her anxiety while
still envisioning the image by lowering his or her finger. Once the client has had the
opportunity to experience successful coping in response to the worrisome scene for
a period of time (about 20 seconds), he or she is instructed to “turn off” the scene
and deepen his or her state of relaxation (about 20 seconds) (Borkovec, 2006). This
technique is repeatedly practiced until the coping strategies become more habitual.
The implementation of self-control desensitization involves both applied relaxation
and coping strategies. By imagining worrisome scenarios and picturing themselves
in a place of enhanced flexibility of responding, clients are in a position more
readily to apply these skills in daily life, thereby enhancing their self-efficacy and
adaptive decision-making ability. Therefore, it is important for clients to monitor
their worry and anxiety consistently and to strengthen their adaptive coping skills
through continued practice.
Cognitive therapy. Cognitive therapy is warranted given the hypervigilance toward

threat cues (Mathews, 1990; Mathews & MacLeod, 1994) observed in GAD. It
is based on the premise that emotional responding is influenced by individuals’
interpretation of specific stimuli (e.g., bodily sensations, external stressors).
Individuals with GAD commonly misjudge the likelihood of feared events. Thus,
cognitive therapy is used to address worry and catastrophic thinking and other
cognitive and perceptual inaccuracies through a number of steps: (a) monitoring
and detecting clients’ way of perceiving themselves and the world, (b) identifying
inaccurate and anxiety-provoking thoughts and cognitive errors, (c) challenging
these cognitions through examination of logic and evidence for the accuracy or
inaccuracy of these thoughts, (d) generating alternative, more accurate perspectives
and beliefs, (e) applying more accurate, logical, and adaptive ways of thinking in daily
life when worry and anxiety are detected, and (f) conducting experiments in daily life
to provide support for using more flexible thinking.
Cognitive restructuring is a useful and effective tool in challenging individuals’
worrisome thoughts. Clients first and foremost learn to recognize their thoughts as
hypotheses, rather than facts, and are encouraged to gather and examine confirming
and disconfirming evidence and avoid common errors, such as confusing thought with
action or thought with fact. This is especially important as individuals’ perceptions and
judgments are likely to be distorted by their emotional reactivity. To illustrate, high
anxiety can result in particular biases where individuals overestimate the likelihood of a
risk or threat (i.e., assuming that negative outcomes are more probable than actuality)
or magnify the valence of negative events (i.e., inflating the meaning of an event
or perceiving it as unmanageable), and whereas these biases can serve a protective
function in response to real threat, they can exacerbate worry and anxiety in the
absence of tangible danger. Thus, cognitive restructuring functions as a management
strategy to correct misinformation and misinterpretations of perceived threat. By
focusing on errors in logic and generating different ways to approach a situation,
clients can learn to countermand their negative automatic thoughts and beliefs.
Overall, cognitive therapy and its related techniques enable clients to reinterpret
stimuli in a more accurate, positive light based on the reality of their environment.
One important focus of cognitive restructuring in persons with GAD is their view
that worry helps them (e.g., Borkovec & Roemer, 1995). Such a perspective can be
an initial roadblock to the success of garnering their cooperation in reducing their
worry. Thus, cognitive therapy often includes behavioral experiments wherein clients
can gather evidence for and against the helpfulness or lack thereof of worry and can
ultimately feel comfortable working with therapists to reduce their worry.
Targeting intolerance of uncertainty. A cognitive model of worry centered on intol-

erance of uncertainty (IU) stipulates that individuals with GAD are characterized
by heightened sensitivity to ambiguous and uncertainty-relevant information (Dugas,
Buhr, & Ladouceur, 2004). IU affects how individuals perceive, interpret, and respond
to situations marked by uncertainty on cognitive, emotional, and behavioral levels,
and is theorized to contribute to the development and maintenance of excessive and
uncontrollable worry in two ways: (a) operation of cognitive biases (direct link with
worry) and (b) facilitation of worry via the processes of positive beliefs about worry,
negative problem orientation, and cognitive avoidance (indirect link with worry)
(Koerner & Dugas, 2006).
Individual and group cognitive behavioral treatment packages have been designed
and implemented to address the four processes implicated in the development and
maintenance of GAD. These processes are intolerance of uncertainty, positive beliefs

about worry, negative problem orientation, and cognitive avoidance (Dugas et al.,
2003; Ladouceur et al., 2000). The principal treatment components include (a)
psychoeducation about CBT and GAD/worry, (b) worry awareness training, (c)
coping with uncertainty, (d) reevaluating beliefs about the usefulness of worry, (e)
improving problem orientation and problem-solving ability, (f) processing core fears
through imaginal exposure, and (g) relapse prevention (Robichaud & Dugas, 2006).
Targeting metacognitive appraisals, beliefs, and strategies. A metacognitive model of

pathological worry and GAD distinguishes between worry (Type 1 worry) and negative
interpretations of worry (Type 2 worry or “meta-worry”) (Wells, 1994). Type 2 worry
captures the negative metacognitive appraisal of worry as dangerous or uncontrollable,
which is implicated in the development of GAD. Conversely, Type 1 worry is triggered
by the positive beliefs people have about worry (e.g., “I can avoid future failure if
I worry about all possibilities”), and is therefore typically employed as a coping
strategy. However, worry can impede more adaptive self-regulatory mechanisms,
thereby activating negative metacognitive beliefs and associated meta-worry (Wells,
2006b).
The primary objectives of metacognitive therapy (MCT) for worry and GAD are to
identify and modify metacognitive appraisals and beliefs about worry and foster a flex-
ible coping approach through use of alternative, more adaptive strategies to deal with
worry triggers (Wells, 2006a). MCT includes individualized case conceptualization;
socialization, or psychoeducation about the nature and structure of the treatment
and the role of worry-related metacognitions; modification of metacognitions related
to the uncontrollability and danger of worry; modification of positive metacognitive
beliefs; and relapse prevention (Wells, 1997, 2006a).
Cognitive bias modification. Individuals with GAD exhibit an attention bias toward
threat (Mathews & MacLeod, 1994), which has been experimentally examined
using the probe detection paradigm (see Mogg & Bradley, 2005, for a review).
Accordingly, an attention modification program (AMP) has been implemented to
decrease attention to threat and anxiety (Amir, Beard, Burns, & Bomyea, 2009). This
computer-administered program involves various combinations of probe type, probe
position, and word type (neutral or threat) and aims to shift individuals’ attention bias
toward threat, thereby reducing symptoms of anxiety. In comparison to an attention
control condition, the AMP significantly modified attention bias toward threat and
reduced self-reported anxiety symptoms (Amir et al., 2009).
Efficacy of Cognitive Behavioral Therapy for

Controlled investigations of the efficacy of CBT and related techniques in treating

GAD have been conducted within the last several decades. Whereas outcome studies
for other anxiety disorders primarily examined the effectiveness of exposure-based
cognitive behavioral interventions, the efficacy of relaxation, imaginal, and cognitive
techniques in treating GAD was evaluated (Newman & Borkovec, 2002). Early clin-
ical trials investigated the treatment of “general anxiety,” a non-DSM category, and
found that combined anxiety management treatments resulted in prolonged symptom
improvement, which sometimes surpassed the effects of individual components
(Newman & Borkovec, 2002). Cognitive therapy interventions were also found
to improve symptoms (Durham & Turvey, 1987; Newman & Borkovec, 2002).
Borkovec and Ruscio (2001) conducted a meta-analysis of 13 controlled clinical
trials examining the efficacy of CBT for GAD, and found highly consistent outcomes.
Importantly, the methodological rigor of the reviewed studies enhances the reliability
and validity of study results. For example, (a) studies selected participants based on
their meeting DSM diagnostic criteria for GAD; (b) most studies incorporated the use
of detailed treatment protocols (n = 9) and conducted adherence checks (n = 8); (c)
some studies assessed nonspecific factors (e.g., the client’s belief in the appropriateness
of the treatment, therapy expectancy) to determine equivalency of conditions (n = 8);
(d) all investigations included follow-up assessments 6 or 12 months posttreatment;
and (e) overall attrition was low in all controlled trials.
This meta-analysis revealed that CBT significantly reduced anxious and depres-
sive symptoms over the course of treatment with an average effect size of 2.48 at
posttreatment and 2.44 at follow-up for anxious symptoms, and 1.13 at posttreat-
ment and 1.22 at follow-up for depression measures, thereby capturing therapeutic
gains in anxious and depressive symptoms. Placebo or alternative psychotherapies
(e.g., nonmanualized psychodynamic psychotherapy, two trials incorporating low
doses of diazepam) resulted in the next highest effect sizes on worry, anxiety, and
depression measures followed by individual CBT components (i.e., behavior therapy
or cognitive therapy), and wait-list/no-treatment conditions. In an examination of
therapeutic efficacy, CBT yielded the greatest reduction of anxious and depressive
symptoms (greatest effect sizes) at posttreatment and follow-up compared to the
other conditions. Between-group comparisons demonstrated that CBT was superior
to wait-list/no-treatment at posttreatment with an average effect size of 1.09 and
0.92 for anxiety and depression measures, respectively. CBT also exhibited greater
efficacy than nonspecific or alternative therapies, with an average effect size for anxiety
and depression measures, respectively, of 0.71 and 0.66 at posttreatment and 0.30
and 0.21 at follow-up; and cognitive or behavioral treatment alone, with an average
effect size of 0.26 for both anxiety and depression measures at posttreatment and
0.54 and 0.45 for anxiety and depression measures, respectively, at follow-up.
Toward Therapeutic Integration

Although CBT for GAD consistently results in significant reductions in anxiety and
mood symptoms, gains that are often maintained at follow-up, GAD still remains
the least successfully treated anxiety disorder (Brown et al., 1994). Approximately
50% of individuals achieve high end-state functioning (range from 40 to 60%) at 6-
and 12-month follow-up (Borkovec & Costello, 1993; Borkovec, Newman, Pincus,
& Lytle, 2002; Borkovec & Whisman, 1996; Dugas et al., 2003; Ladouceur et al.,
2000; Wells et al., 2010), suggesting the need for enhancements to the current CBT
model. Whereas CBT protocols typically adhere to a prescribed number of treatment
sessions, Borkovec et al. (2002) addressed the potential need for additional CBT
sessions to receive maximum benefit by significantly increasing the amount of client
contact time from a previous study (Borkovec & Costello, 1993). However, the rate
of high end-state functioning did not increase, although contact time had doubled.
Another consideration regarded CBT’s lack of focus on critical factors contributing
to the maintenance and development of GAD. Accordingly, treatment for GAD has
been supplemented with additional techniques designed to address aspects of GAD
not commonly targeted in traditional CBT (e.g., interpersonal dysfunction, emotional
processing, emotional dysregulation) in an effort to improve its efficacy.
Integration of interpersonal/experiential therapy. GAD is marked by significant inter-

personal dysfunction and avoidance of emotional processing (Borkovec et al., 2002;
Newman & Erickson, 2010; Przeworski et al., 2011). In terms of interpersonal
problems, it is associated with more marital discord or dissatisfaction than other
anxiety or mood disorders, and distortions in perceptions of negative interpersonal
impact on others (Erickson & Newman, 2007; Newman et al., in press). These inter-
personal factors predict negative CBT outcomes, higher dropout rates, and reduced
probability of remission (Durham, Allan, & Hackett, 1997; Newman et al., in press).
With respect to difficulties with emotion, worry inhibits cardiovascular response to
fearful stimuli (Borkovec & Hu, 1990; Llera & Newman, 2010; Newman & Llera,
2011), thereby diminishing processing of negative emotions. Individuals with GAD
also report greater sensitivity to their negative emotions (Llera & Newman, 2010;
Mennin, Heimberg, Turk, & Fresco, 2005), increased emotional intensity (Mennin
et al., 2005), and heightened reactivity to negative emotional expression in others
(Erickson & Newman, 2007) compared to nonanxious controls. Therefore, interper-
sonal problems, such as clients’ maladaptive ways of relating to others, and deficits in
emotional experience have been targeted through incorporation of interpersonal and
experiential techniques in the context of cognitive behavioral treatment.
Based on Safran and Segal’s (1990) integration of CBT and interpersonal tech-
niques, Newman and colleagues at the Pennsylvania State University adapted this
approach for individuals with GAD and added an experiential focus with the objective
of identifying problematic relationship patterns and facilitating emotional deepening
(Newman, Castonguay, Borkovec, & Molnar, 2004). Dysfunctional relationship pat-
terns were addressed through the exploration of past and current relationships and
identification of ways in which clients create and maintain interpersonal problems,
adoption of alternative ways of relating to others, and use of the therapeutic relation-
ship to explore cognitive and affective processes and challenge interpersonal schemas
(Newman et al., 2004). Emotional awareness and deepening involved tracking markers
of emotionality (e.g., changes in voice quality or pace of conversation) that signi-
fied emotional disruption or disengagement and use of experiential techniques to
engage clients’ comfort and exposure to their emotional experience (Newman et al.,
2004). This treatment was initially tested in an open trial with very promising results
(Newman, Castonguay, Borkovec, Fisher, & Nordberg, 2008).
In the first comparison between standard CBT and an attempt to improve CBT in
a randomized controlled trial of CBT for GAD (Newman et al., 2011), participants
were assigned to either CBT plus supportive listening (SL; n = 40) or CBT plus
interpersonal/emotional processing therapy (I/EP; n = 43) using an additive design.

Both treatments resulted in significant improvement in symptoms at posttreatment.
Therapeutic gains were maintained at 2-year follow-up, such that 75% of participants
in the CBT plus I/EP condition and 63.6% of participants in the CBT plus SL
condition no longer met diagnostic criteria for GAD at follow-up, an improvement
over an average of 50% of participants achieving high end-state functioning found in
previous studies. However, CBT plus I/EP was not statistically superior to CBT plus
SL on any outcome measure. In an effort to understand these null findings, Newman
et al. (2011) provide the following hypotheses: (a) the I/EP techniques chosen may
not have been sufficient to address participants’ interpersonal or emotional difficulties;
(b) I/EP techniques may have been efficacious, but were not superior to SL; and (c)
CBT plus I/EP may only be superior for some types of clients with GAD, such as those
with interpersonal or emotional difficulties. Although between-group differences were
not found, interpersonal problems at posttreatment demonstrate negative associations
with posttreatment and follow-up symptom improvement (Borkovec et al., 2002);
therefore this area would benefit from further investigation.
Emotional contrast exposure therapy. One additional theory about the failure of the
I/EP therapy was put forth by Newman and Llera (2011). These authors theorized
that it is possible that I/EP failed to target the aspect of emotions most feared and
avoided by participants with GAD. Newman and Llera (2011) point to literature
that suggests that rather than enabling emotional avoidance, worry elicits and sustains
negative emotionality as a means to avoid an emotional contrast experience (Brosschot,
Gerin, & Thayer, 2006). Data show that worriers prefer to focus on an unlikely
catastrophic outcome as opposed to being taken off guard or surprised by such an
outcome. Therefore, Newman and Llera proposed that what worriers fear and avoid is
not emotion per se but rather an emotional contrast experience (e.g., a sharp shift in
emotions from feeling fine to suddenly feeling badly). The solution proposed by these
authors is a treatment that exposes participants to the emotional contrast experience
(e.g., relaxation immediately before emotional exposure).
Emotion regulation therapy. The emotion dysregulation model of GAD underscores

the importance of emotion during the worry process (Mennin, Heimberg, Turk,
& Fresco, 2002). Specifically, emotion dysregulation is captured in (a) heightened
intensity of emotions, (b) poor understanding of emotions, (c) negative reactivity to
one’s emotional state, and (d) maladaptive emotional management responses (Mennin
et al., 2002). Preliminary evidence in support of this model found that individuals
with GAD rated their emotional experiences as significantly more intense, experienced
more difficulty describing the motivational content of emotions, understanding their
reactions to shifts in emotional state following mood induction, and self-regulating
following a negative mood, and reported greater fear of negative and positive emotions
than control participants (Mennin et al., 2005). Likewise, deficits in emotional clarity,
acceptance of emotions, ability to engage in goal-directed behaviors when distressed,
impulse control, and access to emotion regulation strategies have been associated
with worry and analogue GAD (Salters-Pedneault, Roemer, Tull, Rucker, & Mennin,
2006).
Thus, emotion regulation therapy (ERT) was established to address the emotional
avoidance of individuals with GAD. ERT integrates experiential and psychody-
namic treatment components into a cognitive behavioral framework, and focuses on
cognitive, emotional, and contextual factors contributing to the maintenance of GAD
(Mennin, 2006). ERT aims to help individuals with GAD (a) to understand and
increase acceptance of their emotional experiences, (b) to enhance their ability to
cope effectively with their emotions, (c) to decrease use of worry and other emotional
avoidance strategies, and (d) to incorporate affective information when identifying
needs, making decisions, motivating behavior, and relating to others (Mennin, 2006).
To achieve these therapeutic objectives, treatment currently comprises four phases.
Phase I focuses on psychoeducation about GAD and use of self-monitoring to track
worry and identify functional patterns of worry and emotions. Phase II centers on
enhancing awareness of bodily reactions and developing emotion regulation skills.
Phase III involves application of skills during exposure to emotionally salient con-
tent. Finally, Phase IV focuses on relapse prevention, termination of the therapeutic
relationship, and future goals (Mennin, 2006). Mennin and colleagues are in the
process of conducting a randomized controlled trial to examine the utility of ERT in
individuals with GAD. Results of this study will have implications for the functionality
of this etiological model and innovative treatments for GAD.
Integration of mindfulness-/acceptance-based techniques. Conceptualizing worry as a

form of avoidance (Borkovec et al., 2004) is central to the application of acceptance-
based treatments to GAD (Roemer & Orsillo, 2002). One particular model of
experiential avoidance suggests that psychological and emotional difficulties manifest
in response to attempts to control or mitigate negative internal experience (Hayes,
Wilson, Gifford, Follette, & Strosahl, 1996). Hayes, Strosahl, and Wilson (1999)
indicate that maladaptive behavior patterns sustained by experiential avoidance can
be modified by adopting a position of acceptance where a person acknowledges the
present moment and endeavors to reduce reliance on emotional and cognitive control
and increase pursuit of meaningful life goals (e.g., interpersonal relationships, physical
well-being) (Roemer & Orsillo, 2002). Acceptance and commitment therapy (ACT)
is an integrative treatment based on these principles and aims (a) to reduce use
of strategies employed to avoid internal experience (e.g., thoughts, feelings, bodily
sensations), (b) to decrease individuals’ negative and literal interpretations of their
thoughts, and (c) to increase individuals’ ability to commit to behavior change in
accordance with their values (Hayes et al., 1999; Roemer & Orsillo, 2002).
Mindfulness techniques, designed to increase awareness and present-moment focus,
have been incorporated into cognitive behavioral treatment for GAD. The objective of
focusing on the here-and-now and making use of all information in one’s environment
is to trade habitual, maladaptive behavioral patterns for more conscious, adaptive,
and flexible ways of responding (Roemer & Orsillo, 2002). The goal is for GAD
clients to eliminate unsuccessful attempts to control internal experience and promote
goal-directed activity (Hayes et al., 1999). Roemer, Orsillo, and Salters-Pedneault
(2008) examined the efficacy of acceptance-based behavioral therapy for GAD.
In comparison to a delayed treatment group, acceptance-based behavioral therapy
resulted in significant reductions in clinician-rated and self-reported GAD symptoms at
posttreatment and 3- and 9-month follow-up. At posttreatment, 77% of participants

achieved high end-state functioning. Overall, the integration of mindfulness- and
acceptance-based interventions into a cognitive behavioral framework demonstrates
promise for the treatment of GAD.
Conclusions
GAD is an intractable condition characterized by pathological worry and cognitive,

behavioral, and experiential avoidance that contribute to the maintenance of this dis-
order and engender significant impairment in life functioning. The last several decades
have been host to an increase in research dedicated to enhancing understanding of
the phenomenology and treatment of GAD. Cognitive behavioral interventions have
consistently demonstrated efficacy in reducing the core and associated symptoms of
GAD, including worry and positive and negative cognitions about worry, information
processing biases, intolerance of uncertainty, and use of avoidance strategies. New
variations on the cognitive behavioral approach to treating GAD have endeavored to
improve individuals’ end-state functioning by targeting areas of deficit (e.g., inter-
personal dysfunction, emotion dysregulation) not generally addressed in traditional
cognitive behavioral protocols. Whereas these integrative treatments have successfully
abated GAD symptomatology and resulted in long-term therapeutic gains, additional
studies utilizing dismantling/additive research designs are needed to evaluate treat-
ment components separately and in combination with the goal of establishing the
relative utility and incremental validity of those therapeutic components.
References
(3rd ed., revised). Washington, DC: Author.
Amir, N., Beard, C., Burns, M., & Bomyea, J. (2009). Attention modification program in
individuals with generalized anxiety disorder. Journal of Abnormal Psychology, 118, 28–33.
doi: 10.1037/a0012589
Ansseau, M., Fischler, B., Dierick, M., Albert, A., Leyman, S., & Mignon, A. (2008).
Socioeconomic correlates of generalized anxiety disorder and major depression in primary
care: The GADIS II Study (Generalized Anxiety and Depression Impact Survey II).
Depression and Anxiety, 25, 506–513. doi: 10.1002/da.20306
Barger, S. D., & Sydeman, S. J. (2005). Does generalized anxiety disorder predict coronary
heart disease risk factors independently of major depressive disorder? Journal of Affective
Disorders, 88, 87–91. doi: 10.1016/j.jad.2005.05.012
Beck, A. T. (2005). The current state of cognitive therapy: A 40-year retrospective. Archives of
Berger, A., Edelsberg, J., Bollu, V., Alvir, J. M., Dugar, A., Joshi, A. V., & Oster, G. (2011).
Healthcare utilization and costs in patients beginning pharmacotherapy for generalized
anxiety disorder: A retrospective cohort study. BMC Psychiatry, 11, 193. doi:10.1186/
1471–244X–11–193
Bernstein, D. A., Borkovec, T. D., & Hazlett-Stevens, H. (2000). New directions in
progressive relaxation training: A guidebook for helping professionals. Westport, CT:
Praeger/Greenwood.
Borkovec, T. D. (2002). Life in the future versus life in the present. Clinical Psychology: Science
and Practice, 9, 76–80. doi: 10.1093/clipsy/9.1.76
Borkovec, T. D. (2006). Applied relaxation and cognitive therapy for pathological worry
and generalized anxiety disorder. In G. C. L. Davey & A. Wells (Eds.), Worry and
its psychological disorders: Theory, assessment and treatment (pp. 273–287). Chichester,
Borkovec, T. D., Alcaine, O., & Behar, E. S. (2004). Avoidance theory of worry and generalized
anxiety disorder. In R. Heimberg, D. Mennin, & C. Turk (Eds.), Generalized anxiety
disorder: Advances in research and practice (pp. 77–108). New York, NY: Guilford Press.
Borkovec, T. D., & Costello, E. (1993). Efficacy of applied relaxation and cognitive-behavioral
therapy in the treatment of generalized anxiety disorder. Journal of Consulting and
Borkovec, T. D., Hazlett-Stevens, H., & Diaz, M. L. (1999). The role of positive beliefs
about worry in generalized anxiety disorder and its treatment. Clinical Psychology and
Psychotherapy, 6, 126–138. doi: 10.1002/(SICI)1099-0879(199905)6:2<126::AID-
CPP193>3.0.CO;2-M
Borkovec, T. D., & Hu, S. (1990). The effect of worry on cardiovascular response to
phobic imagery. Behaviour Research and Therapy, 28, 69–73. doi: 10.1016/0005-
7967(90)90056-O
Borkovec, T. D., Newman, M. G., Pincus, A. L., & Lytle, R. (2002). A component analysis of
cognitive-behavioral therapy for generalized anxiety disorder and the role of interpersonal
problems. Journal of Consulting and Clinical Psychology, 70, 288–298.
Borkovec, T. D., Ray, W. J., & Stober, J. (1998). Worry: A cognitive phenomenon intimately
linked to affective, physiological, and interpersonal behavioral processes. Cognitive Therapy
and Research, 22, 561–576. doi: 10.1023/A:1018790003416
Borkovec, T. D., Robinson, E., Pruzinsky, T., & DePree, J. A. (1983). Preliminary exploration
of worry: Some characteristics and processes. Behaviour Research and Therapy, 21, 9–16.
Borkovec, T. D., & Roemer, L. (1995). Perceived functions of worry among generalized anxiety
disorder subjects: Distraction from more emotionally distressing topics? Journal of Behavior
Therapy and Experimental Psychiatry, 26, 25–30. doi: 10.1016/0005-7916(94)00064-S
Borkovec, T. D., & Ruscio, A. M. (2001). Psychotherapy for generalized anxiety disorder.
Journal of Clinical Psychiatry, 62(Suppl. 11), 37–45.
Borkovec, T. D., & Whisman, M. A. (1996). Psychosocial treatment for generalized anxiety
disorder. In M. R. Mavissakalian & R. F. Prien (Eds.), Long-term treatments of anxiety
disorders (pp. 171–199). Washington, DC: American Psychiatric Association.
Brosschot, J. F., Gerin, W., & Thayer, J. F. (2006). The perseverative cognition hypothesis: A
review of worry, prolonged stress-related physiological activation, and health. Journal of
Psychosomatic Research, 60, 113–124. doi: 10.1016/j.jpsychores.2005.06.074
Brown, T. A., & Barlow, D. H. (1992). Comorbidity among anxiety disorders: Implications
for treatment and DSM-IV. Journal of Consulting and Clinical Psychology, 60, 835–844.
doi: 10.1037/0022-006X.60.6.835
Brown, T. A., Barlow, D. H., & Liebowitz, M. R. (1994). The empirical basis of generalized
anxiety disorder. American Journal of Psychiatry, 151, 1272–1280.
Brown, T. A., Marten, P. A., & Barlow, D. H. (1995). Discriminant validity of the symptoms
constituting the DSM-III-R and DSM-IV associated symptom criterion of generalized
anxiety disorder. Journal of Anxiety Disorders, 9, 317–328. doi: 10.1016/0887-
6185(95)00012-D
Dugas, M., Buhr, K., & Ladouceur, R. (2004). The role of intolerance of uncertainty in etiology
and maintenance. In R. Heimberg, D. Mennin, & C. Turk (Eds.), Generalized anxiety
disorder: Advances in research and practice (pp. 143–163). New York, NY: Guilford Press.
Dugas, M. J., Ladouceur, R., Léger, E., Freeston, M. H., Langolis, F., Provencher, M.
D., & Boisvert, J. M. (2003). Group cognitive-behavioral therapy for generalized anxiety
disorder: Treatment outcome and long-term follow-up. Journal of Consulting and Clinical
Psychology, 71, 821–825. doi: 10.1037/0022-006X.71.4.821
Durham, R. C., Allan, T., & Hackett, C. A. (1997). On predicting improvement and relapse
in generalized anxiety disorder following psychotherapy. British Journal of Clinical
Durham, R. C., & Turvey, A. A. (1987). Cognitive therapy vs. behaviour therapy in the
treatment of chronic general anxiety. Behaviour Research and Therapy, 25, 229–234. doi:
10.1016/0005-7967(87)90051-9
Erickson, T. M., & Newman, M. G. (2007). Interpersonal and emotional processes in
generalized anxiety disorder analogues during social interaction tasks. Behavior Therapy,
38, 364–377. doi: 10.1016/j.beth.2006.10.005
Fifer, S. K., Mathias, S. D., Patrick, D. L., Mazonson, P. D., Lubeck, D. P., & Buesching, D.
P. (1994). Untreated anxiety among adult primary care patients in a Health Maintenance
Organization. Archives of General Psychiatry, 51, 740–750.
Fisher, A. J., Newman, M. G., & Molenaar, P. C. (2011). A quantitative method for the
analysis of nomothetic relationships between idiographic structures: Dynamic patterns
create attractor states for sustained posttreatment change. Journal of Consulting and
Clinical Psychology, 79, 552–563. doi: 10.1037/a0024069
Fogarty, C. T., Sharma, S., Chetty, V. K., & Culpepper, L. (2008). Mental health
conditions are associated with increased health care utilization among urban family
medicine patients. Journal of the American Board of Family Medicine, 21, 398–407. doi:
10.3122/jabfm.2008.05.070082
Goldfried, M. R. (1971). Systematic desensitization as training in self-control. Journal of
Consulting and Clinical Psychology, 37 , 228–234. doi: 10.1037/h0031974
Grant, B. F., Hasin, D. S., Stinson, F. S., Dawson, D. A., Chou, S. P., June Ruan,
W., & Huang, B. (2005). Co-occurrence of 12-month mood and anxiety disorders
and personality disorders in the US: Results from the national epidemiologic sur-
vey on alcohol and related conditions. Journal of Psychiatric Research, 39, 1–9. doi:
10.1016/j.jpsychires.2004.05.004
An experiential approach to behavior change, New York, NY: Guilford Press.
Hayes, S. C., Wilson, K. G., Gifford, E. V., Follette, V. M., & Strosahl, K. (1996). Experimental
avoidance and behavioral disorders: A functional dimensional approach to diagnosis and
Heide, F. J., & Borkovec, T. D. (1983). Relaxation-induced anxiety: Paradoxical anxiety
enhancement due to relaxation training. Journal of Consulting and Clinical Psychology,
51, 171–182. doi: 10.1037/0022-006X.51.2.171
Heide, F. J., & Borkovec, T. D. (1984). Relaxation-induced anxiety: Mechanisms and
theoretical implications. Behaviour Research and Therapy, 22, 1–12. doi: 10.1016/0005-
7967(84)90027-5
Hoehn-Saric, R., & McLeod, D. R. (1988). The peripheral sympathetic nervous system: Its
role in normal and pathologic anxiety. Psychiatric Clinics of North America, 11, 375–386.
Hoffman, D. L., Dukes, E. M., & Wittchen, H.-U. (2008). Human and economic burden of
generalized anxiety disorder. Depression and Anxiety, 25, 72–90.
Holmes, M., & Newman, M. G. (2006). Generalized anxiety disorder. In F. Andrasik (Ed.),
Comprehensive handbook of personality and psychopathology. Vol. 2: Adult psychopathology
(pp. 101–120). New York, NY: John Wiley & Sons, Inc.
doi: 10.1001/archpsyc.62.6.593
Koerner, N., & Dugas, M. J. (2006). A cognitive model of generalized anxiety disorder: The
role of intolerance of uncertainty. In G. C. L. Davey & A. Wells (Eds.), Worry and its
psychological disorders (pp. 201–216). Chichester, England: John Wiley & Sons, Ltd.
Ladouceur, R., Dugas, M. J., Freeston, M. H., Leger, E., Gagnon, F., & Thibodeau, N.
(2000). Efficacy of a cognitive-behavioral treatment for generalized anxiety disorder:
Evaluation in a controlled clinical trial. Journal of Consulting and Clinical Psychology, 68,
957–964. doi: 10.1037/0022-006X.68.6.957
Llera, S. J., & Newman, M. G. (2010). Effects of worry on physiological and subjective
reactivity to emotional stimuli in generalized anxiety disorder and nonanxious control
participants. Emotion, 10, 640–650. doi: 10.1037/a0019351
Lyonfields, J. D., Borkovec, T. D., & Thayer, J. F. (1995). Vagal tone in generalized anxiety
disorder and the effects of aversive imagery and worrisome thinking. Behavior Therapy,
26, 457–466. doi: 10.1016/S0005-7894(05)80094-2
Marten, P. A., Brown, T. A., Barlow, D. H., Borkovec, T. D., Shear, M. K., & Lydiard,
R. B. (1993). Evaluation of the ratings comprising the associated symptom criterion of
DSM-III-R generalized anxiety disorder. Journal of Nervous and Mental Disease, 181,
676–682. doi: 10.1097/00005053-199311000-00005
Massion, A. O., Warshaw, M. G., & Keller, M. B. (1993). Quality of life and psychiatric
morbidity in panic disorder and generalized anxiety disorder. American Journal of
Mathews, A. (1990). Why worry? The cognitive function of anxiety. Behaviour Research and
Therapy, 28, 455–468. doi: 10.1016/0005-7967(90)90132-3
Mathews, A., & MacLeod, C. (1994). Cognitive approaches to emotion and emotional
disorders. Annual Review of Psychology, 45, 25–50. doi: 10.1146/annurev.ps.45.020194.
000325
Mehl-Madrona, L. E. (2008). Prevalence of psychiatric diagnoses among frequent users of
rural emergency medical services. Canadian Journal of Rural Medicine, 13, 22–30.
Mennin, D. S. (2006). Emotion regulation therapy: An integrative approach to treatment-
resistant anxiety disorders. Journal of Contemporary Psychotherapy, 36, 95–105. doi:
10.1007/s10879-006-9012-2
Mennin, D. S., Heimberg, R. G., Turk, C. L., & Fresco, D. M. (2002). Applying an emotion
regulation framework to integrative approaches to generalized anxiety disorder. Clinical
Psychology: Science and Practice, 9, 85–90.
Mennin, D. S., Heimberg, R. G., Turk, C. L., & Fresco, D. M. (2005). Preliminary evidence
for an emotion dysregulation model of generalized anxiety disorder. Behaviour Research
and Therapy, 43, 1281–1310.
Mogg, K., & Bradley, B. P. (2005). Attentional bias in generalized anxiety disorder versus
depressive disorder. Cognitive Therapy and Research, 29, 29–45. doi: 10.1007/s10608-
005-1646-y
Newman, M. G. (2000). Recommendations for a cost-offset model of psychotherapy allocation

using generalized anxiety disorder as an example. Journal of Consulting and Clinical
Psychology, 68, 549–555. doi:10.1037/0022-006X .68.4.549
Newman, M. G., & Borkovec, T. D. (2002). Cognitive behavioral therapy for worry and
generalized anxiety disorder. In G. Simos (Ed.), Cognitive behaviour therapy: A guide for
the practising clinician (pp. 150–172). New York, NY: Taylor & Francis.
Newman, M. G., Castonguay, L. G., Borkovec, T. D., Fisher, A. J., Boswell, J., Szkodny, L.,
& Nordberg, S. S. (2011). A randomized controlled trial of cognitive-behavioral therapy
for generalized anxiety disorder with integrated techniques from emotion-focused and
interpersonal therapies. Journal of Consulting and Clinical Psychology, 79, 171–181. doi:
10.1037/a0022489
Newman, M. G., Castonguay, L. G., Borkovec, T. D., Fisher, A. J., & Nordberg, S. S. (2008).
An open trial of integrative therapy for generalized anxiety disorder. Psychotherapy: Theory,
Research, Practice, Training, 45, 135–147. doi: 10.1037/0033-3204.45.2.135
Newman, M. G., Castonguay, L. G., Borkovec, T. D., & Molnar, C. (2004). Integrative
psychotherapy. In R. G. Heimberg, C. L. Turk, & D. S. Mennin (Eds.), Generalized
anxiety disorder (pp. 320–350). New York, NY: Guilford Press.
Newman, M. G., Crits-Christoph, P., & Szkodny, L. E. (in press). Generalized anxiety disorder.
In L. G. Castonguay & T. G. Oltmanns (Eds.), Psychopathology: Bridging the gap between
basic empirical findings and clinical practice. New York, NY: Guilford Press.
Newman, M. G., & Erickson, T. M. (2010). Generalized anxiety disorder. In J. G. Beck
(Ed.), Interpersonal processes in the anxiety disorders: Implications for understanding
psychopathology and treatment (pp. 235–259). Washington, DC: American Psychological
Association.
Newman, M. G., & Llera, S. J. (2011). A novel theory of experiential avoidance in generalized
anxiety disorder: A review and synthesis of research supporting a contrast avoidance model
of worry. Clinical Psychology Review, 31(3), 371–382. doi: 10.1016/j.cpr.2011.01.008
Newman, M. G., Stiles, W. B., Janeck, A., & Woody, S. R. (2006). Integration of therapeutic
factors in anxiety disorders. In L. G. Castonguay & L. E. Beutler (Eds.), Principles of
therapeutic change that work (pp. 187–202). New York, NY: Oxford University Press.
Olfson, M., & Gameroff, M. J. (2007). Generalized anxiety disorder, somatic pain and health
care costs. General Hospital Psychiatry, 29, 310–316. doi: 10.1016/j.genhosppsych.
2007.04.004
controlled studies. Behaviour Research and Therapy, 25, 397–409. doi: 10.1016/0005-
7967(87)90017-9
Przeworski, A., Newman, M. G., Pincus, A. L., Kasoff, M. B., Yamasaki, A. S., Castonguay,
L. G., & Berlin, K. S. (2011). Interpersonal pathoplasticity in individuals with gener-
alized anxiety disorder. Journal of Abnormal Psychology, 120, 286–298. doi: 10.1037/
a0023334
Robichaud, M., & Dugas, M. J. (2006). A cognitive-behavioral treatment targeting intolerance
of uncertainty. In G. C. L. Davey & A. Wells (Eds.), Worry and its psychological disorders
(pp. 289–304). Chichester, England: John Wiley & Sons, Ltd.
Rodriguez, B. F., Weisberg, R. B., Pagano, M. E., Bruce, S. E., Spencer, M. A., Culpepper,
L., & Keller, M. B. (2006). Characteristics and predictors of full and partial recovery
from generalized anxiety disorder in primary care patients. Journal of Nervous and Mental
Disease, 194, 91–97. doi: 10.1097/01.nmd.0000198140.02154.32
Roemer, L., & Orsillo, S. M. (2002). Expanding our conceptualization of and treatment for
generalized anxiety disorder: Integrating mindfulness/acceptance-based approaches with
existing cognitive-behavioral models. Clinical Psychology: Science and Practice, 9, 54–68.

doi: 10.1093/clipsy/9.1.54
Roemer, L., Orsillo, S. M., & Salters-Pedneault, K. (2008). Efficacy of an acceptance-
based behavior therapy for generalized anxiety disorder: Evaluation in a randomized
controlled trial. Journal of Consulting and Clinical Psychology, 76, 1083–1089. doi:
10.1037/a0012720
Safran, J. D., & Segal, Z. V. (1990). Interpersonal process in cognitive therapy. New York, NY:
Basic Books.
Salters-Pedneault, K., Roemer, L., Tull, M. T., Rucker, L., & Mennin, D. S. (2006). Evidence
of broad deficits in emotion regulation associated with chronic worry and generalized
anxiety disorder. Cognitive Therapy and Research, 30, 469–480.
Sanderson, W. C., & Wetzler, S. (1991). Chronic anxiety and generalized anxiety disorder:
Issues in comorbidity. In R. M. Rapee & D. H. Barlow (Eds.), Chronic anxiety: Generalized
anxiety disorder and mixed anxiety-depression (pp. 119–135). New York, NY: Guilford
Press.
Sanderson, W. C., Wetzler, S., Beck, A. T., & Betz, F. (1994). Prevalence of personality
disorders among patients with anxiety disorders. Psychiatry Research, 51, 167–174. doi:
10.1016/0165-1781(94)90036-1
Stein, D. J. (2001). Comorbidity in generalized anxiety disorder: Impact and implications.
Journal of Clinical Psychiatry, 62(Suppl. 11), 29–36.
Thayer, J., & Borkovec, T. D. (1995, July). Cardiovascular evidence for higher-order classical
aversive conditioning in generalized anxiety disorder. Paper presented at the World
Congress of Behavioural and Cognitive Therapy, Copenhagen, The Netherlands.
Thayer, J. F., Friedman, B. H., & Borkovec, T. D. (1996). Autonomic characteristics
of generalized anxiety disorder and worry. Biological Psychiatry, 39, 255–266. doi:
10.1016/0006-3223(95)00136-0
Todaro, J. F., Shen, B. J., Raffa, S. D., Tilkemeier, P. L., & Niaura, R. (2007).
Prevalence of anxiety disorders in men and women with established coronary heart
disease. Journal of Cardiopulmonary Rehabilitation and Prevention, 27 , 86–91. doi:
10.1097/01.HCR.0000265036.24157.e7
Wells, A. (1994). Attention and the control of worry. In G. C. L. Davey (Ed.), Worrying:
Perspectives on theory, assessment and treatment (pp. 91–114). Chichester, England: John
Wiley & Sons, Ltd.
guide. Hoboken, NJ: John Wiley & Sons, Inc.
Wells, A. (2006a). Metacognitive therapy for worry and generalised anxiety disorder. In
G. C. L. Davey & A. Wells (Eds.), Worry and its psychological disorders (pp. 259–272).
Wells, A. (2006b). The metacognitive model of generalised anxiety disorder. In G. C. L.
Davey & A. Wells (Eds.), Worry and its psychological disorders (pp. 179–200). Chichester,
Wells, A., Welford, M., King, P., Papageorgiou, C., Wisely, J., & Mendel, E. (2010). A pilot
randomized trial of metacognitive therapy vs. applied relaxation in the treatment of adults
with generalized anxiety disorder. Behaviour Research and Therapy, 48, 429–434.
Wittchen, H. U. (2002). Generalized anxiety disorder: Prevalence, burden, and cost to society.
Depression and Anxiety, 16, 162–171. doi: 10.1002/da.10065
Wittchen, H. U., Lieb, R., Pfister, H., & Schuster, P. (2000). The waxing and waning
of mental disorders: Evaluating the stability of syndromes of mental disorders in the
population. Comprehensive Psychiatry, 41(2 Suppl. 1), 122–132. doi:10.1016/S0010-
440X(00)80018-8
Wittchen, H. U., Zhao, S., Kessler, R. C., & Eaton, W. W. (1994). DSM-III-R generalized
anxiety disorder in the National Comorbidity Survey. Archives of General Psychiatry, 51,
355–364.
Yonkers, K. A., Bruce, S. E., Dyck, I. R., & Keller, M. B. (2003). Chronicity, relapse, and
illness-course of panic disorder, social phobia, and generalized anxiety disorder: Findings
in men and women from 8 years of follow-up. Depression and Anxiety, 17 , 173–179. doi:
10.1002/da.10106
Yonkers, K. A., Dyck, I. R., Warshaw, M., & Keller, M. B. (2000). Factors predicting the
clinical course of generalised anxiety disorder. British Journal of Psychiatry, 176, 544–549.
doi: 10.1192/bjp.176.6.544
Yonkers, K. A., Warshaw, M. G., Massion, A. O., & Keller, M. B. (1996). Phenomenology
and course of generalised anxiety disorder. British Journal of Psychiatry, 168, 308–313.
doi: 10.1192/bjp.168.3.308
43
Stefan K. Schmertz
Red Sox Foundation and Massachusetts General Hospital, Harvard Medical School,
United States
Maryrose Gerardi and Barbara O. Rothbaum

Emory University School of Medicine, United States
According to an epidemiological survey (Kessler, Sonnega, Bromet, Hughes, &

Nelson, 1995), between 50 and 60% of the U.S. population will be exposed to a
traumatic event in their lifetime. This may be in the form of childhood emotional,
physical, or sexual abuse or neglect, motor vehicle accidents, natural disasters, military
combat, the sudden loss of a loved one, physical assault or rape, or acts of terror-
ism. Thus, in the field of mental health, trauma is an unavoidable specter. These
prevalence numbers highlight the importance of assessing for trauma exposure with
patients (Engel & Ursano, 2008). Of course, not all traumatic experiences lead to
a diagnosis of posttraumatic stress disorder (PTSD). Trauma may be the catalyst
for bouts of major depression, generalized anxiety, and even the development of
psychotic processes; disorders that are addressed in other chapters of this volume.
Therefore, a strong understanding of the diagnosis and treatment of PTSD becomes
very valuable in differential diagnoses and treatment choices in clients exposed to trau-
matic experiences. Exposure therapy, a form of cognitive behavioral therapy (CBT),
remains the front-line treatment for PTSD (Institute of Medicine [IOM], 2008),
and evidence for the efficacy of other cognitive behavioral interventions continues
to grow (Cukor, Spitalnick, Difede, Rizzo, & Rothbaum, 2009; Hembree & Foa,
2010). The goals of this chapter are to provide the reader with a strong under-
standing of the current cognitive behavioral conceptualization of this disorder and
how this has informed the empirically supported treatments for PTSD, which will be
outlined in some detail. In addition, we will briefly discuss some emerging/adjunct
treatments for PTSD and attempt to address some of the complexities of treating this
disorder.

DOI: 10.1002/9781118528563.wbcbt43
Diagnostic Criteria
According to the Diagnostic and Statistical Manual of Mental Disorders (4th ed.,
text rev.; DSM-IV-TR; American Psychiatric Association [APA], 2000), PTSD is
an anxiety disorder that may develop following exposure to, or the witnessing
of, a traumatic event that involves actual or perceived threat to life or physi-
cal integrity. In addition, one’s emotional reaction to this event is characterized
by intense fear, horror, or helplessness. The symptoms of PTSD are parsed into
three categories; those of (a) reexperiencing, (b) avoidance and numbing, and (c)
hyperarousal. The hallmark symptom of PTSD is “reexperiencing” the traumatic
event in at least one of several ways. These include intrusive and disturbing rec-
ollections of the event, nightmares related to the incident, or experiencing intense
psychological distress or strong physiological reactions when exposed to internal or
external reminders of the event. Some may also report a sense that the event is
happening again that may be accompanied by illusions, hallucinations, or dissoci-
ated flashback episodes. In PTSD, reexperiencing the threat of a traumatic incident
often leads to symptoms of hyperarousal such as difficulty sleeping, difficulty con-
centrating, hypervigilance, increased irritability, and being easily startled. One may
then engage in avoidance of any sort of reminders of the traumatic experience,
as well as efforts to suppress thoughts related to the traumatic event. Avoidance
of, or detaching from, distressing internal experience can lead to symptoms of
emotional numbing such as a restricted range of affect (e.g., unable to have lov-
ing feelings), feeling disconnected from others, and a loss of interest in previously
enjoyed activities. The symptoms of PTSD must be persistently experienced for at
least one month, causing significant distress or impairment of functioning (APA,
2000).
At the time of the writing of this chapter the APA is planning the fifth revi-
sion of the DSM. Although a detailed analysis and commentary is beyond the
scope of this chapter, there are some notable proposed changes to the criteria for
PTSD. In the DSM-5 PTSD may no longer be categorized as an anxiety disorder,
but as a “trauma and stressor related disorder.” The requirement for an emo-
tional response of “fear, horror, or helplessness” during the event will be dropped.
New diagnostic criteria specify the requirement for both avoidance and emotional
numbing symptoms. The emotional numbing symptoms have been expanded and
this cluster is to be called “negative alterations in cognitions and mood.” Added
criteria to this cluster include negative cognitions regarding distorted blame of
self and others, as well as pervasive aversive emotional states such as shame and
guilt (Friedman et al., 2011; www.dsm5.org). These changes are based on con-
firmatory factor analytic studies outlining structurally distinct groups of symptoms
arising from independent mechanisms (e.g., Palmieri, Weathers, Difede, & King,
2007). Whereas these changes may have an impact on diagnostic rates (Forbes
et al., 2011), there is no evidence that current conceptualization of treatment
should be altered. In fact, as will be discussed later in this chapter, some of these
additions seem to be borne of issues that are commonly addressed in CBT for
PTSD.
Posttraumatic Stress Disorder 1025
Prevalence and Comorbidity
Lifetime rates of PTSD in the U.S. population range from around 8 to 14% (Breslau,
1998), and women are twice as likely to develop PTSD as are men (Kessler et al., 1995;
Tolin & Foa, 2006). PTSD is associated with high rates of comorbidity, particularly
mood disorders (61% also meet criteria for a mood disorder), other anxiety disorders
(59%), and substance abuse disorders (46%; Pietrzak, Goldstein, Southwick, & Grant,
2011). The difficulty in treating those with comorbid substance abuse has sparked
the creation of treatments designed to address dual diagnosis patients with PTSD
(see Brady, 2001; McGovern et al., 2009; Najavits, 2002; Najavits, Gallop, & Weiss,
2006). Posttraumatic stress is also associated with increased health problems and a
significant decrease in quality of life (Schnurr & Green, 2004), highlighting the cost
to those who struggle with this disorder.
Cognitive Behavioral Conceptualization of Posttraumatic

Stress Disorder
With the introduction of PTSD to the DSM-III as an anxiety disorder in 1980,

treatment options emerged based on theories of learning, cognition, and fear pro-
cessing. From this research, two main theories have arisen to form the foundation for
the current cognitive behavioral treatment models for PTSD: emotional processing
theory (Foa & Kozak, 1986) and social cognitive theory (Bandura, 1986; Brewin,
2001; Ehlers & Clark, 2000; Resick & Schnicke, 1992).
Emotional Processing Theory

The roots of emotional processing theory lie in work by Lang (1977), who proposed
a bioinformational conceptualization of fear networks that are stored in memory and
act as “programs” for responding to threat. Lang’s theory proposed that the cognitive
structure of the fear memory consists of three parts: (a) a representation of the feared
object (e.g., “bear”), (b) physiological fear responses (e.g., accelerated heart rate),
and (c) the meaning associated with this stimulus (e.g., “bears are dangerous”) (Foa,
Hembree, & Rothbaum, 2007). In normal functioning, this information leads to fear
responses appropriate for the context, such as escape behavior. Elaborating on this
work, Foa and Kozak’s (1985, 1986) emotional processing theory posited that fear
structures become pathological when physiological and escape/avoidance responses
are evoked by harmless stimuli, when harmless stimuli are associated with threat
meaning, and when excessive and easily triggered response elements interfere with
adaptive functioning. In pathological processes such as PTSD, any stimuli present
during the trauma may be included in the trauma memory, such as time of day, or
particular smells that were present, allowing for a broad range of elements erroneously
associated with danger. Further, emotional processing theory outlines how the
pathological fear structure can be altered through (a) activation of the fear structure,
and (b) the introduction of new information that is incompatible with the previously
encoded erroneous information (Foa et al., 2007). Emotional processing theory thus
provides a framework for the mechanisms behind exposure therapy. Through repeated
confrontation of the feared stimuli (e.g., situations, objects, memories) in which a
feared outcome is not realized, new meanings and associations are generated, allowing
for more realistic interpretations of threat. As anxiety decreases in the presence of
the target stimuli through habituation, alternative physiological responses also are
incorporated into the fear structure via classical conditioning (Foa et al., 2007).
Thus, information that once elicited anxiety no longer does so because of successful
alteration of the fear memory.
Social Cognitive Theory

Also important in the current cognitive behavioral conceptualization of PTSD is
social cognitive theory. Broadly, this theory outlined by Bandura (1986) describes the
reciprocal influences of one’s internal world (thoughts, beliefs, and emotions), one’s
behavior, and the environment. The cognitive model of PTSD proposed by Ehlers
and Clark (2000) addresses the processing of trauma, including negative appraisals of
the event or sequelae that lead to a perception of serious, current threat, along with
inadequate elaboration and integration of the trauma memory into autobiographical
memory. The application of social cognitive theory and the cognitive model to PTSD
has focused on the development of distorted or dysfunctional beliefs as one attempts
to reconcile information about the traumatic event with prior schemas in an attempt
to regain a sense of control and mastery in one’s life (Resick, Monson, & Chard,
2008). This typically occurs in one of three ways: assimilation, accommodation, or
over-accommodation. Assimilation refers to altering the event to fit previous beliefs
(e.g., “Because I was assaulted, I must have done something bad to deserve it”).
Accommodation occurs when one alters previous beliefs enough to incorporate new
information (e.g., “although things do happen that are out of one’s control, I have
control over much of my life and keeping myself safe”). Over-accommodation involves
altering one’s previous beliefs to an extreme in order to feel safer or more in control
(e.g., “I should never fully trust anyone again”). In the wake of traumatic experiences
one may develop exaggerated and distorted views about the self, others, and the
world, such as, “I am incapable of protecting myself,” or “The world is entirely
dangerous.” Such beliefs can induce emotions of fear and shame, perpetuating
a perceived lack of self-efficacy, which research has shown to be a mediator of
posttraumatic recovery (Benight & Bandura, 2003). Thus, in treatment, healthy
accommodation of one’s traumatic experience becomes the goal. Interventions based
on social cognitive theory focus on challenging distorted cognitions which maintain
symptoms of PTSD and prevent access to primary emotional responses associated
with trauma that are thought to dissipate quickly once accessed in a direct and
nondefensive manner (Resick et al., 2008). It should be noted that emotional
processing theory and social cognitive theory applied to PTSD are not incompatible.
Both involve gaining access to the cognitive/affective elements of the stored fear
memory and adjusting erroneous or dysfunctional meaning associations (Brewin,
2001).
Posttraumatic Stress Disorder: A Disorder of Impeded Recovery

Because research has demonstrated that almost all those exposed to serious traumatic
events will develop symptoms of PTSD, yet for most symptoms decline within a few
months, it has been suggested that diagnosable PTSD should be viewed more as a
disorder of impeded recovery, rather than the development of a unique pathology
(Resick et al., 2008; Rothbaum, Foa, Riggs, Murdock, & Walsh, 1992). Cognitive
behavioral approaches to PTSD cite two main culprits for this impeded recovery:
(a) avoidance of trauma reminders, and (b) distorted cognitions/beliefs that serve to
maintain negative secondary affective experiences and perpetuate avoidance behaviors.
In the context of emotional processing theory, the avoidance of trauma reminders is
maintained through the process of negative reinforcement. Whereas avoidance leads
to a reduction of anxiety in the short term, in the long term avoidance prevents
emotional processing, thus perpetuating anxiety and other symptoms of PTSD (Foa
et al., 2007). Therefore, PTSD can be viewed as a disorder of extinction.
From a cognitive standpoint, distorted beliefs developed subsequent to trauma
exposure may fuel avoidance behaviors and reduce one’s sense of self-efficacy (e.g., “If
I go out at night, my anxiety will overwhelm me and I will lose control”). Such negative
beliefs about one’s self, others, or the world not only perpetuate secondary emotions
of shame and guilt, but also inhibit processing of primary emotional experiences
associated with the traumatic event (e.g., helplessness) that facilitate emotional
processing. Thus, emotional processing and cognitive restructuring have become the
hallmarks for current CBT treatment for PTSD. Indeed, this conceptualization is
reflected in the revisions to the diagnostic criteria for the DSM-5, that is, the inclusion
of negative cognitions regarding distorted blame of self and others, and pervasive
aversive emotional states (Friedman et al., 2011; www.dsm5.org).
Cognitive Behavioral Interventions for

Elements of Effective Treatment

The psychotherapy approach with the most empirical support for its effectiveness
is CBT, utilizing treatment techniques that are directive, problem-focused, and
delivered short-term. All of the current treatment guidelines for PTSD recommend
CBT treatment (e.g., IOM, 2008). The CBT technique with the most evidence for its
efficacy (24 randomized trials and 9 nonrandomized studies) is exposure therapy, in
which patients are assisted in confronting the trauma-related memories and cues in a
therapeutic manner (Cahill, Rothbaum, Resick, & Follette, 2009). Cognitive therapy,
also recommended as a CBT treatment for PTSD, provides tools for patients to correct
the erroneous cognitions that perpetuate distressing PTSD symptoms. Eye movement
desensitization and reprocessing (EMDR; F. Shapiro, 1995) is recommended in most
guidelines. CBT results in average symptom improvements ranging from 25 to 75%,
with a much smaller percentage of patients in remission and treatment gains generally
maintained at follow-ups of 6 and 12 months posttreatment.
There are four elements most commonly associated with effective CBT treatment for
PTSD: (a) psychoeducation, (b) anxiety management skills (e.g., relaxation/breathing
training), (c) cognitive restructuring, and (d) exposure work to facilitate emotional
processing (Gerardi, Ressler, & Rothbaum, 2010). Psychoeducation typically involves
a discussion of common reactions to trauma as well as a model for the development
of PTSD symptoms which can be an important part of normalizing a patient’s
struggles. Discussion of the treatment rationale also engenders hope and may increase
compliance, which has been shown to improve treatment outcome (Foa, Cahill,
& Pontoski, 2004). Stress management skills may include instruction in slowing
down one’s breathing, progressive muscle relaxation, or grounding techniques to
disengage from negative ruminative processes or dissociation. When identified, specific
erroneous cognitions may be brought into the patient’s awareness and challenged with
more balanced statements based on healthy accommodation of his or her traumatic
experiences. For example, one may learn to evaluate a thought such as, “I can never
be safe” as extreme, and incorporate new self-statements such as, “Although the
world can be dangerous, I am generally safe in the environment and activities of my
life.” Exposure to fear and avoidance-inducing trauma-related cues can be done in
several different ways. In imaginal exposure, the memory of the trauma is repeatedly
recounted in a therapeutic environment. In vivo exposure entails confronting feared
yet safe situations in real-world settings. Interoceptive exposure involves confronting
feared bodily symptoms often associated with PTSD, such as an increased heart
rate and shortness of breath. The most commonly delivered exposure-based therapy,
prolonged exposure (PE), combines imaginal and in vivo exposure.
Prolonged Exposure
Based on Foa and Kozak’s (1986) emotional processing theory and Lang’s (1977)
concept of a fear structure outlined above, PE is thought to (a) activate the fear
structure and (b) incorporate new information which is incompatible with the patho-
logical elements of the fear structure, thus disconfirming those elements. Repeated
confrontation of the trauma memory also serves to organize and integrate the expe-
rience. PE is a manualized treatment consisting of nine to twelve 90-minute sessions,
with sessions one and two consisting of information gathering, treatment preparation,
and psychoeducation, and the remaining sessions involving repeated imaginal expo-
sure to the identified trauma along with in vivo exposure homework assignments.
Well-controlled studies in the literature examining the efficacy of PE have found that
60–95% of participants who received PE no longer met criteria for PTSD follow-
ing treatment (Foa, Rothbaum, & Furr, 2003). Schnurr et al. (2007) conducted
a large multisite randomized clinical trial of PE versus present-centered therapy in
the treatment of female veterans and active-duty personnel with chronic PTSD (68%
reported index trauma as military sexual trauma). Those in the PE condition evi-
denced greater reduction in symptoms at posttreatment and at 3-month follow-up
and were less likely to meet the diagnostic criteria for PTSD; however, there were
no significant differences between conditions at 6-month follow-up. Studies have
also found other variants of exposure therapy effective. Bryant, Moulds, Guthrie,
Dang, and Nixon (2003) investigated exposure therapy, the combination of cognitive
restructuring (CR) and exposure therapy, and supportive counseling (SC), in the treat-
ment of 58 male and female civilian survivors of trauma with chronic PTSD. Those
in the exposure therapy and the CR/exposure therapy conditions showed greater
improvement than those in the SC condition, with evidence of greater symptom
reduction in the combined condition. Nacasch et al. (2011) compared the efficacy
of exposure therapy and treatment as usual (TAU) consisting of psychodynamic
treatment and/or medication and counseling in the treatment of 30 patients with
chronic PTSD following combat or terror related trauma. PTSD symptom severity
improved significantly (along with state and trait anxiety, posttraumatic cognitions,
and depression) in the exposure therapy group from pre- to posttreatment, and
was unchanged in the TAU group. Powers, Halpern, Ferenschak, Gillihan, and Foa
(2010) performed a meta-analysis of 13 randomized controlled exposure therapy trials
(N = 658) which demonstrated that exposure therapy treatment led to significantly
better outcomes than control conditions on measures of PTSD at posttreatment and
at follow-up.
Virtual Reality Exposure

Virtual reality exposure (VRE) is another form of exposure therapy. It is a controlled,
therapist-assisted form of human–computer interaction which allows the participant
to become actively involved in a three-dimensional computer environment via a head-
mounted display consisting of video screens, earphones, and a head-tracking device.
This immersive form of exposure therapy, which includes sights, sounds, smells, and
tactile stimulation, is theorized to overcome some of the avoidance inherent in PTSD,
and to facilitate emotional engagement in the trauma memory. Rothbaum, Hodges,
Ready, Graap, and Alarcon (2001) conducted an open clinical trial using VRE to treat
a small sample of Vietnam combat veterans with PTSD in which participants viewed
the virtual environments including a Huey helicopter and a clearing surrounded
by jungle. PTSD symptoms were significantly reduced from baseline to 6-month
follow-up. In case studies using VRE (Gerardi et al., 2008; Reger & Gahm, 2008),
a reservist’s PTSD symptoms were reduced by 56%, and significant clinical and
functional improvement was demonstrated in an active duty soldier diagnosed with
PTSD. More recent clinical trials using VRE to treat Operation Iraqi Freedom veterans
with PTSD using virtual Iraq Humvee and city environments are ongoing. McLay
et al. (2010) reported a randomized controlled trial of virtual reality graded exposure
therapy (VR-GET) versus TAU in the treatment of PTSD in 20 active duty Operation
Enduring Freedom/Operation Iraqi Freedom military personnel. VR-GET combines
graded exposure with physiologic monitoring and skills training. Seven of 10 VR-GET
participants showed clinically significant (defined as 30% or greater) improvement in
PTSD symptom severity compared with 1 of 9 in TAU.
Difede and Hoffman (2002) developed a simulation of the September 11, 2001
World Trade Center attacks involving a view of the towers with progressive sequences
of a plane flying into the tower. VRE has been successfully used to treat PTSD in
firefighters, disaster relief workers, and civilians using this simulation. In a study com-
paring a 14-session VRE treatment with wait-list control, the VRE group evidenced
significantly greater reductions in clinician-rated PTSD scores (Difede et al., 2007).
Other VR environments include a simulation of a terror bus bombing in Israel (Jos-

man et al., 2006), and a driving environment to treat subsyndromal PTSD related to
motor vehicle accidents (Beck et al., 2007).
Cognitive Processing Therapy

As outlined above, cognitive therapies are based on the theory that the meanings
that we impose on events contribute to emotional states, and therefore the goal of
therapy is to modify these thought processes. Cognitive processing therapy (CPT)
is a particular form of cognitive therapy with an exposure component in which
individuals are taught to challenge faulty assumptions and self-statements and to
modify maladaptive thoughts and overgeneralized beliefs in the areas of safety, trust,
power and control, esteem, and intimacy. CPT includes an exposure component
consisting of a written narrative of the trauma that is read during sessions and at
home. CPT has been found effective in the treatment of PTSD in female sexual assault
victims (Resick et al., 2002) and in male and female veterans with chronic PTSD
(Monson et al., 2006).
In a dismantling study of CPT, the full protocol was compared with its components,
cognitive therapy and written accounts, in 150 adult women with PTSD. Each
treatment was delivered for 6 weeks, with 2 hours of therapy per week. Patients in
all three conditions improved substantially and equivalently on PTSD and related
measures (Resick et al., 2008). Although the authors caution against extrapolating
from these initial results, these data raise the possibility that patients may benefit from
the cognitive component of CPT as a “stand-alone” intervention.
Stress Inoculation Training

Stress inoculation training (SIT; Kilpatrick, Veronen, & Resick, 1982) is based on a
skill deficit model and focuses on managing anxiety that is conditioned at the time of
the trauma and generalizes to other situations. Strategies usually include education,
deep muscle relaxation training, breathing retraining, role playing, covert modeling,
guided self-dialogue, thought stopping, and sometimes graduated in vivo exposure.
SIT received support in studies of female sexual assault victims with PTSD (e.g., Foa
et al., 1999) and for anger management in male veterans with PTSD (Chemtob,
Novaco, Hamada, & Gross, 1997). A staged approach to therapy with adult female
survivors of childhood physical and sexual abuse was found to be successful compared
with a wait-list control condition (Cloitre, Koenen, Cohen, & Han, 2002). The
two-phase treatment condition involved eight weekly individual sessions including
dialectical behavior therapy based affect and interpersonal regulation skills, followed
by eight twice-weekly sessions of PE. CBT treatment programs for PTSD have also
been delivered via the Internet (Lange, van de Ven, Schrieken, & Emmelkamp,
2001) to increase access to treatment. Litz, Engel, Bryant, and Papa (2007) describe
an 8-week “DE-STRESS” Internet-based intervention for the military population,
involving therapist-guided exploration and monitoring of trauma triggers, stress
management, in vivo exposure, trauma writing exercises, and relapse prevention.
At 6-month follow-up, the treatment group evidenced significantly greater decrease

in PTSD symptoms as compared with the Internet-based supportive counseling
group.
Eye Movement Desensitization and Reprocessing

Eye movement desensitization and reprocessing (EMDR; F. Shapiro, 1995) involves
identification of distressing trauma memory images, related negative cognitions, and
alternative positive cognitions. The patient is asked to hold the image in mind
along with the negative cognition and associated bodily sensations while tracking the
therapist’s fingers across their field of vision (saccadic eye movements). However,
recent research on EMDR suggests that the effects of EMDR may be present even
without the specific use of eye movements or other forms of alternating stimulation
(Spates, Koch, Cusack, Pagoto, & Waller, 2009). The cognitive component of
EMDR involves identification and replacement of negative trauma-related thoughts
with positive ones. EMDR is suggested to facilitate incomplete information processing
related to the trauma and/or may function as another form of exposure. In a meta-
analysis of existing studies examining the effectiveness of EMDR compared with
trauma-focused CBT, the treatments were found to be equally efficacious (Seidler
& Wagner, 2006). Recent comparisons of EMDR to PE indicate that they are
roughly equivalent in effectiveness (Spates et al., 2009). For example, Rothbaum,
Astin, and Marsteller (2005) evaluated the efficacy of PE and EMDR compared
with wait-list control in adult female rape victims with PTSD. Results indicated that
both PE and EMDR led to clinically and statistically significant improvements at
posttreatment compared with the control condition, although at 6-month follow-
up, on a measure of good end-state functioning, the participants who received PE
were significantly better than those who received EMDR. A recent review of six
randomized controlled trials and three quasi-experimental studies (Albright & Thyer,
2010) concluded that the evidence supporting EMDR to treat PTSD in combat
veterans is equivocal.
Group Therapy
Studies on group treatment of PTSD have increased over the past decade, but there
have been few with adequate control conditions. The best-powered randomized study
of group interventions for PTSD (Schnurr et al., 2003) found statistically significant
improvements in both the exposure and present-centered therapy groups; however,
these improvements were small. Despite the lack of research, group psychotherapy
remains a common intervention for combat veterans (Shea, McDevitt-Murphy, Ready,
& Schnurr, 2009). One reason may be that psychoeducational or skill-based group
interventions for PTSD are assumed to be more efficient than delivering similar
treatments individually. It is suggested that, compared with individual therapy, group
interventions for PTSD may serve to decrease isolation and allow for reestablishment
of connection and trust with others (Shea et al., 2009). However, few data directly
compare the efficiency or effectiveness of group to individual psychotherapy for
PTSD.
Combination of Psychotherapy and Medication

There are several strategies for combining pharmacotherapy and psychotherapy, with
challenges and advantages to each (Rothbaum, 2008), but the extant data on this
issue are not adequate to determine whether there are additive or interactive effects
(or both) of simultaneously administered pharmacotherapy and psychotherapy for
PTSD. In the first published randomized clinical trial of combined treatment for
PTSD, Rothbaum et al. (2006) treated 88 male and female outpatients with PTSD
with open-label sertraline (up to 200 mg) who were then randomly assigned to
receive continuation with sertraline alone or augmentation with PE, delivered in 10
twice-weekly sessions of 90–120 minutes (Foa et al., 2007). Five additional weeks
of treatment with sertraline alone did not result in further improvement on measures
of PTSD severity, depression, or general anxiety. However, augmentation with PE
resulted in further reduction of PTSD severity only among partial responders to
medication. In a recently published trial with almost a mirror design to the Rothbaum
et al. (2006) study (Simon et al., 2008), participants first received eight sessions of PE
over 4 to 6 weeks and then were randomly assigned to receive paroxetine CR plus five
additional sessions of PE, or placebo plus five additional sessions of PE. The largest
reductions of PTSD symptoms occurred following PE, with no significant differences
between placebo and paroxetine in the augmentation phase.
Schneier et al. (2012) reported on the combined 10-week treatment using parox-
etine and prolonged imaginal exposure, both commenced simultaneously for all
patients, in 27 adult survivors of the World Trade Center attacks of September 11,
2001 with PTSD. The authors concluded that treatment with combined paroxe-
tine plus prolonged exposure was more efficacious than prolonged exposure plus
placebo for PTSD both on response and remission rates. After 10 weeks, all
patients discontinued PE and were offered 12 more weeks of continued double-
blind treatment with paroxetine. The benefit of combined treatment seems to have
disappeared by follow-up, with no differences between those on placebo or active
treatment.
D-cycloserine (DCS) is an N-Methyl-D-aspartate partial agonist that has been
found to facilitate the extinction of fear. DCS by itself has no beneficial effect on
PTSD. However, several ongoing investigations are evaluating the use of DCS to
enhance exposure therapy for PTSD. On the basis of animal research showing that
DCS facilitates extinction of conditioned fear, it was hypothesized that DCS would
facilitate exposure therapy, thereby reducing the number of sessions required for the
same effect compared with exposure therapy alone (Ressler et al., 2004). Clinical
trials using exposure therapy for acrophobia (Ressler et al., 2004), social phobia
(Guastella et al., 2008; Hofmann et al., 2006), and panic disorder (Otto et al.,
2010) have shown that fewer sessions of exposure therapy were needed when DCS
was administered 1 hour before each psychotherapy session. Research currently in
progress will determine whether DCS will also accelerate PTSD treatment with PE
and with VRE.
The use of DCS to facilitate CBT represents a paradigm shift in psychiatry and
psychology. This is a new approach in that pharmacotherapy is only prescribed
to facilitate the learning that takes place during CBT (specifically, exposure-based
therapy) and not because of any direct actions on the symptoms of PTSD or
other anxiety disorders. In contrast, studies that combined “traditional” psychiatric
medications (i.e., antidepressants, benzodiazepines) with CBT for anxiety disorders
have not shown any benefit from adding medication to CBT (Rothbaum, 2008).
Emerging Treatments for PTSD
Despite the success of cognitive behavioral treatments for PTSD, research continues to
address the issue of treatment nonresponders. A recent meta-analysis of 26 controlled
treatment outcome studies revealed that over 30% of those who completed treatment
still met criteria for PTSD (Bradley, Greene, Russ, Dutra, & Westen, 2005). Below,
we review some notable emerging interventions.
Mindfulness- and Acceptance-Based Treatment

Mindfulness has been defined as “the process of intentionally attending moment
by moment with openness and nonjudgmentalness” (S. L. Shapiro, Carlson, Astin,
& Freedman, 2006, p. 378). Applying this approach to one’s daily experience
has been empirically associated with lower levels of depression, negative affect,
and anxiety (Baer, Smith, & Allen, 2004; Brown & Ryan, 2003; Smalley et al.,
2009; Wupperman, Neumann, Whitman, & Axelrod, 2009), as well as increased
emotion regulation (Vujanovic, Bonn-Miller, Bernstein, McKee, & Zvolensky, 2010).
Whereas randomized controlled trials integrating mindfulness-based exercises with
PTSD treatments are lacking (Follette & Vijay, 2009), early work in this area
has been promising (Kearney, McDermott, Malte, Martinez, & Simpson, 2011).
The theoretical and empirical literature suggests that mindfulness may serve several
clinically meaningful functions in alleviating PTSD symptoms.
First, mindfulness may serve as an indirect mechanism of cognitive-affective expo-
sure, as it involves an intrinsic willingness to approach, rather than to avoid, distressing
thoughts and feelings (Vujanovic, Niles, Pietrefesa, Schmertz, & Potter, 2011; Walser
& Westrup, 2007). This may be an especially useful skill for individuals with PTSD,
as it may help facilitate approach-oriented coping with trauma-related internal or
external cues and decrease experiential avoidance. Mindfulness interventions are also
thought to provide a different perspective on one’s internal experience, in which
thoughts, emotions, and sensations are viewed from an observer perspective, as
transient entities that are separate from the person having them. Thoughts such
as “I am incapable of handling my anxiety” might be viewed as “I am having
the thought that I am incapable of handling my anxiety,” and thus become less
threatening and distressful. This perspective is also thought to increase one’s ability
to evaluate and reality-test thoughts and attributions (Kohlenberg, Hayes, & Tsai,
1993).
One intervention that incorporates mindfulness skills is acceptance and commitment
therapy (ACT; Hayes, Strosahl, & Wilson, 1999). Walser and Westrup (2007)
developed an ACT protocol for PTSD which conceptualizes this disorder as stemming
from the use of inherently ineffectual control strategies to avoid unwanted thoughts,
emotions, or sensations associated with one’s traumatic experience. ACT emphasizes

the development of psychological flexibility in the service of movement toward
identified goals and values. Mindfulness exercises are one of a variety of techniques
used to increase willingness to experience thoughts and feelings and thus facilitate
psychological flexibility and participation in valued activity (Walser & Westrup,
2007).
Yoga interventions combine physical activity and breathing techniques with mindful
attention to present experience. Yoga practice has been associated with positive
elements of mental health and has received increased attention as an intervention
for anxiety and mood disorders (Vaghela & Pandya, 2010). Although no controlled
trials have been conducted with PTSD, Brown and Gerbarg (2005) report reductions
in intrusive and hyperarousal symptoms of Vietnam veterans participating in yoga.
In addition, Janakiramaiah et al. (1998) reported treatment gains for depression
including significant reductions in cortisol levels following yoga practice, highlighting
the potential utility for reducing symptoms of hyperarousal in PTSD.
Couple and Family Therapy

Because PTSD has been associated with marital distress and family discord, couple and
family interventions have emerged that attempt to both repair and harness the power
of the family system to relieve symptoms of PTSD (Monson, Fredman, & Adair,
2008). Whereas some approaches focus on restoring balance to the family system
in order to reduce stress, others are more symptom-focused and seek to harness
the support of the partner and/or family to aid in an individual’s recovery (Riggs,
2000). Critical action theory for combat-related PTSD (D. R. Johnson, Feldman,
& Lubin, 1995) and emotion focused therapy (S. M. Johnson & Williams-Keeler,
1998) are family/couple interventions that have been used in the treatment of PTSD;
however, the efficacy of these treatments has yet to be empirically tested (Cukor et al.,
2009).
One promising intervention with early empirical support is cognitive behavioral
conjoint therapy for PTSD (CBCT; Monson et al., 2008). This protocol consists of
fifteen 75-minute sessions in three stages: (a) psychoeducation and safety building,
(b) enhancing relationship satisfaction and undermining avoidance, and (c) cognitive
restructuring to address erroneous meaning making associated with the traumatic
experience (Monson & Fredman, 2012). The primary goal of CBCT is to treat
symptoms of PTSD with the secondary benefit of helping relationships. There
are several ways in which this treatment harnesses the partner relationship to reduce
symptoms. First, improving the relationship context may increase a sense of safety, thus
reducing symptoms of hyperarousal. Teaching patients to better name and share their
emotions may help to reduce emotional numbing and increase emotional connection
in the relationship. Lastly, one’s partner may provide an objective perspective, helping
to facilitate recontextualization of the event and reduce erroneous beliefs associated
with the trauma (Monson & Fredman, 2012). In an uncontrolled trial, Monson
et al. (2011) treated six couples in which one partner held a diagnosis of PTSD.
Results indicated that five of these patients no longer met criteria for PTSD following
treatment. Statistically significant improvement in PTSD symptoms was observed
based on patient, partner, and clinician report, with effect sizes ranging from 1.32 to
1.69. In addition, partners reported clinically significant improvements in relationship
satisfaction. Although patients’ relationship satisfaction was also improved, this change
did not reach statistical significance. Controlled trials are underway to further explore
the efficacy of this intervention (Cukor et al., 2009).
Interpersonal Therapy
Because of the noted disruption of interpersonal relationships often associated with
PTSD, interpersonal interventions have been developed that focus on improved
social functioning as a conduit for change in PTSD symptomatology. Positive social
support following a trauma is indeed associated with improved outcomes and quicker
recovery (Robinaugh et al., 2011). Bleiberg and Markowitz (2005) conducted a
pilot study of such an intervention with 14 subjects with chronic PTSD from various
interpersonal traumas. This intervention focused on increasing trust and addressing
interpersonal conflict, and demonstrated significant improvements in PTSD symptoms
and interpersonal functioning, with 12 of 14 participants no longer meeting criteria for
PTSD following treatment. Several interpersonal interventions have been conducted
in a group context. In a controlled trial, 48 low-income women with chronic
PTSD participated in an interpersonal psychotherapy (IPT) group (Krupnick et al.,
2008). The IPT group produced significantly greater depression and PTSD symptom
reduction than wait-list control. Further controlled trials are needed to determine
if interventions targeting the social aspects of PTSD are sufficient to address PTSD
symptoms, or whether such interventions are better conceptualized as an adjunct
treatment to more established treatments such as exposure therapy (Cukor et al.,
2009).
Summary and Recommendations
PTSD is a debilitating disorder to live with as it may have a negative impact on

many aspects of life, including one’s health and interpersonal functioning. The good
news is that more than several effective treatments have been developed over the
past two decades. Regarding CBT, we are fortunate to be in a position of offering
choices to patients. Everything else being equal, we suggest offering the treatment
for which the patient has expressed a preference. There are data in depression (Kocsis
et al., 2009) and now PTSD (Zoellner, Feeny, & Bittinger, 2009) that patients
improve more when administered their preferred treatment. Both CPT and PE are
being widely disseminated in the Veterans Administration and Department of Defense
settings and are becoming more readily available. Our group has recent evidence in
female rape victims with PTSD that if they have higher avoidant coping styles, they
profit more from an exposure therapy (Leiner, Kearns, Astin, Jackson, & Rothbaum,
2012).
For those patients who have not been treated with an adequate and appropriate
dose of CBT for PTSD and who express no strong preference, we recommend
starting with CBT. The reality in clinical practice is that the majority of individuals
referred for treatment of PTSD are often treated with both psychotherapy and
pharmacotherapy. Regarding the paradigms for combining medication and CBT, for
the antidepressant medication, if they are combined commencing at the same time,
there is the problem of time to response, generally about 4 weeks, for the medication.
It may make more sense to combine these approaches sequentially, starting first with
one and, if there is an insufficient response, then adding the other, ensuring the
administration of a full enough dose and course to expect a response (e.g., at least
4 weeks for selective serotonin reuptake inhibitors). If the antidepressant is the first
treatment, we recommend having it on board at least 4 weeks before commencing with
psychotherapy. Patients who achieve complete remission from medication might not
require any additional treatment, whereas those with a partial response will probably
benefit when CBT is added to pharmacotherapy. For anxiolytic medications other
than the antidepressants, generally the onset of action is much quicker and therefore
they can be combined with psychotherapy from the onset. However, there is some
evidence that they may impede exposure therapy. For the more novel medication
approaches such as DCS, the drug is not expected to afford any benefits in and
of itself, but only in combination with the exposure therapy, so they should be on
board at the same time. It should be noted, however, that PTSD often presents
with a number of psychiatric comorbidities, including major depression and suicidal
ideation, and appropriate treatment is likely to be dependent on the overall clinical
presentation and psychiatric comorbidity. In any case, we think hope is in order. We
have witnessed the resiliency of the human spirit and we know improvement and
recovery is possible, and these treatments reviewed above can help.
References
Albright, D., & Thyer, B. (2010). Does EMDR reduce posttraumatic stress disorder symp-
tomatology in combat veterans? Behavioral Interventions, 25, 1–19. doi: 10.1002/bin.
295
Baer, R. A., Smith, G. T., & Allen, K. B. (2004). Assessment of mindfulness by self-report.
Assessment, 11, 191–206. doi: 10.1177/1073191104268029
Bandura, A. (1986). Social foundations of thought and action: A social cognitive theory.
Englewood, NJ: Prentice-Hall.
Beck, J., Palyo, S., Winer, E., Schwagler, B. E., & Ang, E. J. (2007). Virtual reality exposure
therapy for PTSD symptoms after a road accident: An uncontrolled case series. Behavior
Therapy, 38, 39–48. doi: 10.1016/j.beth.2006.04.001
Benight, C. C., & Bandura, A. (2003). Social cognitive theory of posttraumatic recovery:
The role of perceived self-efficacy. Behavior Research and Therapy, 42, 1129–1148. doi:
10.1016/j.brat.2003.08.008
Bleiberg, K. L., & Markowitz, J. C. (2005). A pilot study of interpersonal psychotherapy
for posttraumatic stress disorder. American Journal of Psychiatry, 162, 181–183. doi:
10.1176/appi.ajp.162.1.181
Bradley, R., Greene, J., Russ, E., Dutra, L., & Westen, D. (2005). A multidimensional meta
analysis of psychotherapy for PTSD [erratum in American Journal of Psychiatry, 162,
832]. American Journal of Psychiatry, 162, 214–227. doi: 10.1176/appi.ajp.162.2.214
Brady, K. T. (2001). Comorbid posttraumatic stress disorder and substance use disorders.
Breslau, N. (1998). Epidemiology of trauma and posttraumatic stress disorder. In R. Yehuda
(Ed.), Psychological trauma (pp. 1–29). Washington, DC: American Psychiatric Press.
Brewin, C. R. (2001). A cognitive neuroscience account of posttraumatic stress disorder and its
treatment. Behavior Research and Therapy, 39, 373–393. doi: 10.1016/S0005-7967(00)
00087-5
Brown, R. P., & Gerbarg, P. L. (2005). Sudarshan Kriya Yogic breathing in the treatment
of stress, anxiety, and depression. Part II: Clinical applications and guidelines. Journal of
Alternative & Complementary Medicine, 11, 711–717. doi: 10.1089/acm.2005.11.711
Brown, K. W., & Ryan, R. M. (2003). The benefits of being present: Mindfulness and its role
in psychological well-being. Journal of Personality and Social Psychology, 84, 822–848.
doi: 10.1037/0022-3514.84.4.822
Bryant, R., Moulds, M., Guthrie, R., Dang, S., & Nixon, R. (2003). Imaginal exposure alone
and imaginal exposure with cognitive restructuring in treatment of posttraumatic stress
disorder. Journal of Consulting and Clinical Psychology, 71, 706–712. doi: 10.1037/0022-
006x.71.4.706
Cahill, S., Rothbaum, B., Resick, P., & Follette, V. (2009). Cognitive behavior therapy for
adults. In E. Foa, T. Keane, M. Friedman, & J. Cohen (Eds.), Effective treatments for
PTSD: Practice guidelines from the International Society for Traumatic Stress Studies, (2nd
Chemtob, C. M., Novaco, R. W., Hamada, R. S., & Gross, D. M. (1997). Cognitive behavioral
treatment for severe anger in posttraumatic stress disorder. Journal of Consulting and
Cloitre, M., Koenen, K., Cohen, L., & Han, H. (2002). Skills training in affective and
to childhood abuse. Journal of Consulting and Clinical Psychology, 70, 1067–1074. doi:
10.1037/0022-006x.70.5.1067
Cukor, J., Spitalnick, J., Difede, J., Rizzo, A., & Rothbaum, B. (2009). Emerging treatments
for PTSD. Clinical Psychology Review, 29, 715–726. doi: 10.1016/j.cpr.2009.09.001
Difede, J., Cukor, J., Jayasinghe, N., Patt, I., Jedel, S., Spielman, L., … Hoffman, H.
G. (2007). Virtual reality exposure therapy for the treatment of posttraumatic stress
disorder following September 11, 2001. Journal of Clinical Psychiatry, 68, 1639–1647.
doi:10.4088/jcp.v68n1102
Difede, J., & Hoffman, H. G. (2002). Virtual reality exposure therapy for World Trade Center
posttraumatic stress disorder: A case report. Cyberpsychology & Behavior, 5, 529–535. doi:
10.1089/109493102321018169
Ehlers, A., & Clark, D. M. (2000). A cognitive model of posttraumatic stress disorder. Behavior
Research and Therapy, 38, 319–345. doi: 10.1016/S0005-7967(99)00123-0
Engel, C. C., & Ursano, R. J. (2008). The importance of assessing exposure to trauma.
Psychiatric Services, 59, 229. doi: 10.1176/appi.ps.59.3.229
Foa, E. B., Cahill, S. P., & Pontoski, K. (2004). Factors that enhance treatment outcome of
cognitive-behavioral therapy for anxiety disorders. CNS Spectrums, 9, 6–17.
Foa, E. B., Dancu, C. V., Hembree, E. A., Jaycox, L. H., Meadows, E. A., & Street, G.
P. (1999). A comparison of exposure therapy, stress inoculation training, and their
combination for reducing posttraumatic stress disorder in female assault victims. Journal
of Consulting and Clinical Psychology, 67 , 194–200. doi: 10.1037/0022-006X.67.2.194
Foa, E. B., Hembree, E. A., & Rothbaum, B. O. (2007). Prolonged exposure therapy for PTSD:
Emotional processing of traumatic experiences, therapist guide. New York, NY: Oxford
University Press.
Foa, E., & Kozak, M. (1985). Treatment of anxiety disorders: Implications for psychopathology.
In H. Tuma & J. Maser (Eds.), Anxiety and the anxiety disorders (pp. 421–452). Hillsdale,
NJ: Erlbaum.
Foa, E., & Kozak, M. (1986). Emotional processing of fear: Exposure to corrective information.
Psychological Bulletin, 99, 20–35. doi: 10.1037/0033-2909.99.1.20
Foa, E., Rothbaum, B., & Furr, J. (2003). Is the efficacy of exposure therapy for posttrau-
matic stress disorder augmented with the addition of other cognitive behavior therapy
procedures? Psychiatric Annals, 33, 47–53.
Follette, V. M., & Vijay, A. (2009). Mindfulness for trauma and posttraumatic stress disorder.
In F. Didonna (Ed.), Clinical handbook of mindfulness (pp. 299–317). New York, NY:
Springer.
Forbes, D., Fletcher, S., Lockwood, E., O’Donnell, M., Creamer, M., Bryant, R. A., … Silove,
D. (2011). Requiring both avoidance and emotional numbing in DSM-V PTSD: Will it
help? Journal of Affective Disorders, 130, 483–486. doi:10.1016/j.jad2010.10.032
Friedman, M. J., Resick, P. A., Bryant, R. A., Strain, J., Horowitz, M., & Speigel, D. (2011).
Classification of trauma and stressor-related disorders in DSM-V. Depression and Anxiety,
28, 737–749. doi:10.1002/da.20845
Gerardi, M., Ressler, K., & Rothbaum, B. (2010). Combined treatment of anxiety disorders.
In D. Stein, M. Hollander, & B. Rothbaum (Eds.), Textbook of anxiety disorders (pp.
147–156). New York, NY: APA Press.
Gerardi, M., Rothbaum, B., Ressler, K., Heekin, M., and Rizzo, A. (2008). Virtual reality
exposure therapy using a virtual Iraq: Case report. Journal of Traumatic Stress, 21,
209–213. doi: 10.1002/jts.20331
and Dadds, M. R. (2008). A randomized controlled trial of D-cycloserine enhancement
of exposure therapy for social anxiety disorder. Biological Psychiatry, 63, 544–549. doi:
10.1016/j.biopsych.2007.11.011
Hayes, S. C., Strosahl, K., and Wilson, K. G. (1999). Acceptance and commitment therapy,
Hembree, E. A., & Foa, E. B. (2010). Cognitive behavioral treatments for PTSD. In G.
M. Rosen & C. B. Frueh (Eds.), Clinician’s guide to posttraumatic stress disorder (pp.
177–203). Hoboken, NJ: John Wiley & Sons, Inc.
Hofmann, S. G., Meuret, A. E., Smits, J. A., Simon, N. M., Pollack, M. H., Eisen-
menger, K., … Otto, M. W. (2006). Augmentation of exposure therapy with D-
cycloserine for social anxiety disorder. Archives of General Psychiatry, 63, 298–304.
doi:10.1001/archpsyc.63.3.298
Institute of Medicine (IOM). (2008). Treatment of posttraumatic stress disorder: An assessment
of the evidence. Washington, DC: National Academies Press.
Janakiramaiah, N., Gangadhar, B. N., Murthy, P. J., Venkatesha, N., Harish, M. G., Shetty,
K., … Vedamurthachar, A. (1998). Therapeutic efficacy of Sudarsham Kriya Yoga (SKY)
in dysthymic disorder. NIMHANS Journal, 16, 21–28.
Johnson, D. R., Feldman, S. C., & Lubin, H. (1995). Critical interaction therapy: Couples
therapy in combat-related posttraumatic stress disorder. Family Process, 34, 401–412.
doi: 10.1111/j1545-5300.1995.00401.x
Johnson, S. M., & Williams-Keeler, L. (1998). Creating healing relationships for couples
dealing with trauma: The use of emotionally focused marital therapy. Journal of Marital
and Family Therapy, 24, 25–40. doi: 10.1111/j17520606.1998.tb01061.x
Josman, N., Somer, E., Reisburg, A., Weiss, P. L., Garcia-Palacios, A., & Hoffman, H. (2006).
Designing a virtual environment for post-traumatic stress disorder in Israel: A protocol.
Cyber Psychology and Behavior, 9, 241–244. doi: 10.1089/cpb.2006.9.241
Kearney, D. J., McDermott, K., Malte, C., Martinez, M., and Simpson, T. L. (2011).
Association of participation in a mindfulness program with measures of PTSD, depression,
and quality of life in a veteran sample. Journal of Clinical Psychology, 68, 101–116. doi:
10.1002/jclp.20853
Kessler, R. C., Sonnega, A., Bromet, E., Hughes, M., & Nelson, C. B. (1995). Posttraumatic
stress disorder in the National Comorbidity Survey. Archives of General Psychiatry, 52,
1048–1060. doi: 10.1001/archpsyc.1995.03950240066012
Kilpatrick, D., Veronen, L., & Resick, P. (1982). Psychological sequelae to rape: Assessment
and treatment strategies. In D. Dolays & R. Meredith (Eds.), Behavioral medicine:
Assessment and treatment strategies (pp. 473–479). New York, NY: Plenum Press.
Kocsis, J. H., Leon, A. C., Markowitz, J. C., Manber, R., Arnow, B., Klein, D. N., &
Thase, M. E. (2009). Patient preference as a moderator of outcome for chronic forms
of major depressive disorder treated with Nefazadone, cognitive behavioral analysis of
psychotherapy, or their combination. Journal of Clinical Psychiatry, 70, 354–361. doi:
10.4088/JCP.08m04371
Kohlenberg, R. J., Hayes, S. C., & Tsai, M. (1993). Radical behavioral psychotherapy: Two
contemporary examples. Clinical Psychology Review, 13, 579–592. doi: 10.1016/0272-
7358(93)90047-P
Krupnick, J. L., Green, B. L., Stockton, P., Miranda, J., Krause, E., & Mete, M. (2008). Group
interpersonal psychotherapy for low-income women with PTSD. Psychotherapy Research,
18, 497–507. doi: 10.1080/10503300802183678
Lang, P. (1977). Imagery in therapy: An information processing analysis of fear. Behavior
Therapy, 8, 862–886. doi: 10.1016/S0005-7894(77)80157-3
Lange, A., van de Ven, J. P., Schrieken, B., & Emmelkamp, P. M. G. (2001). Interapy:
Treatment of post-traumatic stress through the Internet: A controlled trial. Journal
of Behavior Therapy and Experimental Psychiatry, 32, 73–90. doi: 10.1016/S0005-
7916(01)00023-4
Leiner, A. S., Kearns, M., Astin, M., Jackson, J., & Rothbaum, B. O. (2012). Avoidant coping
and treatment outcome in rape-related posttraumatic stress disorder. Journal of Consulting
and Clinical Psychology, 80, 317–321. doi: 10.1037/a0026814
Litz, B. T., Engel, C. C., Bryant, R. A., & Papa, A. (2007). A randomized, controlled proof
of concept trial of an Internet based, therapist assisted self-management treatment for
posttraumatic stress disorder. American Journal of Psychiatry, 164, 1676–1683. doi:
10.1176/appi.ajp.2007.06122057
McGovern, M. P., Lambert-Harris, C., Acquilano, S., Xie, H., Alterman, A. I., & Weiss, R. D.
(2009). A cognitive behavioral therapy for co-occurring substance use and posttraumatic
stress disorder. Addictive Behaviors, 34, 892–897. doi: 10.1016/j.addbeh.2009.03.009
McLay, R., Wood, D., Webb-Murphy, J., Spira, J., Wiederhold, M., Pyne, J., & Wieder-
hold, B. (2010). A randomized controlled trial of virtual reality-graded exposure therapy
for posttraumatic stress disorder in active duty service members with combat-related
posttraumatic stress disorder. Cyberpsychology Behavior and Social Networking, 13, 3–11.
doi: 10.1089/cyber.2011.0003
Monson, C., & Fredman, S. J. (2012). Cognitive-behavioral conjoint therapy for posttraumatic
stress disorder: Harnessing the healing power of relationships, New York, NY: Guilford Press.
Monson, C., Fredman, S. J., & Adair, K. C. (2008). Cognitive-behavioral conjoint therapy
for posttraumatic stress disorder: Application of Operation Enduring and Iraqi Freedom
veterans. Journal of Clinical Psychology, 64, 958–971. doi: 10.1002/jclp.20511
Monson, C., Fredman, S. J., Adair, K. C., Stephens, S. P., Resick, P. A., Schnurr, P. P., …
MacDonald, A. (2011). Cognitive behavioral conjoint therapy for PTSD: Pilot results from
a community sample. Journal of Traumatic Stress, 24, 97–101. doi:10.1002/jts.20604
Monson, C., Schnurr, P., Resick, P., Friedman, M., Young-Xu, Y., & Stevens, S. (2006). Cog-
nitive processing therapy for veterans with military-related posttraumatic stress disorder.
Journal of Consulting and Clinical Psychology, 74, 898–907. doi: 10.1037/0022-
006x.74.5.898
Nacasch, N., Foa, E., Huppert, J., Tzur, D., Fostick, L., Dinstein, Y., … Zohar, J. (2011).
Prolonged exposure therapy for combat- and terror-related posttraumatic stress disorder:
A randomized control comparison with treatment as usual. Journal of Clinical Psychiatry,
72, 1174–1180. doi:10.4088/JCP.09m05682blu
Najavits, L. M. (2002). Seeking safety: A treatment manual for PTSD, New York, NY: Guilford
Press.
Najavits, L. M., Gallop, R. J., & Weiss, R. D. (2006). Seeking safety therapy for adolescent
girls with PTSD and substance use disorder: A randomized controlled trial. Journal of
Health Services and Research, 43, 453–463. doi:10.1007/s11414-006–9034–2
Otto, M. W., Tolin, D. F., Simon, N. M., Pearlson, G. D., Basden, S., Meunier, S. A., …
Pollack, M. H. (2010). Efficacy of D-cycloserine for enhancing response to cognitive-
behavioral therapy for panic disorder. Biological Psychiatry, 67 , 365–370. doi:10.1016/
j.biopsych.2009.07.036
Palmieri, P. A., Weathers, F. W., Difede, J., & King, D. W. (2007). Confirmatory factor
analysis of the PTSD Checklist and the Clinician Administered PTSD Scale in disaster
workers exposed to World Trade Center Ground Zero. Journal of Abnormal Psychology,
116, 329–341. doi: 10.1037/0021-843X116.2.329
Pietrzak, R. H., Goldstein, R. B., Southwick, S. M., & Grant, B. F. (2011). Prevalence of Axis
I comorbidity of full and partial posttraumatic stress disorder in the United States: Results
from Wave 2 of the National Epidemiologic Survey on Alcohol and Related Conditions.
Journal of Anxiety Disorders, 25, 456–465. doi: 10.1016/j.janxdis.2010.11.010
Powers, M., Halpern, J., Ferenschak, M., Gillihan, S., & Foa, E. (2010). A meta-analytic review
of prolonged exposure for posttraumatic stress disorder. Clinical Psychology Review, 30,
635–641. doi: 10.1016/j.cpr.2010.04.007
Reger, G., & Gahm, G. (2008). Virtual reality exposure therapy for active duty soldiers. Journal
of Clinical Psychology, 64, 940–946. doi: 10.1002/jclp.205.12
Resick, P. A., Monson, C. M., & Chard, K. M. (2008). Cognitive processing therapy vet-
eran/military version: Therapist’s manual, Washington, DC: Department of Veteran’s
Affairs.
Resick, P. A., Nishith, P., Weaver, T. L., Astin, M. C., & Feuer, C. A. (2002). A comparison
of cognitive-processing therapy with prolonged exposure and a waiting condition for
the treatment of chronic post-traumatic stress disorder in female rape victims. Journal of
Consulting and Clinical Psychology, 70, 867–879. doi: 10.1037/0022-006X.70.4.867
Resick, P. A., & Schnicke, M. K. (1992). Cognitive processing therapy for sexual assault
victims. Journal of Consulting and Clinical Psychology, 60, 748–756. doi: 10.1037/0022-
006X.60.5.748
Ressler, K., Rothbaum, B., Tannenbaum, L., Anderson, P., Graap, K., Zimand, E., … David,
M. (2004). Cognitive enhancers as adjuncts to psychotherapy: Use of D-cycloserine in
phobics to facilitate extinction of fear. Archives of General Psychiatry, 61, 1136–1144.
doi:10.1001/archpsyc.61.11.1136
Riggs, D. S. (2000). Marital and family therapy. In E. B. Foa, T. M. Keane, & M. J. Friedman
(Eds.), Effective treatments for PTSD (pp. 280–301). New York, NY: Guilford Press.
Robinaugh, D. J., Marques, L., Traeger, L. N., Marks, E. H., Sung, S. C., Gayle, B. J., …
Simon, N. M. (2011). Understanding the relationship of perceived social support to
post-trauma cognitions and posttraumatic stress disorder. Journal of Anxiety Disorders,
25, 1072–1078. doi:10.1016/j.janxdis.2011.07.004
Rothbaum, B. O. (2008). Critical parameters for D-cycloserine enhancement of cognitive-

behavioral therapy for obsessive compulsive disorder. American Journal of Psychiatry,
165, 293–296. doi: 10.1176/appi.ajp.2007.07121871
Rothbaum, B., Astin, M., & Marsteller, F. (2005). Prolonged exposure versus eye movement
desensitization and reprocessing (EMDR) for rape victims. Journal of Traumatic Stress,
18, 607–616. doi: 10.1002/jts.20069
Rothbaum, B., Cahill, S., Foa, E., Davidson, J., Compton, J., Connor, K., … Hahn, C. (2006).
Augmentation of sertraline with prolonged exposure in the treatment of posttraumatic
stress disorder. Journal of Traumatic Stress, 19, 625–638. doi:10.1002/jts20170
Rothbaum, B., Foa, E. B., Riggs, D. S., Murdock, T., & Walsh, W. (1992). A prospective
examination of post-traumatic stress disorder in rape victims. Journal of Traumatic Stress,
5, 355–475. doi: 10.1002/jts52490050309
Rothbaum, B., Hodges, L. F., Ready, D., Graap, K., & Alarcon, R. D. (2001). Virtual reality
exposure therapy for Vietnam veterans with posttraumatic stress disorder. Journal of
Schneier, F. R., Neria, Y., Pavlicova, M., Hembree, E., Jung Suh, E., Amsel, L., & Marshall,
R. D. (2012). Combined prolonged exposure therapy and paroxetine for PTSD related
to the World Trade Center attack: A randomized controlled trial. American Journal of
Psychiatry, 169, 80–88. doi: 10.1176/appi.ajp.2011.11020321
Schnurr, P. P., Friedman, M. J., Engel, C. C., Foa, E. B., Shea, M. T., Chow, B. K., …
Bernardy, N. (2007). Cognitive behavioral therapy for post traumatic stress disorder in
women: A randomized controlled trial. Journal of the American Medical Association, 297 ,
820–830. doi:10.1001/jama.297.8.820
Schnurr, P. P., Friedman, M., Foy, D., Shea, M., Hsieh, F., Lavori, P., … Bernardy,
N. C. (2003). Randomized trial of trauma-focused group therapy for posttraumatic stress
disorder. Archives of General Psychiatry, 60, 481–489. doi:10.1001/archpsyc.60.5.481
Schnurr, P. P., & Green, B. L. (2004). Understanding relationships among trauma, posttrau-
matic stress disorder, and health outcomes. Advances in Mind-Body Medicine, 20, 18–29.
doi: 10.1037/10723-010
Seidler, G. H., & Wagner, F. E. (2006). Comparing the efficacy of EMDR and trauma
focused cognitive-behavioral therapy in the treatment of PTSD: A meta-analytic study.
Psychological Medicine, 36, 1515–1522. doi: 10.1017/S0033291706007963
Shapiro, F. (1995). Eye movement desensitization and reprocessing: Basic principles, protocols and
procedures, New York, NY: Guilford Press.
Shapiro, S. L., Carlson, L. E., Astin, J. A., & Freedman, B. (2006). Mechanisms of mindfulness.
Journal of Clinical Psychology, 62, 373–386. doi: 10.1002/jclp.20237
Shea, M. T., McDevitt-Murphy, M., Ready, D. J., & Schnurr, P. P. (2009). Group therapy. In
E. B. Foa, T. M. Keane, M. J. Friedman, & J. A. Cohen (Eds.), Effective treatments for
PTSD: Practice guidelines from the International Society for Traumatic Stress Studies (2nd
Simon, N., Conner, K., Lang, A. J., Rauch, S., Krulewicz, S., Lebeau, R. T., …
Pollack, M. H. (2008). Paroxetine CR augmentation to posttraumatic stress disorder
refractory to prolonged exposure therapy. Journal of Clinical Psychiatry, 69, 400–405.
doi:10.4088/JCP.v69n0309
Smalley, S. L., Loo, S. K., Hale, T. S., Shrestha, A., McGough, J., Flook, L., & Reise, S. (2009).
Mindfulness and attention deficit hyperactivity disorder. Journal of Clinical Psychology,
65, 1087–1098. doi: 10.1002/jclp.20618
Spates, C. R., Koch, E., Cusack, K., Pagoto, S., & Waller, S. (2009). Eye movement
desensitization and reprocessing. In E. B. Foa, T. M. Keane, M. J. Friedman, &
J. A. Cohen, Eds.), Effective treatments for PTSD: Practice guidelines from the International
Society for Traumatic Stress Studies, (pp. 279–305) New York, NY: Guilford Press.
Tolin, D.F. and Foa, E.B. (2006). Sex differences in trauma and posttraumatic stress disorder:
A quantitative review of 25 years of research. Psychological Bulletin, 132, 959–992. doi:
10.1037/1942-9681.S.1.37
Vaghela, S., & Pandya, M. (2010). Impact of yoga on mental health. Indian Journal of
Community Psychology, 6, 310–312.
Vujanovic, A. A., Bonn-Miller, M. O., Bernstein, A., McKee, L. G., & Zvolensky, M. J.
(2010). Incremental validity of mindfulness skills in relation to emotional dysregulation
among a young adult community sample. Cognitive Behaviour Therapy, 39, 203–213.
doi: 10.1080/16506070903441630
Vujanovic, A. A., Niles, B., Pietrefesa, A., Schmertz, S. K., & Potter, C. (2011). Mindfulness
in the treatment of posttraumatic stress disorder among military veterans. Professional
Psychology: Research and Practice, 42, 24–31. doi: 10.1037/a0022272
Walser, R. D., & Westrup, D. (2007). Acceptance & commitment therapy for the treatment of
post-traumatic stress disorder and trauma-related problems: A practitioner’s guide to using
mindfulness and acceptance strategies. Oakland, CA: New Harbinger Publications.
Wupperman, P., Neumann, C. S., Whitman, J. B., & Axelrod, S. R. (2009). The role of
mindfulness in borderline personality disorder features. Journal of Nervous and Mental
Disease, 197 , 766–771. doi: 10.1097/NMD.0b013e3181b9734
Zoellner, L. A., Feeny, N. C., & Bittinger, J. N. (2009). What you believe is what you
want: Modeling PTSD treatment preferences for sertraline or prolonged exposure.
Journal of Behavior Therapy and Experiential Psychiatry, 40, 455–467. doi: 10.1016/
j/jbtep.2009.06.0
44
Jonathan S. Abramowitz and Brittain L. Mahaffey
University of North Carolina at Chapel Hill, United States
Obsessive-compulsive disorder (OCD) is characterized by (a) recurrent, unwanted,

and seemingly bizarre thoughts, images, or doubts that provoke affective distress
(obsessions; e.g., the image of harming a child), and (b) repetitive behavioral or
mental rituals performed to reduce this distress (compulsions; e.g., constantly asking
others for reassurance that one did not harm anyone). Obsessional fears generally
relate to uncertainty about personal safety or the safety of others. Compulsions are
deliberately performed to reduce this uncertainty. Consistent studies on the various
manifestations of OCD (e.g., Abramowitz et al., 2010) indicate that certain types
of obsessions and compulsions co-occur within patients, including: (a) obsessions
regarding contamination and decontamination rituals (e.g., excessive cleaning); (b)
obsessions regarding responsibility for harm and checking or reassurance-seeking ritu-
als; (c) unwanted, repugnant violent, sexual, or blasphemous obsessional thoughts and
covert compulsions or “neutralizing strategies” (e.g., mental rituals such as praying);
and (d) obsessions concerning symmetry and orderliness and ordering/arranging
rituals.
Although most people with OCD recognize that their obsessions and rituals are
senseless and excessive, some strongly believe that their rituals serve to prevent the
occurrence of disastrous consequences; that is, they have “poor insight.” Clinical
observations suggest that a patient’s degree of insight can vary over time as well as
across symptom categories. For example, one patient evaluated in our clinic realized
that her fear of causing her mother to die of cancer just by thinking about it was
unrealistic (although she tried to prevent such thoughts just to be on the safe side),
yet she was strongly convinced that if she did not put all items in a special oven
before bringing them into the house, she would become infected with bed bugs. It is
important to ascertain patients’ degree of insight into the senselessness of their OCD
symptoms as poorer insight can negatively impact treatment outcome.
The lifetime prevalence rate of OCD in adults is 2–3% (e.g., Kessler et al., 2005).
Although symptoms typically wax and wane as a function of general life stress, a chronic
and deteriorating course is the norm if adequate treatment is not sought. In many
cases, fears, avoidance, and rituals impair various areas of functioning including job

DOI: 10.1002/9781118528563.wbcbt44
or academic performance, social functioning, and leisure activities. Many individuals

with OCD also experience other Axis I disorders such as mood and anxiety problems
(Abramowitz, 2011). This chapter begins with an overview of cognitive behavioral
therapy (CBT) for OCD, including a description of the interventions and techniques
as well as their conceptual underpinnings. We also review the latest treatment outcome
research establishing the effectiveness of CBT for OCD. A case is then presented to
illustrate the use of CBT techniques for this problem.
Conceptual Basis of Cognitive Behavioral Therapy for

Before the 1970s, treatment for OCD consisted largely of psychodynamic psy-
chotherapy derived from psychoanalytic ideas of unconscious motivation. There are
virtually no scientific studies of the effectiveness of this approach, yet the general
consensus of that era—that OCD was an unmanageable condition with a poor
prognosis—demonstrates how little confidence clinicians placed in this form of treat-
ment. What literature is available suggests that the effects of psychodynamic therapies
are neither robust nor durable for OCD (Steketee, 1993). By the last quarter of the
twentieth century, however, the prognostic picture for OCD had improved drastically;
this was due in large part to Victor Meyer (1966) and other behaviorally oriented
clinicians and researchers who conducted laboratory experiments and derived a learn-
ing model and behavioral treatment approach to OCD. With the cognitive revolution
of the 1980s and 1990s, theorists such as Paul Salkovskis (1985) and Jack Rachman
(1997) added to these models by describing the development of obsessional fear as
involving dysfunctional beliefs and appraisals.
Behavioral Theory and Therapy

Mowrer’s (1960) two-stage learning theory of anxiety disorders was the first (and
perhaps the most) influential conceptual model in the development of contemporary
CBT for OCD. This model explains the acquisition of fear as involving classical
conditioning, and the maintenance of the conditioned fear response (and resulting
avoidance and compulsive rituals) as involving operant conditioning. For example,
a patient might develop a fear of knives after hearing about someone who had
been violently stabbed and then having unconditionally fear-provoking thoughts
(i.e., reminders of the stabbing) come to mind in the presence of a knife (classical
conditioning). She might then avoid knives whenever possible, pray that she does
not “lose control and stab anyone,” or keep all knives in the home locked away.
These avoidance and ritualistic behaviors might immediately reduce her fear (albeit
temporarily), yet this also negatively reinforces such behaviors (operant conditioning)
and therefore they are likely to be repeated (compulsively). Moreover, the avoidance
and rituals prevent her from learning that the conditioned stimulus (i.e., using knives)
is generally not dangerous; and her fear and avoidance therefore persist. Accordingly,
successful treatment of OCD must promote extinction of the conditioned anxiety
response through confrontation with erroneously feared objects and situations, and
Obsessive-Compulsive Disorder 1045
also eliminate avoidance and rituals that impede extinction learning: hence exposure
and response prevention.
Meyer (1966) elaborated quite eloquently on this idea from a more cognitive (as
opposed to a strictly learning/conditioning) perspective:
Learning theories take into account the mediation of responses by goal expectancies,
developed from previously reinforcing situations. When these expectations are not fulfilled,
new expectancies may evolve, which, in turn, may mediate new behavior. Thus, if the
obsessional is persuaded or forced to remain in feared situations and prevented from
carrying out the rituals, he may discover that the feared consequences no longer take
place. Such modification of expectations should result in the cessation of ritualistic
behavior. (p. 275)
Essentially, Meyer argued that when a patient with OCD confronts his or her obses-
sional fear, without performing rituals, over-estimates of the probability and costs
of feared outcomes are able to be corrected, leading to the reduction of obsessive
fear and ritualistic behavior. These procedures form the backbone of contemporary
CBT.
In Meyer’s (1966) initial study using what is now commonly referred to as
exposure and response prevention (ERP), his patients deliberately confronted for
2 hours each day obsessional situations and stimuli they usually avoided (e.g.,
floors, bathrooms), while also refraining from compulsive rituals (e.g., no washing
or checking). Most of these individuals demonstrated at least partial improvement at
posttreatment and very few relapsed at follow-up (Meyer, Levy, & Schnurer, 1974).
The interest generated by these initial findings led to additional studies in centers
around the world using more advanced methodology in both inpatient and outpatient
settings. Research conducted in the United Kingdom (Hodgson, Rachman, & Marks,
1972), Holland (Emmelkamp & Kraanen, 1977), Greece (Rabavilas, Boulougouris,
& Stefanis, 1976), and the United States (Foa & Goldstein, 1978) with hundreds
of patients and many therapists affirmed the beneficial effects and generalizability
of exposure-based treatment for OCD. By the end of the 1980s, ERP was widely
considered the psychosocial treatment of choice for obsessions and compulsions
(Steketee, 1993).
Contemporary ERP entails therapist-guided systematic repeated and prolonged
exposure to situations that provoke obsessional fear along with abstinence from
compulsive behaviors. This might occur in the form of repeated actual confrontation
with feared low-risk situations (i.e., in vivo exposure), or in the form of imaginal
confrontation with the feared disastrous consequences of confronting the low-risk
situations (imaginal exposure). For example, an individual who fears turning into a
child molester if he gives his baby boy a bath and washes his penis would practice
doing these activities repeatedly. He would also resist the urge to analyze or dismiss
any thoughts of molesting the child that come to mind. Similarly, someone with
obsessional fears of germs from toilet seats would touch toilet seats and imagine
possibly contracting illnesses from the germs.
Refraining from compulsive rituals (response prevention) is a vital component
of treatment because the performance of such rituals to reduce obsessional anxiety
would prematurely discontinue exposure and rob the patient of learning that (a) the
obsessional situation of acceptable risk, and (b) anxiety subsides on its own even if
the ritual is not performed. Thus, successful ERP requires that the patient remain
in the exposure situation without attempting to reduce the distress by withdrawing
from the situation or by performing compulsive rituals or neutralizing strategies. In
the examples above, the first patient would refrain from seeking assurances that he is
not a child molester; the second patient would refrain from washing or cleaning.
At the start of exposure tasks (situational and imaginal), the patient typically
experiences a rapid elevation in subjective anxiety and physiological arousal. In fact,
patients are told that they must engage in the exposure task fully until such experiences
are evoked. During the course of an exposure session, however, the subjective distress
(and associated physiological response) usually subsides, even if the individual remains
exposed to the feared stimulus. Furthermore, extinction occurs more rapidly with
repeated exposure to the same stimulus over subsequent sessions and the obsessional
fear progressively abates (Foa & Kozak, 1986).
Cognitive Theory and Therapy

Although behavioral models of OCD satisfactorily explain the persistence of com-
pulsive rituals, they do not adequately account for the development of obsessional
fears. Very few patients with OCD, for example, recount conditioning experiences in
which fear would be expected to have become paired with obsessional triggers (Clark,
2004). Cognitive models of OCD were therefore developed in an effort to understand
obsessions better, and to shift the focus of treatment onto these phenomena as well.
Such approaches begin with the well-established finding that intrusions (thoughts,
images, and impulses that intrude into consciousness (e.g., unwanted thoughts of
harming a loved one) are experienced by most people (i.e., normal intrusions), but
can develop into obsessions when appraised as posing a threat for which the individual
is personally responsible (e.g., “Having thoughts about harming Mother means I’m
a dangerous person who must take extra care to ensure that I don’t lose control”;
Salkovskis, 1996). Such appraisals evoke distress and motivate the person to try to
suppress or neutralize the unwanted intrusion (e.g., by replacing it with a “good”
thought), and to attempt to prevent any harmful events associated with the intrusion
(e.g., by avoiding driving).
According to the cognitive model, compulsions are conceptualized as efforts to
remove intrusions and to prevent any perceived harmful consequences. Salkovskis
(1985) advanced two main reasons that compulsions become persistent and excessive:
First, they are reinforced by immediate distress reduction and by temporary removal
of the unwanted thought (negative reinforcement, as in the conditioning model).
Second, they prevent the person from learning that their appraisals are unrealistic
(e.g., the person fails to learn that unwanted harm-related thoughts do not lead
to acts of harm). Compulsions influence the frequency of intrusions by serving as
reminders of intrusions, and thereby triggering their reoccurrence. For example,
compulsive hand-washing can remind the person that he or she may have become
contaminated. Attempts at distracting oneself from unwanted intrusions may para-
doxically increase the frequency of intrusions, possibly because the distractors become
reminders (retrieval cues) of the intrusions. Compulsions can strengthen one’s per-
ceived responsibility. That is, the absence of the feared consequence after performing
the compulsion reinforces the belief that the person is responsible for removing the
threat.
As derived from this conceptual model, cognitive therapy for OCD (e.g., Wilhelm
& Steketee, 2006) involves a mix of didactic and Socratic dialogue along with
“experiments” used to deepen the patient’s conviction in his or her new, functional
beliefs and appraisals. Didactic information includes being taught the cognitive model
and that intrusive thoughts are normal experiences which become obsessions only
when appraised as significant in a way that is distressing (e.g., “Thoughts of violence
are equivalent to committing violent acts”). Socratic and experiential techniques are
used to help patients challenge and correct their erroneous beliefs and appraisals, such
as discussions about dysfunctional thinking patterns and behavioral experiments in
which the patient enters and observes situations that exemplify his or her fears, and
then collects information that allows him or her to revise judgments about the degree
of risk associated with obsessions. Although the rationale for behavioral experiments
in cognitive therapy is somewhat different than the rationale for exposure exercises
in ERP, there is procedural overlap, and fundamental differences between the two
techniques may be difficult to discern.
The Delivery of Cognitive Behavioral Therapy for

Contemporary CBT for OCD involves a blend of the ERP and cognitive therapy
techniques as described above. We believe that notions of “behavioral” versus “cog-
nitive” therapy represent a false dichotomy: In clinical practice, the largely academic
differences in conceptual emphasis are outweighed by their overlaps, and both make
important contributions to the treatment of OCD for most patients. One format that
is highly successful is a few sessions of assessment, psychoeducation, and treatment
planning, followed by twice-weekly sessions of ERP and cognitive therapy, lasting
about 90 to 120 minutes each, spaced over about 8 weeks (Abramowitz, Foa, &
Franklin, 2003). Generally, the therapist supervises the exposure sessions and assigns
self-exposure practice to be completed by the patient between sessions. Depending
on the patient’s symptom presentation and the practicality of confronting actual
feared situations, treatment sessions might involve varying amounts of situational
and imaginal exposure practice. Cognitive techniques are used informally throughout
treatment to help weaken dysfunctional beliefs and prepare patients for confronting
their fears and resisting compulsive urges (Abramowitz, 2006).
A course of CBT typically begins with the assessment of (a) obsessional thoughts,
ideas, and impulses, (b) stimuli that trigger the obsessions, (c) rituals and avoidance
behavior, and (d) the anticipated harmful consequences of confronting feared situ-
ations without performing rituals (i.e., the cognitive links between obsessions and
compulsions). Psychoeducation is woven into this assessment as the therapist uses
examples from the patient’s repertoire of OCD symptoms to illustrate and teach the
patient how the principles of learning and emotion are involved in the problem (e.g.,
Salkovskis, 1996). The patient is also given a clear rationale for how CBT is expected
to be helpful in reducing OCD. This psychoeducational component is an important
step in therapy because it helps to motivate the patient to tolerate the distress and
uncertainty that typically accompanies exposure practice. A helpful rationale includes
information about how ERP involves the provocation and reduction of distress during
prolonged exposure. Information gathered during the assessment sessions is then used
to plan, collaboratively with the patient, the specific exposure exercises that will be
pursued (Abramowitz, 2006).
In addition to explaining and planning a hierarchy of exposure exercises, the edu-
cational stage of ERP also acquaints the patient with response prevention procedures.
The term “response prevention” does not imply that the therapist actively prevents
the patient from performing rituals. Instead, the therapist must help the patient to
resist urges to perform rituals on his or her own. Self-monitoring of rituals is often
used in support of this goal. The patient is taught to keep track of the date, time,
triggers of, and time spent ritualizing using forms designed for this purpose.
Implementing Exposure Therapy

Situational (in vivo) exposure. The exposure exercises themselves typically begin with
the patient confronting moderately distressing situations and stimuli. Stimuli that
trigger low levels of anxiety are omitted from the treatment plan since these would not
teach the patient how to manage obsessional anxiety. The treatment plan is arranged
so that gradually the patient practices confronting more and more difficult situations
until the most distressing situations are presented. Beginning with less anxiety-evoking
exposure tasks increases the likelihood that the patient will learn to manage his or
her distress and complete the exposure exercise successfully (Abramowitz, 2006).
Moreover, having success with initial exposures increases confidence in the treatment
and helps motivate the patient to persevere during later, more difficult, exercises
(Abramowitz, 2006). The most feared items must be confronted in treatment to
allow the patient to learn that even these stimuli are manageable. Moreover, exposure
to the most anxiety-evoking situations is not left to the end of the treatment, but
rather is practiced about midway through the schedule of exposure tasks. This allows
the patient ample opportunity to repeat exposure to the most difficult situations in
different contexts to allow generalization of treatment effects. At the end of each
treatment session, the therapist instructs the patient to continue exposure for several
hours and in different contexts without the therapist.
Imaginal exposure. In contrast to situational fear cues, which are often concrete,
obsessional thoughts, ideas, and images are intangible, and therefore can be elusive
targets when designing exposure. Although in vivo exposure often evokes obsessional
thoughts, imaginal exposure provides a more systematic way of exposing the patient to
the key fear-evoking elements of his or her obsessions. The recommended methods for
conducting imaginal exposure include (a) using digital voice recorders or audiocassette
tapes (continuous loop tapes work especially well) or (b) written scripts containing
the anxiety-evoking material (Freeston et al., 1997). Both of these media allow the
therapist to prolong the patient’s confrontation with an otherwise covert event and, if
necessary, manipulate the content of the stimulus. The use of a digital voice recorder
or audio tape further ensures that unsupervised (homework) exposure will include
confrontation with the correct stimuli.
Abramowitz (2006) described three types of imaginal exposure that can be used
based on the specifics of the patient’s symptoms. Primary imaginal exposure is essen-
tially situational exposure to unwanted thoughts. It involves directly and repeatedly
confronting spontaneously occurring repugnant thoughts, images, and urges (i.e.,
violent, sexual, or blasphemous obsessions). Secondary imaginal exposure is used
when situational exposure evokes fears of disastrous consequences. In such instances,
imaginal exposure is begun during or after situational exposure, and should involve
visualizing the feared outcomes or focusing on uncertainty associated with the risk
of feared outcomes. Finally, preliminary imaginal exposure entails imagining con-
fronting a feared stimulus as a preliminary step in preparing for situational exposures.
For example, a patient might vividly imagine touching the bathroom floor before
actually engaging in situational exposure to the bathroom floor. This type of exposure
might be used as an intermediate step in preparing the patient to confront a situation
of which he or she is extremely fearful.
Using Cognitive Therapy

As mentioned previously, cognitive therapy techniques might be used throughout
treatment to illustrate dysfunctional beliefs, help patients change such cognitive
distortions, and help prepare patients for especially fear-provoking exposure tasks.
Indeed, the therapist should take an active role in facilitating cognitive change
during exposure by helping the patient challenge dysfunctional beliefs about feared
stimuli and feared consequences relevant to the exposure exercise. Commonly, such
discussions turn to risk-taking and the importance of learning how to manage
acceptable (everyday) degrees of uncertainty. Rather than provide reassurance or
argue with patients about the exact probabilities of their most feared consequences, it
is useful to emphasize the practicalities of taking the low-level risks presented during
exposure. That is, learning to live with a reasonable amount of risk and uncertainty is
preferable to the consequences of trying to demand absolute certainty and eliminate all
risk (i.e., avoidance), or performing compulsive rituals in order to secure an absolute
guarantee of safety—which is not feasible. Importantly, it is counterproductive to
try to convince the patient that exposure situations are “not dangerous.” This is for
the patient to discover for him- or herself through experience. Risk levels are best
described as “acceptably low” rather than “zero.” A few specific cognitive techniques
used in the treatment of OCD are described next.
For patients with overestimates of personal responsibility, the “pie technique”
(Clark 2004) involves the patient giving an initial estimate of the percentage of
responsibility that would be attributable to him or her if a feared consequence were to
occur. The patient then generates a list of the parties (other than him- or herself) that
would also have some responsibility for the feared consequence. They then draw a pie
chart, each slice of which represents one of the responsible parties identified. Next,
the patient labels all parties’ slices according to their percentage of responsibility and
labels his or her own slice last. By the exercise’s end, it is generally clear to patients
that the majority of the responsibility for the feared event would not be their own.
For patients with difficulty discriminating between unwanted obsessional thoughts
and actions, the “cognitive continuum” technique involves the patient rating how
immoral he or she perceives him- or herself to be for having the intrusive obsessional
thoughts. Next, the patient rates the morality level of other individuals who have
committed acts of varying degrees of immorality (e.g., a serial rapist, abusive parents).
Then, the patient re-rates him- or herself and reevaluates how immoral he or she is
for simply experiencing intrusive thoughts.
Procedural Variations
A range of methods have been developed for conducting exposure therapy. Most
OCD symptoms may be treated with any of the various methods of implementation;
some approaches, however, are more effective in producing change for specific types
of obsessions and rituals.
In-session versus homework exposure. In some CBT programs, therapy session time is
used for practicing exposure under the supervision of the therapist. In addition to this
“therapist-supervised exposure,” homework exposure—usually involving repeating
the same tasks practiced in session—is assigned for each day between sessions. In
other programs, session time is devoted only to planning and discussing exposure
assignments, which are carried out exclusively as homework assignments (self-directed
exposure). There are advantages of therapy programs using exclusively self-directed
exposure, including reduced therapist time. Self-directed exposure also circumvents
the problem of generalizing the effects of therapy from the treatment session to the
patient’s everyday environment. That is, the therapist’s presence during exposure can
serve as a safety signal and prevent the evocation of anxiety. For example, OCD
patients with compulsive checking rituals may experience fewer obsessional doubts
(e.g., of hitting pedestrians while driving) and urges to check (e.g., the roadside)
when accompanied by the therapist during exposures (e.g., driving through a business
district), as compared to when conducting such exposures on their own (Abramowitz,
2006; Tolin & Hannan, 2005).
On the other hand, confronting extremely frightening stimuli and resisting the
urge to carry out rituals is a demanding task that requires no small degree of courage.
It is to be expected that patients will at some point cut corners to avoid facing the
most frightening aspects of their exposure assignments. They might also prematurely
terminate the exposure if it becomes highly anxiety-provoking rather than remaining in
the situation until habituation occurs. Although these behaviors might not represent a
deliberate attempt to undermine the therapy, they can dilute the integrity of exposure
and lead to attenuated outcome. Thus, it is important that therapist supervision of
exposure occur at least to some degree to ensure the authenticity of exposure.
We suggest using a fading procedure in which the patient first practices and learns
how to conduct exposure correctly under the therapist’s careful supervision. Then,
the therapist gradually fades him- or herself from involvement in these exercises.
The patient learns to decide on exposure tasks, arrange them, and execute them
sufficiently. In our clinic we use both therapist-supervised and self-directed exposure.

Specifically, patients receive therapist-supervised exposure during most treatment
sessions, and the therapist assigns for homework the repetition of what was practiced
during the session. This allows the patient an opportunity to generalize what was
learned in session by affording him or her the opportunity to practice exposure in
varied contexts.
Full versus partial response prevention. Another common variant of ERP involves the
way in which response prevention is used. While some therapists insist that patients
stop all ritualizing during the entire time that they are in treatment, others use a partial
response prevention approach in which rituals are stopped during exposure sessions
and, perhaps, for a specific period of time afterward. Given the relationship between
response prevention and eventual reduction of the frequency and intensity of OCD
symptoms, it would seem important to encourage patients to target complete ritual
abstinence early on in treatment. At times, however, this goal may be inconsistent
with that of systematic, gradual exposure using a hierarchy. Indeed, patients may have
chance encounters with frightening stimuli which evoke high urges to ritualize, but
which have not yet been practiced in session. A related difficulty is that patients could
become demoralized if they feel overwhelmed, or think that they cannot achieve
complete ritual abstinence immediately. An alternative to full response prevention is
a graded approach in which instructions for stopping rituals parallel the progress up
the exposure hierarchy with the goal being complete ritual abstinence midway into
treatment.
Proposed Mechanisms of Change
Three potential mechanisms of change have been proposed to account for the
reduction of obsessions and compulsions during ERP. From a learning perspective,
ERP is thought to be effective because it provides an opportunity for the extinction
of conditioned fear responses. That is, repeated and uninterrupted exposure to feared
stimuli produces habituation—an inevitable natural decrease in conditioned fear.
Response prevention fosters habituation by blocking the performance of anxiety-
reducing behaviors (i.e., rituals) which would foil the habituation process. Extinction
of conditioned fear occurs when the obsessional stimulus is repeatedly paired with the
natural reduction of anxiety.
From a cognitive perspective, ERP is thought to correct dysfunctional beliefs that
underlie OCD symptoms, such as overestimates of threat and the importance of
intrusive thoughts, by presenting the patient with information that disconfirms these
beliefs. For example, when a patient confronts feared situations and refrains from
rituals, he or she finds out that feared outcomes such as disease or bad luck are
unlikely to occur. This evidence is processed and incorporated into the patient’s belief
system.
Finally, ERP is thought to help patients gain self-efficacy by demonstrating to them
that they have mastered their fears without having to rely on avoidance or safety
behaviors. The importance of this sense of mastery is an oft-overlooked effect of ERP.
Foa and Kozak (1986) have drawn attention to three indicators of change during
exposure-based treatment. First, physiological arousal and subjective fear must be
evoked during exposure. Second, the fear responses gradually diminish during the
exposure session (within-session habituation). Third, the initial fear response at
the beginning of each exposure session declines across sessions (between-sessions
habituation).
How Effective Is Cognitive Behavioral Therapy for

Obsessive-Compulsive Disorder?
Numerous studies of CBT for OCD have been conducted with thousands of patients
and hundreds of therapists in countries around the world. The treatment programs in
these studies have varied with respect to their emphasis on exposure versus cognitive
therapy, but most have included at least some elements of both. Randomized
controlled trials (RCTs) provide the most convincing evidence for the efficacy of
this treatment and consistently show the superiority of CBT over credible control
therapies such as progressive muscle relaxation training (e.g., Fals-Stewart, Marks, &
Shafer, 1993), anxiety management training (Lindsay, Crino, & Andrews, 1997),
and pill placebo (Foa et al., 2005). Studies have also found that CBT can be more
effective than serotonergic antidepressants often used in pharmacotherapy for OCD
(e.g., Foa et al., 2005). Symptom reduction rates across studies (as measured by the
Yale-Brown Obsessive-Compulsive Scale [YBOCS; Goodman et al., 1989a, 1989b])
typically fall in the 50–60% range, with most patients maintaining their gains long-
term and experiencing mild to moderate residual symptoms at follow-up. Thus,
despite clinically significant improvement, patients rarely achieve complete symptom
remission with CBT (Abramowitz, 1998).
Whereas most individuals with OCD exhibit overt compulsive rituals (e.g., washing,
checking), a substantial subset report severe obsessional symptoms in the absence of
observable compulsive behaviors (Abramowitz, Franklin, Schwartz, & Furr, 2003).
Patients with this presentation of OCD (sometimes called “pure obsessional” or
“pure-O”) typically perform mental rituals and other subtle anxiety-reduction strate-
gies to manage obsessional distress, but which might be difficult to distinguish from
obsessions. Accordingly, some experts have considered such patients nonresponsive
to CBT (Jenike, 1993). Freeston et al. (1997), however, developed and tested a
specialized CBT program for this OCD manifestation that involved psychoeducation,
cognitive techniques, and repeated imaginal exposure to descriptions of obsessional
thoughts (via audio recording) and abstinence from mental ritualizing. In a compar-
ison to wait-list, patients receiving this program improved more than 50% from pre-
to posttest, and maintained their gains at 3-month follow-up, while there was no
improvement in the wait-list group.
Group Cognitive Behavioral Therapy

The vast majority of studies evaluating the effects of CBT for OCD have focused on
individual treatment. Group CBT programs, however, have also proven effective in
reducing OCD symptoms (Anderson & Rees, 2007; Cordioli et al., 2003; McLean
et al., 2001). In one study, 12 weeks of group CBT emphasizing exposure therapy
was more effective than group therapy emphasizing cognitive therapy, although
both programs were more effective than wait-list (McLean et al., 2001). In another
investigation, group CBT resulted in significant improvement relative to wait-list,
and patients continued to improve at 3-month follow-up (Cordioli et al., 2003). In
the only study directly comparing individual and group CBT for OCD, Anderson
and Rees (2007) found that 10 weeks of either treatment format was more effective
than wait-list, but there were no differences between treatments. Therapy included
exposure and cognitive therapy techniques, and at posttest and follow-up, symptom
severity ranged from mild to moderate. The strengths of a group approach to CBT
for OCD include the support and cohesion of the group. Potential disadvantages,
however, include the relative lack of attention to each individual’s particular symptom
presentation, particularly given the heterogeneity of OCD.
Cognitive Behavioral Therapy as an Adjunct to Pharmacotherapy

Although pharmacotherapy is the most widely used treatment for OCD, the average
symptom reduction with the most potent agents (i.e., the serotonin reuptake inhibitors
[SRIs]) is only in the 20–40% range (e.g., Greist, Jefferson, Kobak, Katzelnick,
& Serlin, 1995). Thus, even an adequate SRI trial leaves patients with clinically
significant OCD symptoms. As a result, researchers have examined whether adding
CBT improves outcome following one or more adequate trials of an SRI. Tenneij,
van Megen, Denys, and Westenberg (2005), for example, randomly assigned 96
OCD patients on adequate medication trials to receive either 6 additional months
of their medication or CBT emphasizing ERP. Those who received ERP showed a
19% improvement in symptoms on average, while patients who continued on their
medication actually got worse (mean 21% increase in symptoms). Even medication
responders benefitted further from adjunctive CBT.
In another CBT augmentation study, Simpson et al. (2008) randomly assigned
108 OCD patients with clinically significant symptoms despite a 12-week adequate
SRI trial to receive either 17 sessions of CBT or stress management training while
continuing SRI pharmacotherapy. They found that CBT was superior to stress
management in reducing OCD symptoms. At week 8, significantly more patients
receiving ERP than receiving stress management training had a symptom decrease
of at least 25% and achieved scores in the mild range of the YBOCS. The clinical
implications of these findings are important because medication is the most widely
available and most widely used form of treatment for OCD, yet it typically produces
only modest benefits.
Effectiveness Studies
Although RCTs have yielded sound evidence for the efficacy of CBT for OCD,
this conclusion is based primarily on studies employing carefully selected patient
samples and highly trained therapists that are not representative of typical clinical
service settings. For example, despite the high frequency with which comorbid
conditions exist in patients with OCD, individuals with comorbid disorders (e.g.,
Axis II, major depression) are usually excluded from RCTs. Most therapists also do
not receive regular supervision from experts in the field. Thus, effectiveness studies
are designed to address such methodological concerns and examine the effects of
treatments in more representative patient samples treated in typical clinical settings.
The aim of effectiveness research is to bridge the gaps between research and clinical
practice.
In one such study, Franklin, Abramowitz, Kozak, Levitt, and Foa (2000) examined
outcome for 110 consecutively referred individuals with OCD who received 15
sessions of intensive CBT (daily ERP sessions) on an outpatient fee-for-service basis.
Half of this sample had comorbid Axis I or Axis II diagnoses and patients were only
denied CBT if they were actively psychotic, abusing substances, or suicidal (conditions
under which CBT is contraindicated). On average, these patients underwent a
60% reduction in OCD symptoms from pretest to posttest, and only 10 patients
dropped out of treatment prematurely. Warren and Thomas (2001) replicated these
results in a smaller study (N = 26) conducted within a private practice setting.
They reported a 50% symptom decrease from pre- to posttest. In a multicultural
naturalistic study, Friedman et al. (2003) found that whereas CBT was effective
in reducing OCD and depressive symptoms, many patients reported significant
residual symptoms after therapy. Taken together, the findings from these studies
indicate that CBT for OCD can be transported successfully from highly controlled
research settings to more routine clinical settings that serve representative patient
populations.
Predictors of Response
While exposure-based CBT is effective for most OCD patients who receive this
treatment, about 25–30% drop out of therapy prematurely. Among those who
remain in treatment, about 80% respond well, yet 20% or more do not. Therefore,
about 50% of patients referred with OCD are not significantly improved with CBT,
and it is important to consider this alongside the impressive data for this treatment’s
effectiveness. Next, we turn to a discussion of factors that predict response to CBT,
namely: (a) insight into OCD symptoms, (b) depression, and (c) family expressed
emotion.
Insight
As mentioned at the beginning of this chapter, individuals with OCD vary in the
degree to which they are able to recognize their obsessions and compulsions as
senseless and excessive. Foa, Abramowitz, Franklin, and Kozak (1999) found that
the presence of poor insight into the senselessness of obsessional fears was related
to poorer outcome following CBT. Perhaps patients with poor insight have great
difficulty learning and consolidating information that is inconsistent with their OCD
beliefs. Alternatively, because of their extreme fear, these patients might not adhere
to ERP instructions as closely as patients with better insight.
Comorbid Depression
Depression often co-exists with OCD (Ricciardi & McNally, 1995), and whereas
mild to moderate levels of depression do not appear to attenuate response to CBT,
Abramowitz, Franklin, Street, Kozak, and Foa (2000) found that severely depressed
OCD patients (i.e., those with a comorbid diagnosis of major depressive disorder) do
not respond as well. One explanation is that their high emotional reactivity interferes
with the normal pattern of habituation during exposure therapy. Thus, severely
depressed patients do not have the therapeutic experience of feeling comfortable
in the presence of feared stimuli, and therefore fail to learn that obsessive doubts
are unrealistic. Strongly held negative self-referent beliefs might also interfere with
cognitive therapy, and create motivational difficulties which make it difficult for such
patients to work hard at therapeutic exercises.
Expressed Emotion
The way in which family members respond to a loved one with OCD (or any
problem) is called expressed emotion (EE). EE can be conceptualized as emotional
overinvolvement, hostility, and perceived criticism. Chambless and Steketee (2000)
examined EE as a predictor of CBT outcome with OCD and found that hostility
was the most consistent predictor of poor response: When relatives were hostile
to the identified patient, the odds of dropping out of treatment were about six
times greater than when relatives were not hostile. Hostility was also associated with
poorer response in patients who completed treatment. Interestingly, once hostility
was statistically controlled, criticism had a positive effect. This suggests that when
relatives express dissatisfaction with patients’ symptoms, but do not express personal
rejection, criticism may have motivational properties that enhance treatment response.
This underscores the importance of educating family members about OCD and how
to assist therapeutically with CBT exercises during treatment. Our research group has
recently completed a study testing a couples-based CBT program for OCD in which
we trained patients’ partners/spouses to reduce their hostility and engage properly in
treatment (Abramowitz et al., in press; see also section on “Conclusions and Future
Directions”).
Case Example
Background
Kristen was a Caucasian 42-year-old graduate student enrolled in a Master of Business
Administration program at a local university. She had two young children and had
been happily married for 10 years. She presented to our clinic complaining of
frequent “inappropriate” thoughts about animals. Further evaluation revealed that
these thoughts were of a sexual nature and mostly pertained to dogs. She had
no history of substance abuse, sexual or physical abuse, or psychotic illness. She
did, however, report a history of OCD, describing a period in high school during
which she was “overly concerned” about germs. These concerns were accompanied
by compulsive behaviors such as excessive hand-washing and sanitization (e.g.,
wiping down surfaces with disinfectant), and avoidance behaviors such as opening
doors with her elbows and not using public restrooms. Although these symptoms
were initially distressing and time-consuming, they abated to subclinical levels in
college.
Assessment
Assessment began with a general clinical interview focusing on the onset and nature
of her symptoms. Kristen reported that her symptoms had begun the previous year,
shortly after her sister got a new Labrador puppy. Kristen was visiting her sister
and playing with the puppy when she first had an intrusive thought about touching
the puppy’s genitals. She was extremely upset by this thought and described it as
“repugnant.” The thoughts soon became more graphic and frequent, and they were
triggered by reminders of her sister and of dogs. By the time she came to our
clinic, she was avoiding anything that would remind her of dogs, including parks,
visiting her sister, and pet stores. The intrusive thoughts had also begun to occur
uncued while she was doing other activities such as watching television or studying.
These thoughts had become so frequent that she was having a great deal of difficulty
studying and her grades were suffering as a consequence. Kristen also reported feeling
guilty that she was not able to focus on her children when she was spending time
with them.
As part of the intake interview, the therapist also conducted a functional assessment
to identify any avoidance or compulsive rituals that Kristen was engaging in to reduce
anxiety related to her intrusions. Other than avoiding certain places and activities,
Kristen denied engaging in compulsive rituals. In fact, she reported that she had
diagnosed herself as having the “pure obsessions” form of OCD. Given that people
with OCD characterized by concerns about immorality or immoral thoughts often
engage in covert mental rituals (Abramowitz et al., 2010), the therapist asked Kristen
about mental rituals, specifically her frequent praying for forgiveness due to her
obsessional thoughts. She also imagined cleansing her body with fire after having
them in an attempt to reduce her distress. When the therapist clarified the precise
reasons that Kristen was avoiding dogs, Kristen revealed that rather than a fear of
dogs per se, she was afraid that interacting with dogs would provoke the unwanted
sexual thoughts.
In addition to the functional assessment, the therapist inquired about Kristen’s
beliefs about the nature and importance of thoughts. Kristen reported that her
intrusive thoughts prompted her to feel that she was a bad person and worry that she
might actually want to act on them. She was also afraid she was more likely to engage
in sexual behaviors with dogs as a consequence of having such thoughts. Kristen
further stated that she wanted to know with one hundred percent certainty that she
did not want to act on these thoughts and that they did not mean anything about her
morally.
Treatment
Kristen was enrolled in our clinic’s twice-weekly CBT program for OCD. The first
two treatment sessions focused on psychoeducation about the nature of OCD and
involved planning for exposure therapy and goal setting.
Session 1. During the first session the therapist normalized the experience of intrusive
thoughts by providing common examples that most people report experiencing (e.g.,
thoughts about screaming in church, or driving one’s car off the road). The therapist
also explained that intrusive thoughts were like “mental noise” and that it is only
when a person ascribes importance to them that they become anxiety-provoking.
Specifically, the therapist helped Kristen to understand how her dysfunctional beliefs
make these otherwise meaningless thoughts seem very frightening and important.
Kristen recognized that her thoughts about dogs had become anxiety-provoking
because of how worried she was that they meant something about her as a
person.
Throughout this session and subsequent interactions with the therapist, Kristen
continued to seek reassurance that having the thoughts did not mean that she was
a bad person. Because reassurance seeking can function to maintain distress in the
long term, the therapist encouraged Kristen to recall their previous conversations and
answer her own questions (i.e., “Based on our previous conversations, what do these
thoughts mean about you as a person?”). The therapist also explained that they would
be using ERP to treat Kristen’s OCD and that they would discuss this further in the
next session.
Session 2. During the treatment planning phase, Kristen stated that she wanted to, “get
rid of the thoughts” and that this would be the only successful outcome of treatment.
It is common for patients with OCD to believe that the only way to reduce their
distress is by eliminating their obsessional thoughts altogether (Abramowitz, 2006).
This is problematic because it encourages thought suppression attempts and increases
frustration with therapy when the therapist asks patients to engage in activities that will
initially increase the frequency of intrusions. Thus, the therapist explained to Kristen
about the problems with thought suppression. Specifically, she illustrated how people
are generally not successful at thought suppression, and that the act of attempting to
suppress a thought implies that the thought is bad or dangerous. She explained that
a more effective strategy for reducing Kristen’s anxiety would be to help her confront
her intrusive thoughts without using mental rituals, escape, or avoidance to reduce
her fear in the short term.
The therapist then explained how ERP is thought to reduce OCD symptoms.
Specifically, she enlisted Kristen’s assistance to develop a model of her own idiosyn-
cratic obsessions and rituals, explaining how the rituals paradoxically increase the
frequency of Kristen’s intrusions by making them seem more threatening and by
serving as reminders of the intrusions. For example, they identified that praying about
the thoughts reminded Kristen of the very thoughts she was trying to dismiss, thus
increasing the frequency of intrusions. The therapist then explained the concept of fear
habituation and how exposure helps people to recognize that the intrusive thoughts
themselves are not dangerous and that the anxiety they provoke will naturally subside
if the individual refrains from neutralizing.
Session 3. The third session was dedicated to developing a fear hierarchy that graduated
from situations Kristen felt would provoke only moderate anxiety (e.g., going to her
sister’s house, seeing dogs on television) to those she believed would evoke extreme
anxiety (e.g., allowing herself to have the unwanted sexual thoughts while in the
presence of a dog, being licked by a dog, touching a dog’s stomach). The therapist
explained that Kristen was the “expert” on her own OCD symptoms, and that it would
be important for her to participate actively in identifying scenarios and situations that
would provoke anxiety for her. Collaboratively they generated a list of situations and
assigned each a rating on a Subjective Units of Distress scale (SUDs) from 0 (not at
all anxiety-provoking) to 100 (intensely anxiety-provoking). Using these ratings, they
created an ordered list of exposure activities for Kristen to complete. The therapist
emphasized that they would only move up the hierarchy as Kristen mastered lower
levels.
Sessions 4–10. Given that Kristen’s anxiety was provoked by both thoughts and
environmental stimuli, her hierarchy involved both imaginal and situational exposure
exercises. For example, many of the early exposure exercises involved imaginal
exposure to the thoughts without engaging in mental neutralizing behaviors (e.g.,
prayer). The therapist helped Kristen to write scripts that described her more vivid
dog-related intrusions. These were then read aloud and recorded on a digital voice
recorder for loop play back. Initially in session, and then at home, Kristen listened
to the recordings and allowed the thoughts to come to mind without pushing them
away or using mental rituals. During the in-session exposures, the therapist helped
Kristen monitor herself for subtle avoidance strategies such as letting her mind wander
to other topics. They also used the SUDs ratings to track Kristen’s anxiety before,
during, and after each exposure at 5-minute intervals. The therapist encouraged
Kristen to continue with each exposure practice until her fear had dropped at least
50% from her highest or “peak” fear level.
Once Kristen understood the concept of how to conduct effective exposure
exercises, she was assigned homework practice. For example, after session 5 she was
asked to practice two to three times daily with the audio recording. As Kristen
progressed and her mastery of the concepts of ERP increased, she was encouraged
to design her own exposure exercises at home and to take advantage of natu-
rally occurring exposure opportunities (e.g., seeing a dog in the park while out
jogging).
In addition to continuing in-session exposure exercises throughout therapy, the
therapist also used cognitive therapy strategies such as Socratic questioning techniques
to help Kristen challenge her maladaptive beliefs about the need for certainty. For
example, Kristen struggled with the need for a guarantee that on some level she
did not really want to engage in sexual activities with animals. Her therapist asked
questions to explore the concept of uncertainty and illustrate that uncertainty is
ubiquitous. For example, they discussed the idea that neither Kristen nor the therapist
knew for certain whether they would have a car accident on their way home from the
session; and yet both assumed they would be safe. The point of this exercise was to
show Kristen that she can manage acceptable levels of uncertainty, and in fact does
so on a daily basis. Kristen was encouraged to generalize this to her own experiences
with intrusive thoughts.
Kristen responded favorably to treatment, showing a significant decrease in the
frequency of her intrusions and her level of distress associated with them. By session 8
they began working toward consolidating Kristen’s treatment gains and planning for
treatment termination. Termination planning involved spending time helping Kristen
to summarize what she learned over the course of treatment. For example, she was able
to articulate that she was “certain enough” that she did not wish to engage in sexual
acts with dogs. She could also recognize that accepting some degree of uncertainty was
both necessary and possible. Kristen and the therapist also spent time reviewing the
core principles of ERP and how to design exposure exercises if novel obsessions arose
in the future. The therapist also assisted Kristen in identifying idiosyncratic cues which
might warn of an impending relapse in symptoms. For example, Kristen noted that one
of the early warning signs of her present episode was withdrawing from her husband
sexually. Finally, they discussed circumstances which might mean Kristen would want
to seek further therapy in the future. The therapist encouraged Kristen to recognize
that knowing when to seek further therapy was a strength, rather than a sign of failure.
Summary and Future Directions
As illustrated in the case example above, CBT is the most effective short- and
long-term treatment for OCD. These encouraging findings notwithstanding, full
remission is not the standard. Evidence from effectiveness studies also suggests
that this approach is transportable to nonresearch settings, and therefore should
be a “first-line” treatment modality for OCD in all settings. Although response to
treatment is highly variable, we are beginning to uncover factors that may reliably
predict poorer response, such as poor insight into the senselessness of obsessional
fears, severe depression, and family hostility.
Although the research to date has addressed many critical issues in the treatment of
OCD, there are still important topics that require further study. For example, given
how patients’ family members are often involved in OCD symptoms by taking part in
avoidance or rituals, or by providing reassurance, it is important to develop treatments
that help teach family members about OCD and its treatment, and then train them
in how to assist effectively with a loved one’s therapy. Couple-based CBT for OCD
(Abramowitz et al., ) might involve partner-assisted exposure therapy, helping the
couple work to reduce behaviors that function to accommodate or reinforce OCD
symptoms, as well as general couples therapy to enhance communication and reduce
general stress levels.
It is also important to develop and test motivational (“readiness”) programs to
help individuals with a great deal of ambivalence about getting started in treatment
resolve their ambivalence in a way that helps them see that the advantages of reducing
their symptoms outweigh the anxiety-evoking nature of ERP, which is often a
roadblock. Providing access to case histories, or even to former patients who can
discuss what treatment is like, might decrease refusal rates and increase treatment
compliance. Finally, providing successful CBT for OCD can be a challenge, and
very few centers offer the training needed to become proficient in these procedures.
Therefore, development of programs for psychology and psychiatry trainees might
improve access to this effective therapy.
References
Abramowitz, J. S. (1998). Does cognitive-behavioral therapy cure obsessive-compulsive disor-
der? A meta-analytic evaluation of clinical significance. Behavior Therapy, 29, 339–355.
doi: 10.1016/S0005-7894(98)80012-9
Abramowitz, J. S. (2006). Understanding and treating obsessive-compulsive disorder: A cognitive-
behavioral approach, Mahwah, NJ: Erlbaum.
Abramowitz, J. S. (2011). Obsessive-compulsive disorder and comorbid mood disorders. In
R. Hudak & D. D. Dougherty (Eds.), Clinical obsessive-compulsive disorder in adults and
children (pp. 61–70). Cambridge, England: Cambridge University Press.
Abramowitz, J. S., Baucom, D. H., Wheaton, M. G., Boeding, S., Fabricant, L. E., Paprocki,
C., & Fischer, M. S. (in press) Enhancing exposure and response prevention for OCD: A
couple-based approach. Behavior Therapy. doi: 10.1016/j.beth.2013.02.005
Abramowitz, J. S., Deacon, B., Olatunji, B., Wheaton, M. G., Berman, N., Losardo, D., …
Hale, L. (2010). Assessment of obsessive-compulsive symptom dimensions: Development
and evaluation of the Dimensional Obsessive-Compulsive Scale. Psychological Assessment,
22, 180–198. doi:10.1037/a0018260
Abramowitz, J. S., Foa, E. B., & Franklin, M. E. (2003). Exposure and ritual prevention for
obsessive-compulsive disorder: Effects of intensive versus twice-weekly sessions. Journal
of Consulting and Clinical Psychology, 71, 394–398. doi: 10.1037/0022-006X.71.2.394
Abramowitz, J. S., Franklin, M., Schwartz, S., & Furr, J. (2003). Symptom presentation and
outcome of cognitive-behavioral therapy for obsessive-compulsive disorder. Journal of
Consulting and Clinical Psychology, 71, 1049–1057. doi: 10.1037/0022-006X.71.6.1049
Abramowitz, J., Franklin, M., Street, G., Kozak, M., & Foa, E. (2000). Effects of comorbid
depression on response to treatment for obsessive-compulsive disorder. Behavior Therapy,
31, 517–528. doi: 10.1016/S0005-7894(00)80028-3
Anderson, R. A., & Rees, C. S. (2007). Group versus individual cognitive-behavioural treatment
for obsessive-compulsive disorder: A controlled trial. Behaviour Research and Therapy, 45,
123–137. doi: 10.1016/j.brat.2006.01.016
Chambless, D. L., & Steketee, G. (2000). Expressed emotion and behavior therapy outcome:
A prospective study with obsessive-compulsive and agoraphobic outpatients. Journal of
Consulting and Clinical Psychology, 67 , 658–665.
Clark, D. A. (2004). Cognitive-behavioral therapy for OCD, New York, NY: Guilford Press.
Cordioli, V., Heldt, A., Braga, E., Bochi, D., Margis, R., Basso de Sousa, M., … Kapczin-
ski, F. (2003). Cognitive-behavioral group therapy in obsessive-compulsive disorder: A
randomized clinical trial. Psychotherapy and Psychosomatics, 72, 211–216. doi:10.1159/
000070785
Emmelkamp, P. M. G., & Kraanen, J. (1977). Therapist-controlled exposure in vivo versus self-
controlled exposure in vivo: A comparison with obsessive-compulsive patients. Behaviour
Fals-Stewart, W., Marks, A. P., & Schafer, J. (1993). A comparison of behavioral group therapy
and individual behavior therapy in treating obsessive-compulsive disorder. Journal of
Nervous and Mental Disease, 181, 189–193. doi:10.1097/00005053-199303000-00007
Foa, E. B., Abramowitz, J. S., Franklin, M. E., & Kozak, M. J. (1999). Feared consequences,
fixity of belief, and treatment outcome in patients with obsessive-compulsive disorder.
Behavior Therapy, 30, 717–724. doi: 10.1016/S0005-7894(99)80035-5
Foa, E. B., & Goldstein, A. (1978). Continuous exposure and complete response prevention
in the treatment of obsessive-compulsive neurosis. Behavior Therapy, 9, 821–829.
Foa, E. B., & Kozak, M. (1986). Emotional processing of fear: Exposure to corrective
Foa, E. B., Liebowitz, M. R., Kozak, M. J., Davies, S., Campeas, R., Franklin, M. E., … Tu, X.
(2005). Treatment of obsessive-compulsive disorder by exposure and ritual prevention,
clomipramine, and their combination: A randomized, placebo controlled trial. American
Journal of Psychiatry, 162, 151–161. doi:10.1176/appi.ajp.162.1.151
Franklin, M. E., Abramowitz, J. S., Kozak, M. J., Levitt, J., & Foa, E. B. (2000). Effectiveness of
exposure and ritual prevention for obsessive-compulsive disorder: Randomized compared
with nonrandomized samples. Journal of Consulting and Clinical Psychology, 68, 594–602.
doi: 10.1037/0022-006X.68.4.594
Freeston, M. H., Ladouceur, R., Gagnon, F., Thibodeau, N., Rheaume, J., Letarte, H., &
Bujold, A. (1997). Cognitive-behavioral treatment of obsessive thoughts: A controlled
study. Journal of Consulting and Clinical Psychology, 65, 405–413. doi: 10.1037/0022-
006X.65.3.405
Friedman, S., Smith, L. C., Halpern, B., Levine, C., Paradis, C., Viswanathan, R., … Ackerman,
R. (2003). Obsessive-compulsive disorder in a multi-ethnic urban outpatient clinic: Initial
presentation and treatment outcome with exposure and ritual prevention. Behavior
Therapy, 34, 397–410. doi:10.1016/S0005-7894(03)80008-4
Goodman, W. K., Price, L. H., Rasmussen, S. A., Mazure, C., Fleischmann, R. L., Hill, C. L., …
Charney, D. S. (1989a). The Yale-Brown Obsessive Compulsive Scale, I: Development,
use, and reliability. Archives of General Psychiatry, 46, 1006–1011.
Goodman, W. K., Price, L. H., Rasmussen, S. A., Mazure, C., Delgado, P., Heninger, G. R.,
& Charney, D. S. (1989b). The Yale-Brown Obsessive Compulsive Scale, II: Validity.
Greist, J. H., Jefferson, J. W., Kobak, K. A., Katzelnick, D. J., & Serlin, R. C. (1995). Efficacy
and tolerability of serotonin transport inhibitors in obsessive compulsive disorder: A
meta-analysis. Archives of General Psychiatry, 52, 53–60.
Hodgson, R., Rachman, S., & Marks, I. (1972). The treatment of chronic obsessive-compulsive
neurosis: Follow-up and further findings. Behaviour Research and Therapy, 10, 181–189.
Jenike, M. A. (1993). Obsessive-compulsive disorder: Efficacy of specific treatments as assessed
by controlled trials. Psychopharmacology Bulletin, 29, 487–499.
Kessler, R., Berglund, P., Demler, O., Jin, R., Merikangas, K. R., & Walters, E. E. (2005).
Lindsay, M., Crino, R., & Andrews, G. (1997). Controlled trial of exposure and response
prevention in obsessive-compulsive disorder. British Journal of Psychiatry, 171, 135–139.
doi: 10.1192/bjp.171.2.135
McLean, P. D., Whittal, M. L., Thordarson, D. S., Taylor, S., Sochting, I., Koch, W. J., …
Anderson, K. W. (2001). Cognitive versus behavior therapy in the group treatment
of obsessive-compulsive disorder. Journal of Consulting and Clinical Psychology, 69,
205–214. doi:10.1037/0022-006X.69.2.205
Meyer, V. (1966). Modification of expectations in cases with obsessional rituals. Behaviour
Meyer, V., Levy, R., & Schnurer, A. (1974). The behavioral treatment of obsessive-compulsive
disorders. In H. R. Beech (Ed.), Obsessional states (pp. 233–258). London, England:
Methuen.
Mowrer, O. (1960). Learning theory and behavior, New York, NY: John Wiley & Sons, Inc.
Rabavilas, A., Boulougouris, J., & Stefanis, C. (1976). Duration of flooding sessions in
the treatment of obsessive-compulsive patients. Behaviour Research and Therapy, 14,
349–355.
Rachman, S. (1997). A cognitive theory of obsessions: Elaborations. Behaviour Research and
Therapy, 36, 385–401.
Ricciardi, J. N., & McNally, R. J. (1995). Depressed mood is related to obsessions but not
compulsions in obsessive-compulsive disorder. Journal of Anxiety Disorders, 9, 249–256.
doi: 10.1016/0887-6185(95)00006-A
Salkovskis, P. M. (1985). Obsessional-compulsive problems: A cognitive-behavioural analysis.
Salkovskis, P. M. (1996). Cognitive-behavioral approaches to the understanding of obsessional
problems. In R. Rapee (Ed.), Current controversies in the anxiety disorders (pp. 103–133).
Simpson, H. B., Foa, E., Liebowitz, M., Ledley, D., Huppert, J., Cahill, S., … Hahn, C.
(2008). A randomized controlled trial of cognitive-behavior therapy for augmenting
pharmacotherapy in obsessive-compulsive disorder. American Journal of Psychiatry, 165,
621–630. doi:10.1176/appi.ajp.2007.07091440
Steketee, G. (1993). Treating obsessive-compulsive disorder, New York, NY: Guilford Press.
Tenneij, N., van Megen, H., Denys, D., & Westenberg, H. (2005). Behavior therapy augments
response of patients with obsessive-compulsive disorder responding to drug treatment.
Tolin, D. F., & Hannan, S. (2005). The role of the therapist in behavior therapy for OCD. In
J. S. Abramowitz & A. C. Houts (Eds.), Concepts and controversies in obsessive-compulsive
disorders (pp. 317–332). New York, NY: Springer.
Warren, R., & Thomas, J. C. (2001). Cognitive-behavior therapy of obsessive-compulsive
disorder in private practice: An effectiveness study. Journal of Anxiety Disorders, 15,
277–285.
Wilhelm, S., & Steketee, G. (2006). Cognitive therapy for obsessive-compulsive disorder,
Oakland, CA: New Harbinger.
45
Tourette Syndrome and Tic
Disorders
Matthew R. Capriotti, Flint M. Espil,
and Douglas W. Woods
University of Wisconsin-Milwaukee, United States
Tourette Syndrome and Tic Disorders
Tourette syndrome (TS) has a tumultuous history within the field of psychology.
Early psychoanalytic efforts to treat TS were aimed at resolving the supposed root
psychological conflict causing tics (Kushner, 1999). In the 1970s, biological treat-
ments came into favor, as it was discovered that TS could be successfully managed
with antipsychotics (Shapiro & Shapiro, 1968). This biological conceptualization of
TS became prominent throughout the last quarter of the twentieth century, although
behavioral psychologists continued to develop and test interventions aimed at teach-
ing tic management strategies and minimizing the effects of contextual factors on
the expression of tics. The last two decades have seen a surge of research on these
behavioral interventions (see reviews by Bate, Malouf, Thorsteinsson, & Bhullar,
2011; Cook & Blacher, 2007; Himle, Woods, Piacentini, & Walkup, 2006) and
a unification of biological and behavioral views of TS into a more unitary biobe-
havioral conceptualization of tic disorders (e.g., Conelea & Woods, 2008; Lavoie,
Imbriglo, Stip, & O’Connor, 2011; Piacentini et al., 2010; Wang et al., 2011;
Woods, Piacentini, Himle, & Chang, 2005). At present, cognitive behavioral ther-
apy (CBT) for TS has earned recognition as an efficacious, acceptable, and durable
treatment option. This chapter reviews information about TS and common comorbid
conditions, summarizes the evidence base of CBT strategies that have (and have
not) proven efficacious, and presents information on evidence-based assessment and
treatment tactics.

DOI: 10.1002/9781118528563.wbcbt45
Tourette Syndrome: Epidemiology and Phenomenology
Definition, Prevalence, and Course

Tics are rapid, unintentional movements or vocalizations that occur frequently.
Between 2% and 20% of children have at least one tic for a month or longer at some
point in their lives (Costello et al., 1996). For most, these tics are benign, transient
phenomena that cause little distress or change in daily functioning. A majority of these
children quickly “outgrow” their tic(s), thus never attaining a diagnosis of chronic tic
disorder or TS (Costello et al., 1996).
For some, tics may persist over an extended period of time, become more numerous
and intense, and cause significant distress and functional impairment. This pattern
of persistent, chronic, difficult-to-deal-with tics represents the various tic disorders
described in the Diagnostic and Statistical Manual of Mental Disorders (4th ed., text
rev.; DSM-IV-TR; American Psychiatric Association, 2000). TS, the most prevalent
and well-known tic disorder, involves the presence of multiple motor tics and at least
one vocal tic over a period of one year or longer. If a patient has a history solely
of motor or vocal tics, a diagnosis of chronic motor tic disorder or chronic vocal tic
disorder is given. In cases where tics have not been present for one year or longer,
but are causing significant distress and/or impairment, a diagnosis of transient tic
disorder may be given.
The lifetime prevalence of TS appears to be between 0.4% and 3.8% (Robertson,
2008), indicating that the disorder is much more prevalent than once thought. The
disorder occurs more commonly in males than females, with most studies finding
a gender ratio between two-to-one and six-to-one (Coffey et al., 2000; Kadesjo &
Gillberg, 2000). Tics most often begin around age 5 or 6 (Leckman et al., 1998).
In those whose tics continue, symptoms become more severe throughout childhood
and early pubertal stages, usually peaking in severity between ages 10 and 12. As
children with TS transition into early adulthood, tics tend to become less severe. One
longitudinal study (Leckman et al., 1998) found that 57% of individuals with a history
of TS were nearly or completely tic free by age 18. However, 27% of those assessed
continued to experience fairly moderate tic symptoms, and 11% experienced severe
symptoms. Unfortunately, few predictors of future remission have been identified,
although some evidence suggests that children with poor fine motor abilities have
a somewhat poorer prognosis in regard to future tic severity (Bloch, Sukhodolsky,
Leckman, & Schultz, 2006).
While some important questions still remain as to the precise developmental
trajectory of TS, it is clear the disorder tends to remit spontaneously in many
individuals. It is important for both patients and clinicians to understand the variability
in patterns of remission, as well as the fact that tics tend to wax and wane across
periods of weeks and months (Leckman et al., 1998).
Tourette Syndrome and Tic Disorders 1065
Phenomenology and Tic-Related Urges

Although tics are the defining symptoms of TS and other tic disorders, virtually all
adolescents and adults with chronic tic disorders (CTDs) experience uncomfortable
somatosensory sensations prior to the tics (i.e., “premonitory urges”) that remit
temporarily when a tic is performed (Leckman, Walker, & Cohen, 1993). These
premonitory urges have been reported to begin around the age of 10 (Leckman et al.,
1993) but may occur earlier (Woods et al., 2005) and are believed to play a central role
in the expression of tics (Conelea & Woods, 2008; Kane, 1994; Leckman et al., 1993;
Scahill, Leckman, & Marek, 1995). Consistent with these findings, patients often
report that tics are not “involuntary” actions, but rather “semivoluntary” behaviors
that occur in response to premonitory urges (Koller & Biary, 1989). Understanding
these urges is important for CBT practitioners, because (a) the urges can cause
substantial distress in their own right (Kane, 1994; Leckman et al., 1993), (b) urges
play a key role in administering CBT-based treatments for CTDs, and (c) reducing
premonitory urges and/or one’s behavioral response when the urge arises may be a
key change mechanism in treating CTDs using CBT.
Comorbidity
Individuals with CTDs often present with other Axis I psychopathology. Attention-
deficit/hyperactivity disorder (ADHD) and obsessive-compulsive disorder (OCD)
have been discussed as the most common comorbidities associated with CTDs. In
a review of a large, international sample of over 6,800 children with CTDs, Freeman
et al. (2000) found that 55% of children also had ADHD. Three large-scale epidemi-
ological studies (Kadesjo & Gillberg, 2000; Khalifa & von Knorring, 2003; Scahill,
Bitsko, Visser, & Blumberg, 2009) found that 64–68% of children also met diagnostic
criteria for ADHD. Two of these studies also investigated the prevalence of OCD
among children with CTDs and found higher rates than in the pediatric population at
large. Kadesjo and Gillberg (2000) found a 38% prevalence rate of OCD in children
with a CTD, and Khalifa and von Knorring (2006) noted a 10% coincidence. The
discrepancy in these figures likely stems from the fact that in the latter study OCD was
diagnosed only when full diagnostic criteria were met, while in the former study an
OCD diagnosis was conferred on the basis of two or more parent-reported compulsive-
type behaviors. Additionally, recent evidence suggests that the prevalence of these two
conditions among individuals with CTDs may be somewhat lower among those who
present for psychological treatment of their tics (26% for ADHD and 19% for OCD;
Specht et al., 2011). Specht et al. (2011) found that social anxiety and generalized
anxiety disorder were also highly prevalent among the pediatric sample (20% and 21%,
respectively). Other studies (e.g., Kadesjo & Gillberg, 2000; Scahill et al., 2009) have
also noted relatively high rates of anxiety and other problems within CTD populations,
but have assessed these issues less systematically. Although questions remain as to the
“true” rates of Axis I comorbidities in patients with CTDs, it is clear that clinicians
must be prepared to treat CTDs in the context of ADHD, OCD, and other anxiety
disorders.
Differential Diagnosis
In most cases, a patient with a suspected tic disorder should be evaluated by a neurol-
ogist or psychiatrist trained in movement disorders before CBT is recommended. Tics
can often be confused with other neurological or psychiatric conditions; thus is it is
imperative to obtain an accurate diagnostic profile. Below, we briefly review common
questions regarding the differential diagnosis of tics and other disorders.
Stereotypy versus tics. Stereotypies are rhythmic, repetitive behaviors that can include
movements and vocalizations. Often believed to occur almost exclusively in children
with autism spectrum disorders and other developmental disabilities, stereotypies
have also been noted to occur in typically developing children (Harris, Mahone, &
Singer, 2008; J. M. Miller, Singer, Bridges, & Waranch, 2006). In this latter group
of individuals, the movements may be confused with tics and lead patients to seek
treatment for CTDs. Practitioners can distinguish tics from stereotypies in a number
of ways. First, stereotypies often occur continuously for a period of many seconds
or minutes at a time, whereas tics tend to occur in several seconds or less. Second,
stereotypies are experienced as pleasurable and are rarely preceded by somatosensory
urges (Singer, 2009), whereas tics are most often described as unwanted movements
that “must” be done to alleviate aversive sensations (Leckman et al., 1993). Finally,
stereotypies tend to onset early in development (81% of stereotypies in typically
developing children onset by age 2; Harris et al., 2008), whereas tics typically onset
around ages 5–6 (Leckman et al., 1998). Distinguishing between tics and stereotypies
is important for diagnosis and case conceptualization, but research suggests that
behavioral interventions delivered on an outpatient basis can be effective in treating
stereotypies in typically developing individuals (Miller et al., 2006; Ricketts et al.,
2013).
Obsessive-compulsive disorder versus tics. Another common difficulty in differential

diagnosis arises when trying to determine whether a particular behavior is a complex
tic or a compulsion associated with OCD. For instance, a patient who repetitively taps
on surfaces may be demonstrating a complex tic (i.e., a multipart tic that resembles a
purposive act) or a compulsion (i.e., a behavior that is performed to alleviate distress
associated with anxiety and/or obsessive cognitions). These two classes of behavior
are differentiated in a number of ways. First, complex motor tics generally appear at
a later age than simple tics (e.g., eye blinking, facial twitches; Leckman et al., 1998).
Thus, in patients with no history of simple tics, complex repetitive behaviors are most
likely associated with OCD or stereotypic movement disorder.
Second, in those with co-occurring CTD and OCD, complex movements can
be categorized by the feelings and/or thoughts the patient experiences before the
occurrence. Complex tics are often associated with a vague somatosensory urge to
engage in the behavior, whereas compulsions are typically preceded by physiological

signs of anxiety (e.g., sweating, increased heart rate) or specific cognitions (e.g., “My
family will be harmed if I don’t tap on this table”; Miguel, Coffey, Baer, & Savage,
1995). It is worth noting that the question of differentiating between complex tics
and the “not just right” subtype of OCD is not yet well established. Indeed, based on
current definitions in the literature, informed clinicians might differ in their diagnostic
opinions of such a movement (Miguel et al., 1995). However, concerns surrounding
this issue are mitigated by the fact that exposure-based treatment approaches are
likely to be similarly effective for both complex tics and “not just right” compulsions
(Abramowitz, 1997; March, Franklin, Nelson, & Foa, 2001; Verdellen, Keijsers,
Cath, & Hoogduin, 2004).
Tics versus other movement disorders. Psychologists who work with individuals with
tics must also have a working knowledge of other movement disorders that involve
involuntary motor and vocal acts. These include Sydenham’s chorea, myoclonus,
and fasciculations. In general, these movements can be distinguished from tics
by their phenomenology, degree of interference with volitional movements, and
suppressibility. Tics are generally accompanied by some sort of premonitory sensation
or “urge,” are usually “overridden” by intentional movements, and can be suppressed
briefly. In contrast, movements associated with these other neurological conditions
occur without sensory signals or urges, often interfere with voluntary movements, and
cannot be suppressed (Singer, Mink, Gilbert, & Jankovic, 2010). Differentiating tics
from these other types of movements is critical to ensuring good patient outcomes.
Behavioral interventions have not been shown to be effective for treating these
movements, while prognosis is generally quite good if appropriate pharmacotherapy
is received (Singer et al., 2010). Additionally, some disordered movements can be a
signal of other neurological problems (e.g., brain tumors, encephalitis), necessitating
appropriate referral if such movements are present.
Neurobehavioral Models of Compulsive Tic Disorder

Etiology, Maintenance, and Clinical Change Mechanisms
To date, research suggests that tics and CTDs involve a dynamic, complex interaction
of biological and environmental influences. Evidence suggests that tics initially arise
from neurobiological dysfunction involving abnormalities in cortico-striatal-thalamo-
cortical circuits involved in motor planning and response selection (Mink & Pleasure,
2003; Wang et al., 2011). In persons with CTDs, multiple studies have found
decreased volume of structures in the basal ganglia, which are involved in selection of
motor acts (Peterson et al., 2003). Such results suggest that dysfunction of the brain’s
first-line mechanisms for inhibiting unwanted motor responses may be impaired in
people with CTDs. Research has also identified neural correlates of compensatory
mechanisms (i.e., voluntary tic suppression). For instance, Baym, Corbett, Wright,
and Bunge (2007) have found that people with CTDs exhibit enhanced “top-down”
control of motor acts, and higher frontal lobe activation during tasks requiring
effortful control.
Although neuroscience research has elucidated neural mechanisms central to CTD,

it is clear that environmental factors play a large role in CTD expression and
maintenance. Various studies have identified robust environmental influences on tic
expression (for a review, see Conelea & Woods, 2008), including both antecedents
and consequences surrounding ticcing. Both observable or “public” events, as well as
internal or “private” events, have been found to affect tic expression. In terms of the
effects public events have on tics, several studies have shown that tic-contingent social
attention and escape from task demands can inadvertently reinforce tics (Carr, Taylor,
Wallander, & Reiss, 1996; Scotti, Schulman, & Hojnacki, 1994; Watson & Sterling,
1998). Likewise, antecedent “triggers” of tics can include certain people, places, or
activities where tics are more likely to happen (e.g., a child sitting down to take an
exam).
In addition to public factors, it appears that “private” factors occurring within the
patient’s body also exert a significant influence on tic maintenance and expression.
As discussed earlier, premonitory urges are centrally important to tic expression, as
performing a tic brings about a temporary decrease in their strength. Functionally,
the urge can be thought of as a reflexive establishing operation (J. Michael, 2000),
in that its presence establishes its removal as reinforcing. Upon noticing the aversive
premonitory urge, individuals are cued to perform a tic in order to terminate it. This
is consistent with findings from a recent functional magnetic resonance imaging study
that found increased activation of the amygdala, hippocampus, and somatosensory
cortex to coincide with the premonitory urge experience (Wang et al., 2011). These
converging lines of evidence from neuroimaging and behavioral research provide
robust evidence of the emotional and sensory salience of the urge experience, the
reinforcing value of its alleviation, and the likely importance of the premonitory urge
as a proximal determinant of tic expression.
Mechanisms of Change
Various lines of evidence about CTD phenomenology and treatment suggest potential
mechanisms through which clinically significant change might be achieved.
Perhaps the most obvious target for decreasing tic severity is to correct the
neurobiological dysfunction that comprises the fundamental neurobiologic cause of tic
expression. Typically, this has been attempted by prescribing neuroleptic medications
(e.g., risperidone, olanzapine, haloperidol; Harrison, Schneider, & Walkup, 2007).
Neuroleptic pharmacotherapy has proven efficacious in decreasing tic severity (for a
review, see Pringsheim et al., 2012), but often carries substantial side effects that
cause many to discontinue treatment (Silva, Muñoz, Daniel, Barickman, & Friedhoff,
1996).
The behavioral model of CTDs suggests two primary avenues through which CBT
can affect clinical change. The first involves altering social consequences that may be
functioning as reinforcers for ticcing. As discussed above, these factors can include tic-
contingent attention (social positive reinforcement) and tic-contingent escape from
aversive tasks (social negative reinforcement). For instance, a parent might respond
to a child’s loud coughing tic by consoling him or her. Although this arises from the
parent’s understandable desire to support his or her child, it may indeed function as a
reinforcing social consequence for the coughing tic (for a similar case, see Watson &
Sterling, 1998). Alternatively, when a child tics during algebra class, he or she might
be allowed to leave the classroom to “let the tics out.” This situation could serve as
a negative reinforcement loop, in which the child’s ticcing produces escape from an
aversive activity (sitting in algebra class), thereby making the tic more likely to occur
in the future. By identifying and altering these types of patterns in the patient’s daily
life, clinicians can work to minimize inadvertent socially mediated reinforcement of
ticcing.
The second primary environmental mechanism for change in CBT involves altering
internal or “private” events that also establish tics as reinforcing. Ticcing is known
to produce temporary relief from premonitory urges (Bullen & Hemsley, 1983;
Leckman et al., 1993). This process can be described as an automatic negative
reinforcement contingency (Miltenberger, 2005), wherein the urge functions as a
reflexive establishing operation, or a stimulus whose mere presence serves as motivation
for its removal (Michael, 2000). Clinicians may attempt to alter this relationship by
taking steps to decrease the perceived magnitude of the negative reinforcer (i.e.,
the premonitory urge). This can be accomplished directly by providing experiences
where the client experiences these urges for a prolonged period (several minutes)
without ticcing (Verdellen, Hoogduin, & Keijsers, 2007). It may also be possible
to teach coping strategies that lessen the perceived magnitude of the urge, and,
subsequently, the patient’s motivation to perform a tic. In the next section, we discuss
efficacious CBT techniques that have grown out of an integrated neurobehavioral
view of TS.
Empirically Validated Interventions

Throughout the past 40 years, many behavioral interventions for CTDs have been
developed and tested. Ultimately, habit reversal training (HRT) and comprehensive
behavioral intervention for tics (CBIT) have emerged as the most efficacious options
for TS (Cook & Blacher, 2007; Himle et al., 2006). Exposure and response prevention
(ERP) has demonstrated efficacy in a single clinical trial and a previous small-N study,
but the evidence supporting its efficacy is still developing (Cook & Blacher, 2007).
In this section, we describe these treatment approaches, review the evidence on their
efficacy, and discuss their suitability for various populations.
Habit reversal training. HRT, the longest-standing behavioral treatment for tics,
teaches skills to minimize and manage tics as they occur in daily life. HRT is a
multicomponent treatment package whose primary components include (a) awareness
training, (b) competing response training (CRT), and (c) social support. These
components are applied sequentially to each tic, one at a time, starting with the tic
the patient finds most bothersome.
Awareness training. Awareness training involves teaching the patient to detect tics
and premonitory sensations as they occur in real time. Some patients may be able to do
these things without explicit training. In such cases, awareness training will proceed
quickly but should never be omitted. In other patients, including most pediatric
patients, tic detection skills must be built through a more extended awareness training
process. To begin this process, the patient and therapist create a detailed operational
definition of the target tic. Next, the patient practices detecting tics as they occur in
real time during a non-tic-related conversation. After the patient is able to reliably
detect tics and premonitory sensations for the target tic, CRT begins.
Competing response training. In CRT, the patient and therapist work together to select
a physical “exercise” to be used when tics and/or premonitory sensations occur. The
exercise involves engaging in a specific behavior that is physically incompatible with
the tic, relatively inconspicuous, and sustainable for at least one minute. After a
competing response has been selected for the targeted tic, the patient is told to use
this exercise for at least one minute (or until the urge goes away, whichever is longer)
whenever he or she notices the urge or when a tic occurs. The patient practices this
for the remainder of the session, with the therapist providing prompts and positive
feedback in a manner similar to that used during awareness training.
Social support. To encourage use of competing response exercises outside of the

therapeutic context, social support is also included as part of the HRT protocol
(Azrin & Nunn, 1973). This involves finding a support person (e.g., parent, spouse,
roommate) who is trained both to praise the patient for using the competing response
when it is done correctly, and nonjudgmentally to prompt the patient to use the
competing response when a tic occurs but the patient does not engage in the exercise.
With children, social support may also involve providing tangible rewards contingent
on regular competing response use. It is important to note that social support never
involves delivering praise or prompts contingent on occurrence or nonoccurrence of
tics, but rather on the use of competing response exercises.
Comprehensive Behavioral Intervention for Tics

CBIT is an elaborated CBT treatment package that combines traditional HRT com-
ponents with other techniques suggested by a contemporary behavioral understanding
of CTDs (Woods et al., 2008).
In addition to HRT, CBIT includes a functional assessment/function-based inter-
vention protocol to address the contextual factors that impact tic expression. The
assessment process identifies likely “tic triggers” and potentially tic-reinforcing conse-
quences. During the functional assessment, the therapist interviews the patient and his
or her parents about common factors that are present and potentially influencing tics
during periods of tic exacerbation. This process provides the therapist with a work-
ing model of the patient’s unique pattern of tic-exacerbating environmental factors.
From here, the therapist works with the client to devise function-based interventions,
which are changes in these environmental factors made to minimize contact with
tic-triggering events. For instance, functional assessment might reveal that a child’s
tics are exacerbated during math class, and that his math teacher often asks if he
is OK when the ticcing worsens. A function-based strategy for this situation would
involve asking the teacher to stop checking in with the child after he tics and replace
this by checking in with him at random intervals, regardless of whether or not his
tics had just occurred. In this case, the function-based intervention plan accomplishes
the therapeutic goal of limiting social reinforcement for ticcing, while providing an
alternative “tic-neutral” way for the child to receive attention from his teacher and
the opportunity to express concerns to him or her.
CBIT also includes relaxation training and psychoeducation as part of the treat-
ment program. Relaxation training involves teaching diaphragmatic breathing and
progressive muscle relaxation. Although relaxation has been shown to be ineffective as
a stand-alone treatment for TS (Bergin, Waranch, Brown, Carson, & Singer, 1998),
this component is added, as it is thought to facilitate successful use of compet-
ing response exercises. This idea is based on evidence showing that tic suppression
abilities decrease when individuals experience stress (Conelea, Brandt, & Woods,
2011). Psychoeducation in CBIT involves educating the patient (and parents of pedi-
atric patients) about the nature of TS. During this component, the clinician provides
information about the prevalence, course, common phenomenological characteristics,
and underlying neuropathology. Psychoeducation has demonstrated beneficial effects
for various psychiatric conditions (e.g., Kendall et al., 2008; Miklowitz, George,
Richards, Simoneau, & Suddath, 2003) and provides a logical starting point for
beginning psychological treatment.
Other Interventions
Other cognitive behavioral treatments for TS have been designed and tested, but
evidence supporting their efficacy is less clear (Cook & Blacher, 2007). An exhaustive
discussion of all CBT interventions is beyond the scope of this chapter, but a few
recent examples are worth mentioning. O’Connor’s research group has developed a
treatment package (O’Connor, 2005) that incorporates cognitive therapy techniques
with traditional HRT components. This combination of cognitive therapy plus HRT
has been found to have comparable efficacy to HRT alone (O’Connor, Gareau,
& Borgeat, 1997), suggesting the added components do not substantially enhance
treatment efficacy.
Other researchers have sought to improve HRT’s efficacy by adding components
of acceptance and commitment therapy (ACT), a third-wave behavioral therapy that
aims to change clinically relevant behavior by promoting psychological flexibility in
the way that patients experience aversive cognitions, emotions, and events. An initial
pilot study (Franklin, Best, Wilson, Loew, & Compton, 2011) found that the ACT
plus HRT combination did not produce better results than HRT alone. However, the
aim of changing the way patients with TS respond to premonitory urges and social
consequences of tics remains an intriguing goal for treatment development.
Efficacy of cognitive behavioral therapy. A large body of evidence supports the efficacy
of HRT and its modern variant, CBIT. At least 16 randomized controlled trials and
controlled small-N studies support the efficacy of HRT in decreasing tics (Himle et al.,
2006). In a recent review of HRT for tics, Cook and Blacher (2007) found that HRT
met American Psychological Association Division 12 criteria as a “well-established”
treatment for tics (Chambless & Ollendick, 2001). In addition, a recent meta-analysis
by Bate et al. (2011) found that HRT produces large effects (Cohen’s d = 0.8),
that are similar in magnitude to those found in clinical trials of widely prescribed
pharmacotherapies for CTDs (Piacentini et al., 2010).
In addition to the robust support for traditional HRT, two multisite randomized
controlled trials have found positive results for the efficacy of CBIT. In each trial,
participants were randomized to receive eight hour-long, weekly sessions of either
CBIT or psychoeducation and supportive therapy (PST), which was intended as a
control comparison condition to account for the influence of nonspecific factors. Both
trials demonstrated superior treatment outcomes for CBIT compared to the control
condition (Piacentini et al., 2010; Wilhelm et al., 2012). These differences were
highly clinically significant, with between-group effect sizes in the moderate-to-large
range (d = 0.68 in the pediatric trial and d = 0.58 in the adult trial).
ERP has also demonstrated promising efficacy in one small-N design (Hoogduin,
Verdellen, & Cath, 1997) and one randomized controlled trial (Verdellen et al.,
2004). In the randomized controlled trial comparing ERP and HRT with adult and
adolescent patients, a similar response to both interventions was found, although this
finding was somewhat obfuscated by the fact that the ERP treatment involved 24
hours of treatment (twelve 2-hour sessions), while the HRT intervention included
10 hours (ten 1-hour sessions) and lacked a social support component. Nonetheless,
this trial demonstrated that good acute clinical outcomes (within-group effect size:
d = 0.84) can be obtained by utilizing an ERP approach.
Important Treatment, Patient, and Clinician Characteristics

in Habit Reversal Training/Comprehensive Behavioral
Intervention for Tics
A number of factors appear to affect the effectiveness of CBT approaches. These

include treatment-specific factors, patient characteristics, and clinician factors.
Treatment Factors
Active components. Since Azrin and Nunn (1973) first published the HRT protocol,
clinical researchers have sought to identify the “active ingredients” of the 11-
component protocol. In an effort to simplify the protocol, Miltenberger and Fuqua
(1985) compared an abbreviated version, consisting of awareness training, CRT, and
social support components, to a full HRT package, and found the two versions were
equivalent. A subsequent dismantling study of this simplified HRT package found
that each of the three components used by Miltenberger and Fuqua was “active”
in that its inclusion was necessary to generate treatment response in at least one of
the four individuals studied (Woods, Miltenberger, & Lumley, 1996). Given these
findings, subsequent HRT research generally incorporated these three components,
in order to simplify the protocol and make it more accessible to clinicians.
Treatment duration. The “dose” of treatment necessary for CBT to produce clini-
cally significant improvement is not clear. Although earlier studies involved weekly
outpatient sessions for as long as 8 months (e.g., Azrin & Peterson, 1988, 1990),
across several recent trials CBT delivered in eight to ten 1-hour sessions (Piacentini
et al., 2010; Verdellen et al., 2004; Wilhelm et al., 2012) has produced large,
durable symptom decreases. Positive treatment effects have also been noted with as
few as three sessions of HRT (Woods, Twohig, Flessner, & Roloff, 2003). Future
research is needed to analyze parametrically the effects of treatment “dose” on
symptom reduction and durability of gains. Additionally, it is important to establish
whether a short-duration, high-intensity treatment (such as that described in a case
study by Flancbaum, Rockmore, & Franklin, 2011) could reliably produce clinically
significant, long-lasting gains. Given the current state of the evidence, we advise
practitioners to tailor the duration of treatment to the patient’s needs and resources.
In the absence of a sound empirical rationale for extending acute HRT/CBIT
beyond eight sessions, clinicians are advised to use this dose as a heuristic “starting
point” but extend or shorten the protocol based on the needs of the patient. In
the case of ERP, clinicians should expect to administer approximately twelve 2-hour
sessions, as this is the duration found efficacious in the Verdellen et al. (2004)
trial.
Treatment setting and telehealth. Recent studies have also shown that CBT can
effectively reduce tic severity when delivered remotely via videoconferencing tech-
nology (Himle, Olufs, Himle, Tucker, & Woods, 2010). This mode of treatment
delivery may be particularly useful in increasing the availability of CBT for TS,
which is currently lacking in most areas of the United States (Woods, Conelea,
& Himle, 2010). In an initial pilot study, Himle et al. (2010) showed clinically
significant decreases in tic frequency for three children receiving remotely deliv-
ered CBIT. A larger study (Himle et al., 2012) found that this “tele-CBIT”
treatment was as effective as face-to-face CBIT. Overall, telehealth technology
is a viable option for delivering CBT for TS when logistics preclude face-to-
face treatment. Of course, therapists should consider factors such as confiden-
tiality, suicide risk, patient access to reliable videoconferencing equipment, and
licensing issues when considering a telehealth approach (Mathy, Kerr, & Haydin,
2003).
Patient Variables
Age. Behavior therapy has demonstrated efficacy in children, adolescents, and adults
with CTDs. In the CBIT trials (Piacentini et al., 2010; Wilhelm et al., 2012), pediatric
patients responded to CBIT at a higher rate than adults (53% vs. 38%). However, this
may speak to factors other than the specific efficacy of CBIT among these populations,
as children also responded more than adults to the control treatment (psychoeducation
and supportive therapy; 19% versus 7%). Behavior therapy has demonstrated efficacy
in samples including children as young as age 9 (e.g., the pediatric CBIT trial;
Piacentini et al., 2010). ERP has also proven efficacious for children of 9–10 years
of age, but may be less acceptable to pediatric clients (according to Hoogduin
et al., 1997, p. 134, children described ERP sessions as “those awful two hour
sessions”). Although CBT for TS has not been thoroughly investigated in children
younger than 9, successful outcomes have been reported with children as young as 4
years old (Watson & Sterling, 1998). Based on these studies, interventions targeting
functional interventions may be particularly crucial in working with these younger
clients.
Intellectual functioning. Traditional CBT approaches involve “self-management”

strategies that clients perform independently according to multistep instructions. As
a result, such therapies are typically implemented and studied within samples of
individuals with typical cognitive functioning. Among this population, intelligence
does not appear to affect treatment outcomes. Some efforts have been made to
treat tics with behavioral procedures in individuals with intellectual disabilities. Such
treatments have involved more direct differential reinforcement procedures (Varni,
Boyd, & Cataldo, 1978). We are aware of no published reports of ERP or HRT
for treating tics in individuals with intellectual disabilities. However, ERP may be
a more feasible treatment choice for this population, as it requires less complex
instruction-following on the part of the patient than HRT does.
Comorbidity. Since individuals with CTDs often present with comorbid psychiatric
symptomology, it is important to understand the influences of these factors on
treatment. Several studies have shown successful clinical outcomes for tics in samples
with relatively high levels of comorbidity (Piacentini et al., 2010; Verdellen et al.,
2004; Wilhelm et al., 2003; Wilhelm et al., 2012). However, little is known about
the potential moderating effects of comorbid psychopathology (e.g., ADHD, OCD)
on outcomes for CBT for TS. Given the importance of this question, future research
is needed to identify the efficacy of CBT for tics in subpopulations of children also
affected by comorbid psychiatric conditions. At present, the literature suggests that
the mere presence of these conditions does not contraindicate the use of CBT.
Clinicians are advised to base treatment planning on their assessment of the client’s
readiness for CBT and to prioritize treatment goals according to the patient’s global
clinical presentation.
Concomitant pharmacotherapy. For most patients, psychosocial intervention is not the

first line of CTD treatment. A substantial proportion of individuals seen in psycholog-
ical clinics are already taking medication to manage their symptoms. Unfortunately,
little is known about the interactions between behavior therapy and pharmacother-
apy effects, and it is not clear whether medication status moderates the efficacy of
CBT. However, some relevant findings do exist and can inform clinical practice. For
instance, basic research studies have shown that individuals with a CTD who are
taking neuroleptics show less sensitivity to reward than their unmedicated counter-
parts (Palminteri et al., 2009). Since CBT often involves rewarding tic-management
behaviors (e.g., using tangible rewards or social praise for correctly using a competing
response), decreasing sensitivity to reward may lessen CBT’s efficacy. Nonetheless,
Piacentini et al. (2010) did not find a moderating effect of medication status on CBIT
outcomes, although these researchers did not specifically look at the moderating
effects of different medication classes.
Clinician Variables
Most published studies of CBT for CTD have employed master’s- or doctoral-level
clinical psychologists as therapists. However, with proper training and supervision
by an experienced practitioner, it may be possible for other health professionals
to implement psychosocial interventions for TS. Currently, our research group is
conducting a study examining the effectiveness of CBIT delivered in neurology clinics
by neurologists and nurses familiar with CTDs, but not with behavioral therapy in
general.
Assessment
Before beginning treatment, it is important to conduct a comprehensive assessment

of the patient’s tic history, current symptoms, and overall psychological functioning.
We recommend that initial diagnosis be made by a physician, preferably a neurologist,
prior to the psychologist’s intake assessment. After this, the psychological practitioner
can confirm the initial tic diagnosis either via unstructured interviewing centered
around DSM diagnostic criteria, or by using the Tic Disorders modules of the
Mini International Neuropsychiatric Interview (MINI-KID; Sheehan et al., 2010)
or Anxiety Disorders Interview Schedule (ADIS; Silverman & Albano, 1996). In
addition to establishing diagnostic status, an initial interview should determine age of
onset, patterns of symptom waxing and waning since onset, and tic treatment history.
Assessment of tic severity should rely on information from multiple informants,
collected through multiple modalities, and should assess multiple aspects of tics
and related distress and impairment. The clinician-rated Yale Global Tic Severity
Scale (YGTSS; Leckman, Riddle, Hardin, & Ort, 1989) is considered the “gold
standard” measure of tic severity and may be administered at the beginning of
treatment and periodically thereafter to track broad symptom severity. The YGTSS is
administered via a semistructured interview that takes 20–30 minutes to administer
and has demonstrated good psychometric properties (Leckman et al., 1989). Based
on the responses of the patient and his or her parent, clinicians make separate ratings
of motor and vocal tics across five different dimensions (i.e., number, frequency,
intensity, complexity, and interference). Each dimension is rated along a 0–5 scale.
Scores from all dimensions are summed separately for motor and vocal tics, yielding
motor and vocal tic severity scores (range: 0–25 each). Motor and vocal severity
scores are summed to create a total tic severity score (range: 0–50). The YGTSS also
includes a global tic-related impairment scale (range: 0–50).
The Parent Tic Questionnaire (PTQ) is a validated parent-report measure of tic
severity that provides indices of number, frequency, and intensity of motor and
vocal tics (Chang, Himle, Tucker, Woods, & Piacentini, 2009). The PTQ can be
completed quickly and is well suited for use as a weekly symptom tracking measure for
pediatric patients. For older adolescents and adults, the PTQ may be modified into a
self-report format and used similarly. Since premonitory urges play an important role
in a cognitive behavioral conceptualization of CTDs and in CBT for these conditions,
it is important to assess these phenomena. This can be done via unstructured interview
about the nature of any sensations, associated distress or impairment, and whether
or not they reduce when a tic occurs. The Premonitory Urge for Tics Scale (PUTS;
Woods et al., 2005) may also be administered to provide a dimensional measure of
premonitory urge severity.
Initial Interview
After a diagnosis of tic disorder has been established, but before starting CBT, the first
session with the patient should involve building rapport, providing psychoeducation,
and obtaining additional information if necessary—especially if the initial assessment
was conducted by someone other than the therapist.
Building rapport and motivation. Patients with CTDs may feel reluctant to discuss
their tics, especially if they have a history of others reacting negatively to their
symptoms (Cutler, Murphy, Gilmour, & Heyman, 2009). Because patient compliance
is crucial in determining clinical benefit, it is important to build rapport with the
patient. To help establish a therapeutic relationship, therapists should introduce
therapy in a way that emphasizes its collaborative nature; that is, that the therapist and
patient are going to work together to help the patient manage tics more effectively.
Therapists should explain to patients that the goal of therapy is to make patients just
as competent as the therapist in treating tics, and to achieve that goal, patients are
going to learn a set of skills they can use for the rest of their lives.
If patients are resistant or have low motivation to engage in treatment, it can be
helpful to generate a list of psychosocial consequences the tics have produced. This
list might include places they avoid, school or work productivity, close relationships,
and other areas often endorsed by individuals with tic disorders (Conelea, Woods,
et al., 2011). For example, a patient with TS may have loud vocal tics that have
prevented him or her from going to restaurants, movie theaters, or even grocery
shopping. Motivational interviewing (Miller & Rollnick, 2002) techniques may also
help therapists motivate clients to engage in treatment who may be resistant or
ambivalent toward working on tics.
History of tic disorder and treatment. A detailed account of onset, tic symptomology,
and course of tics should be obtained in the initial interview. The therapist should
inquire as to when the tics began, and how they were discovered. Given the nature of
tics, patients may currently not be presenting with the same tics they had when first
diagnosed. Therapists should collect information related to severity: which tics are
most severe, and whether there have been any physical complications due to the tics.
While collecting information about tic onset, history, and course, the therapist should
also focus on learning about the client’s interests, hobbies, and personal history. This
information can also be used during conversations while conducting HRT in later
sessions.
Therapists should also obtain a history of prior treatment. Many patients are often
referred to our clinic from neurologists. If patients have not yet seen a neurologist,
we recommend they do so before starting treatment. Therapists should establish
whether patients have seen other health care professionals for their tics in the past
and, if so, whether treatment was effective. Such information can help therapists
determine patients’ level of knowledge, treatment buy-in, and any potential barriers
to treatment. If patients report prior, unsuccessful sessions of CBIT, therapists should
make every effort to determine why those sessions were unsuccessful.
If the patient is currently taking medication for tics, therapists should create a list of
the specific drug, dosage, start date, whether the patient finds the medication helpful,
and whether the patient wishes to continue taking the medication. Therapists should
consult with the prescribing physicians. This can be helpful in coordinating patient
care consistent with the patient’s wishes.
Patients may also present with a history of other problems. Given the high
comorbidity with other conditions, patients may present for treatment with one or
more other disorders. In the initial interview, therapists should determine the presence
of other disorders, establish which is primary, and determine whether appropriate
steps are being taken to alleviate other disorders. If another disorder is the primary
concern, then it may be in the patient’s best interests to have that disorder treated first.
If therapists are not qualified to treat a separate, primary disorder, they should refer
patients to an appropriate specialist. After the primary disorder has been effectively
managed, patients could then return to work on their tic disorder. If patients are
receiving concurrent treatment for another disorder, therapists may treat the tic
disorder providing the other treatment does not interfere (e.g., the client has ample
time to work on both conditions).
Psychoeducation and treatment rationale. After obtaining background information

and treatment history, therapists should provide patients with an overview of tic
disorders. A description of motor versus vocal tics and simple versus complex tics is
typically a helpful place to begin. Providing the basic DSM-5 criteria for tic disorders
can also be helpful, especially when explaining the different types of tic disorders.
Reviewing disorder criteria may be helpful in reducing patient and parental anxiety
surrounding tic disorders by putting TS into perspective and showing that it is really
not much different diagnostically from other, seemingly more benign disorders.
In addition to tic type and disorders, clients can benefit from a discussion of tic phe-
nomenology and natural history. Data on the average age of onset and worst severity
usually align well to the patient’s self-reported history. Explanations of the waxing
and waning nature of tics as well as the premonitory urge should also be included in
this discussion. When discussing etiology of tic disorders, common metaphors may
be more effective than a lecture on specific genetic findings and neuroanatomy. Com-
paring the brain’s creation of tics with leaky brakes in an automobile is an example of
one metaphor commonly used when discussing neuropathology. The remainder of
the psychoeducation piece should include epidemiological data as well as important
resources (e.g., the Tourette Syndrome Association) for patients and family members.
After psychoeducation, the therapist and patient should review treatment options
and briefly discuss what the patient feels most comfortable pursuing. This should
involve a discussion of behavior therapy, medication, and the natural course of tics
if left untreated. Therapists should present findings from empirical studies, including
the efficacy of treatment options, strengths, and weaknesses. For example, behavior
therapy involves much work on the part of patients and their families. If the child
and family cannot devote the time and resources to pursue this option, other avenues
should be considered. Pharmacotherapy, on the other hand, involves significantly less
patient effort, but can have significant side effects.
When discussing behavior therapy as an option, therapists should describe the two
primary goals of treatment: (a) to mitigate the effects of tic-exacerbating antecedents
and consequences on tics, and (b) to teach patients skills to manage tics (i.e., com-
peting responses). Therapists should also outline the course of treatment. Therapists
should explain that sessions occur weekly and typically last 60–90 minutes, and that
patients should expect to work on therapy skills for 30–45 minutes a day outside of
treatment time. Parents or guardians of patients should understand that they also play
a key role in treatment and should expect to invest a considerable amount of time as
well.
When discussing medications, a salient issue for most patients involves the side
effects. Because side effects can vary by medication type, it is important for therapists
to have a working understanding of the various drug classes (e.g., alpha agonists,
atypical neuroleptics, SRIs, etc.) and the side effects typically caused by such drugs.
Should patients choose to pursue pharmacotherapy, therapists should be able to make
appropriate referrals.
Session by Session
The following session-by-session description of CBIT is included to demonstrate to
clinicians how behavior therapy for tics may be generally structured.
Session 1. The goals of the first session are to build rapport, provide psychoeducation,
obtain tic history and assess current functioning, introduce the concept of function-
based assessment, create a rewards program, and assign homework. Therapists work
with patients to develop a comprehensive list of all current tics, which are organized
within a tic hierarchy. After identifying all current tics, patients rate how distressing
or impairing each tic is on a scale of 0–10 (where “0” indicates that the tic did not
happen or is nondistressing, and higher numbers indicate more frequent, distressing
tics). These ratings should be updated at the beginning of each session, and the most
bothersome tic in the hierarchy is usually the first tic targeted in treatment. After
creating the hierarchy, therapists introduce the concept of function-based assessment,
and create a reward program to reinforce patients for their efforts in managing tics.
The reward program is typically omitted when working with adults. Between sessions
1 and 2, patients and a designated support person (usually a parent) should monitor
the first tic in the hierarchy during 20-minute blocks two to three times per week.
Session 2. The goals of session 2 are to review monitoring homework, introduce

function-based interventions, and conduct HRT for the first tic in patients’ hierarchies.
Therapists should use information from the monitoring homework to help with the
functional assessment. During the functional assessment, therapists develop a list
of all antecedents and consequences associated with increases in tic frequency for
the first tic on the hierarchy. To do this, therapists should assess several situations
for the effects on ticcing, including the classroom, public places other than school,
watching television, playing video games, mealtimes, playing sports, in the car, when
stressed/anxious, and during periods of excitement or anticipation. In each of these
situations, if tics are typically exacerbated, an effort should be made to assess various
social reactions to tics that may be inadvertently reinforcing the behavior. After the
assessment, therapists can develop function-based interventions. These interventions
should attempt to minimize the impact of tic-exacerbating situations on patients. For
example, if a child reports ticcing more while working on homework immediately
after school, parents might allow 15 minutes of free time before the child is expected
to begin working.
Following the functional interventions, therapists should introduce and conduct
HRT. This process involves awareness training, CRT, and social support. During
awareness training, therapists should obtain a detailed description of the target tic,
including any evidence of a premonitory urge, or warning signal that the tic is about
to occur. Next, the therapist and patient should conduct a casual conversation for
a few minutes. During the conversation the patient should acknowledge any time
the tic occurs. The therapist should provide praise for correct detection and prompts
when the tics are exhibited but not recognized by the client.
After the patient becomes proficient at recognizing the occurrence of the tic, a
competing response can be developed. Following treatment guidelines (Woods et al.,
2008), each competing response (CR) should adhere to the following criteria:
1. The CR should be physically incompatible with the target tic.

2. The CR should be held for at least one minute or until the premonitory urge
goes away.
3. The CR should be inconspicuous and able to be performed anywhere.
After demonstrating the appropriate use of the CR, therapists should have the
client practice the CR. They should converse for a few minutes, and the patient
should practice using the CR as necessary. During this time, therapists should prompt
patients to use the CR if the tic occurs and praise patients for correctly using the
CR. After patients learn to use a CR, a parent or guardian should be trained to help
implement CRs outside of therapy. For adults, a spouse or close friend are common
options. The support person should be someone with whom patients are comfortable
working and already have a strong relationship. The support person should praise
patients for correctly implementing the CR and gently remind patients to use the
CR when necessary. The support person also conducts planned CR practice with the
patient at least three or four times each week, for at least 30 minutes each time.
Sessions 3 and 4. Sessions 3 and 4 are identical to session 2. After patients obtain
a working understanding of functional assessment, intervention, and competing
responses, a new tic is monitored each week and then worked on during the
following session. In session 4, the therapist introduces relaxation training, specifically
diaphragmatic breathing. Patients with TS or chronic vocal tic disorder may have
already learned controlled breathing if it was used as a CR for a vocal tic. Even so, a
review at this stage can be helpful, especially within the larger context of learning to
manage stress and anxiety as antecedents to tics.
When introducing controlled breathing, therapists should first demonstrate the

appropriate technique before asking patients to do it. For children and others who
may struggle learning the concept, it may be helpful to have them place one hand
on their stomach and another on their chest. The hand on the stomach should
move inward and outward as the patient breathes, but the hand on the chest
should stay relatively still (Woods et al., 2008). Therapists should again be sure
to collaborate with patients to determine what is comfortable. After introducing
controlled breathing, patients should practice the technique three or four times for
at least 5 minutes per practice over the following week (in addition to tic monitoring
and CR practice).
Session 5. In session 5, therapists review previous functional interventions and com-

peting responses and make any necessary improvements. Afterwards, therapists design
functional interventions and conduct HRT for the tic monitored between sessions
4 and 5. Therapists also review controlled breathing from the last session and trou-
bleshoot any problems patients may be having with the technique. Therapists then
introduce the second component of the relaxation treatment element, progressive
muscle relaxation (PMR). This procedure, used often in behavior therapy (Goldfried
& Davison, 1994), involves tensing and then relaxing various muscle groups through-
out the body. The goal of PMR is to help patients reduce muscle tension and relax
during stressful situations, both of which are common tic antecedents. Several scripts
exist to help therapists accomplish this task (Goldfried & Davison, 1994; Woods
et al., 2008), but regardless of the script used, therapists should make every effort to
demonstrate the process before asking patients to engage in the process.
Sessions 6, 7, and 8. Session 6 involves a review of everything covered up to that point,

but no new material is introduced. The therapist and patient work on the next tic
in the hierarchy and practice the relaxation techniques. In standard CBIT, sessions 7
and 8 include a discussion of relapse prevention and termination.
During the relapse prevention component, the patient should be encouraged to
remain vigilant for tics during stressful times, notice and react appropriately to
common symptom waxing, and have the social support person encourage the patient
to use competing responses as well as stress management techniques (e.g., PMR
and controlled breathing). Both the patient and support person should be aware of
emotional, situational, and physical triggers that tend to exacerbate tics, and if tics
reappear or worsen, the same protocol learned in treatment should be reviewed and
re-established. If tics become too complicated and unmanageable, patients should
consider returning to treatment.
Termination should involve a summary of the patients’ progress throughout
treatment and, ideally, some form of outcome assessment such as the YGTSS. It is
often helpful to contrast severity ratings from the outset and conclusion of therapy
to help patients see their progress. Age-appropriate acknowledgement (e.g., therapy
completion certificates) can also occur. Therapists should also elicit patient and family
feelings towards termination and try to resolve any anxiety surrounding the end of
the therapeutic relationship.
Conclusion
In this chapter we reviewed the literature on tic disorders and their treatment and
provided a session-by-session overview of CBIT. Although CBT for tic disorders
has gained much more attention in the last decade, more research is needed on the
mechanisms of change in therapy and improvement of treatment outcome. Research
should also focus on extending the efficacy of CBT for tic disorders into populations
with comorbid anxiety disorders and disruptive behavior disorders (e.g., ADHD).
Long-term follow-up data for CBT are also lacking, and should explore factors that
may or may not enhance long-term treatment gains.
References
Abramowitz, J. S. (1997). Effectiveness of psychosocial and pharmacological treatments for
obsessive-compulsive disorder: A quantitative review. Journal of Consulting and Clinical
Psychology, 65, 44–52. doi:10.1037/0022-006X.65.1.44
Azrin, N. H., & Nunn, R. G. (1973). Habit-reversal: A method of eliminating nervous
habits and tics. Behaviour Research and Therapy, 11, 619–628. doi:10.1016/0005-
7967(73)90119-8
Azrin, N. H., & Peterson, A. L. (1988). Habit reversal for the treatment of Tourette
syndrome. Behaviour Research and Therapy, 26, 347–351. doi:10.1016/0005-7967(88)
90089-7
Azrin, N. H., & Peterson, A. L. (1990). Treatment of Tourette syndrome by habit rever-
sal: A waiting-list control group comparison. Behavior Therapy, 21, 305–318. doi:
10.1016/S0005-7894(05)80333-8
Bate, K. S., Malouff, J. M., Thorsteinsson, E. T., & Bhullar, N. (2011). The efficacy of habit
reversal therapy for tics, habit disorders, and stuttering: A meta-analytic review. Clinical
Baym, C. L., Corbett, B. A., Wright, S. B., & Bunge, S. A. (2007). Neural correlates of tic
severity and cognitive control in children with Tourette syndrome. Brain, 131, 165–179.
doi:10.1093/brain/awm278
Bergin, A., Waranch, H. R., Brown, J., Carson, K., & Singer, H. S. (1998). Relaxation
therapy in Tourette syndrome: A pilot study. Pediatric Neurology, 18, 136–142. doi:
10.1016/S0887-8994(97)00200-2
Bloch, M. H., Sukhodolsky, D. G., Leckman, J. F., & Schultz, R. T. (2006). Fine-motor skill
deficits in childhood predict adulthood tic severity and global psychosocial functioning
in Tourette’s syndrome. Journal of Child Psychology and Psychiatry, 47 , 551–559. doi:
10.1111/j.1469-7610.2005.01561.x
Bullen, J. G., & Hemsley, D. R. (1983). Sensory experience as a trigger in Gilles de la Tourette’s
syndrome. Journal of Behavior Therapy and Experimental Psychiatry, 14, 197–201. doi:
10.1016/0005-7916(83)90048-4
Carr, J. E., Taylor, C. C., Wallander, R. J., & Reiss, M. L. (1996). A functional-analytic
approach to the diagnosis of a transient tic disorder. Journal of Behavior Therapy and
Experimental Psychiatry, 27 , 291–297. doi:10.1016/S0005-7916(96)00025-0
Chambless, D. L., & Ollendick, T. H. (2001). Empirically supported psychological inter-

ventions: Controversies and evidence. Annual Review of Psychology, 52, 685–716. doi:
10.1146/annurev.psych.52.1.685
Chang, S., Himle, M. B., Tucker, B. T. P., Woods, D. W., & Piacentini, J. (2009). Initial
psychometric properties of a brief parent-report instrument for assessing tic severity in
children with chronic tic disorders. Child & Family Behavior Therapy, 31, 181–191. doi:
10.1080/07317100903099100
Coffey, B. J., Biederman, J., Geller, D. A., Spencer, T., Park, K. S., Shapiro, S. J., & Garfield,
S. B. (2000). The course of Tourette’s disorder: A literature review. Harvard Review of
Psychiatry, 8, 192–198. doi:10.1080/hrp_8.4.192
Conelea, C. A., Brandt, B. C., & Woods, D. W. (2011). The impact of a stress induction task
on tic frequencies in youth with Tourette syndrome. Behaviour Research and Therapy, 49,
492–497. doi: 10.1016/j.brat.2011.05.006
Conelea, C. A., & Woods, D. W. (2008). The influence of contextual factors on tic expression
in Tourette syndrome: A review. Journal of Psychosomatic Research, 65, 487–496. doi:
10.1016/j.jpsychores.2008.04.010
Conelea, C. A., Woods, D. W., Zinner, S. H., Budman, C., Murphy, T., Scahill, L. D.,
… Walkup, J. (2011). Exploring the impact of chronic tic disorders on youth: Results
from the Tourette syndrome impact survey. Child Psychiatry & Human Development, 42,
219–242. doi:10.1007/s10578-010-0211-4
Cook, C. R., & Blacher, J. (2007). Evidence-based psychosocial treatments for tic dis-
orders. Clinical Psychology: Science and Practice, 14, 252–267. doi:10.1111/j.1468-
2850.2007.00085.x
Costello, E. J., Angold, A., Burns, B. J., Stangl, D. K., Tweed, D. L., Erkanli, A., & Worthman,
C. M. (1996). The Great Smoky Mountains Study of Youth. Goals, design, methods, and
the prevalence of DSM-III-R disorders. Archives of General Psychiatry, 53, 1129–1136.
doi:10.1001/archpsyc.1996.01830120067012
Cutler, D., Murphy, T., Gilmour, J., & Heyman, I. (2009). The quality of life of young
people with Tourette syndrome. Child: Care, Health & Development, 35, 496–504.
doi:10.1111/j.1365-2214.2009.00983.x
Flancbaum, M., Rockmore, L., & Franklin, M. E. (2011). Intensive behavior therapy for
tics: Implications for clinical practice and overcoming barriers to treatment. Journal of
Developmental and Physical Disabilities, 23, 61–69. doi:10.1007/s10882-010-9222-0
Franklin, M. E., Best, S. H., Wilson, M. A., Loew, B., & Compton, S. N. (2011). Habit reversal
training and acceptance and commitment therapy for Tourette syndrome: A pilot project.
Journal of Developmental and Physical Disabilities, 23, 49–60. doi:10.1007/s10882-010-
9221-1
Freeman, R. D., Fast, D. K., Burd, L., Kerbeshian, J., Robertson, M. M., & Sandor, P.
(2000). An international perspective on Tourette syndrome: Selected findings from 3,500
individuals in 22 countries. Developmental Medicine and Child Neurology, 42, 436–447.
Goldfried, M. R., & Davison, G. C. (1994). Clinical behavior therapy. New York, NY: John
Wiley & Sons, Inc.
Harris, K. M., Mahone, E. M., & Singer, H. S. (2008). Nonautistic motor stereotypies:
Clinical features and longitudinal follow-up. Pediatric Neurology, 38, 267–272. doi:
10.1016/j.pediatrneurol.2007.12.008
Harrison, J., Schneider, B., & Walkup, J. (2007). Medical management of Tourette’s syndrome
and other associated repetitive behaviors. In D. W. Woods, J. Piacentini, & J. Walkup
(Eds.), Treating Tourette syndrome and tic disorders: A guide for practitioners (pp.
Himle, M. B., Olufs, E., Himle, J., Tucker, B. T. P., & Woods, D. W. (2010). Behavior
therapy for tics via videoconference delivery: An initial pilot test in children. Cognitive
and Behavioral Practice, 17 , 329–337. doi:10.1016/j.cbpra.2010.02.006
Himle, M. B., Woods, D. W., Freitag, M. J., Franklin, S., Ely, L. J., & Walther, M. (2012).
A randomized pilot trial comparing videoconference versus face-to-face delivery of CBIT
for Tourette syndrome. Behavior Research and Therapy, 50, 565–570.
Himle, M. B., Woods, D. W., Piacentini, J. C., & Walkup, J. T. (2006). Brief review of
habit reversal training for Tourette syndrome. Journal of Child Neurology, 21, 719–725.
doi:10.1177/08830738060210080101
Hoogduin, K., Verdellen, C., & Cath, D. (1997). Exposure and response prevention in the
treatment of Gilles de la Tourette’s syndrome: Four case studies. Clinical Psychology
& Psychotherapy, 4, 125–135. doi:10.1002/(SICI)1099-0879(199706)4:2<125::AID-
CPP125>3.0.CO;2-Z
Kadesjo, B., & Gillberg, C. (2000). Tourette’s disorder: Epidemiology and comorbidity in
primary school children. Journal of the Academy of Child and Adolescent Psychiatry, 39,
548–555. doi:10.1097/00004583-200005000-00007
Kane, M. J. (1994). Premonitory urges as “attentional tics” in Tourette’s syndrome.
doi:10.1097/00004583-199407000-00005
Kendall, P. C., Hudson, J. L., Gosch, E., Flannery-Schroeder, E., & Suveg, C. (2008).
Cognitive-behavioral therapy for anxiety disordered youth: A randomized clinical trial
evaluating child and family modalities. Journal of Consulting and Clinical Psychology, 76,
282–297. doi:10.1037/0022-006X.76.2.282
Khalifa, N., & von Knorring, A. L. (2003). Prevalence of tic disorders and Tourette syndrome
in a Swedish school population. Developmental Medicine and Child Neurology, 45,
1346–1353.
Koller, W. C., & Biary, N. M. (1989). Volitional control of involuntary movements. Movement
Disorders, 4, 153–156. doi:10.1002/mds.870040207
Kushner, H. I. (1999). A cursing brain? The histories of Tourette syndrome. Cambridge, MA:
Harvard University Press.
Lavoie, M. E., Imbriglio, T. V., Stip, E., & O’Connor, K. P. (2011). Neurocognitive changes
following cognitive-behavioral treatment in Tourette syndrome and chronic tic disorder.
International Journal of Cognitive Therapy, 4, 34–50. doi:10.1521/ijct.2011.4.1.34
Leckman, J. F., Riddle, M. A., Hardin, M. T., & Ort, S. I. (1989). The Yale Global Tic Severity
Scale: Initial testing of a clinician-rated scale of tic severity. Journal of the American
198907000-00015
Leckman, J. F., Walker, D. E., & Cohen, D. J. (1993). Premonitory urges in Tourette’s
syndrome. American Journal of Psychiatry, 150, 98–102.
Leckman, J. F., Zhang, H., Vitale, A., Lanin, F., Lynch, K. A., & Peterson, B. S. (1998).
Course of severity in Tourette syndrome: The first two decades. Pediatrics, 102, 14–19.
doi:10.1542/peds.102.1.14
March, J. S., Franklin, M., Nelson, A., & Foa, E. (2001). Cognitive-behavioral psychotherapy
for pediatric obsessive-compulsive disorder. Journal of Clinical Child Psychology, 30, 8–18.
doi:10.1207/S15374424JCCP3001_3
Mathy, R. M., Kerr, D. L., & Haydin, B. M. (2003). Methodological rigor and ethical
considerations in Internet-mediated research. Psychotherapy: Theory, Research, Practice,
Training, 40, 77–85. doi:10.1037/0033-3204.40.1-2.77
Michael, J. (2000). Implications and refinements of the establishing operation concept. Journal
of Applied Behavior Analysis, 33, 401–410. doi.org/10.1901/jaba.2000.33-401
Michael, R. P. (1957). Treatment of a case of compulsive swearing. British Medical Journal,

20, 1506–1507. doi:10.1136/bmj.1.5034.1506
Miguel, E. C., Coffey, B. J., Baer, L., & Savage, C. R. (1995). Phenomenology of intentional
repetitive behaviors in obsessive-compulsive disorder and Tourette’s disorder. Journal of
Miklowitz, D. J., George, E. L., Richards, J. A., Simoneau, T. L., & Suddath, R. L. (2003).
A randomized study of family-focused psychoeducation and pharmacotherapy in the
outpatient management of bipolar disorder. Archives of General Psychiatry, 60, 904–912.
doi:10.1001/archpsyc.60.9.904
Miller, J. M., Singer, H. S., Bridges, D. D., & Waranch, H. R. (2006). Behavioral therapy for
treatment of stereotypic movements in nonautistic children. Journal of Child Neurology,
21, 119–125. doi:10.1177/08830738060210020701
Miltenberger, R. G. (2005). The role of automatic negative reinforcement in clinical problems.
International Journal of Behavioral Consultation and Therapy, 1, 1–11.
Miltenberger, R. G., & Fuqua, R. W. (1985). A comparison of contingent vs. non-contingent
competing response practice in the treatment of nervous habits. Journal of Behavior
Therapy and Experimental Psychiatry, 16, 195–200. doi:10.1016/0005-7916(85)
90063-1
Mink, J. W., & Pleasure, D. E. (2003). The basal ganglia and involuntary movements:
Impaired inhibition of competing motor patterns. Archives of Neurology, 60, 1365–1368.
doi:10.1001/archneur.60.10.1365
O’Connor, K. P. (2005). Cognitive-behavioral management of tic disorders. Chichester,
England: John Wiley & Sons, Ltd. doi:10.1002/9780470713518
O’Connor, K. P., Gareau, D., & Borgeat, F. (1997). A comparison of a behavioural
and a cognitive-behavioural approach to the management of chronic tic disor-
ders. Clinical Psychology and Psychotherapy, 4, 105–117. doi:10.1002/(SICI)1099-
0879(199706)4:2<105::AID-CPP126>3.3.CO;2-P
Palminteri, S., Lebreton, M., Worbe, Y., Grabli, D., Hartmann, A., & Pessiglione, M.
(2009). Pharmacological modulation of subliminal learning in Parkinson’s and Tourette’s
syndromes. Proceedings of the National Academy of Sciences, 106, 19179–19184. doi:
10.1073/pnas.0904035106
Peterson, B. S., Thomas, P., Kane, M. J., Scahill, L., Zhang, H., Bronen, R., … Staib, L.
(2003). Basal ganglia volumes in patients with Gilles de la Tourette syndrome. Archives
of General Psychiatry, 60, 415–424. doi:10.1001/archpsyc.60.4.415
Piacentini, J., Woods, D. W., Scahill, L., Wilhelm, S., Peterson, A. L., Chang, S., …
Walkup, J. (2010). Behavior therapy for children with Tourette disorder: A random-
ized controlled trial. Journal of the American Medical Association, 303, 1929–1937.
doi:10.1001/jama.2010.607
Pringsheim, T., Doja, A., Gorman, D., McKinlay, D., Day, L., Billinghurst, L., …
Sandor, P. (2012). Canadian guidelines for the evidence-based treatment of tic disorders:
Pharmacotherapy. Canadian Journal of Psychiatry, 57 , 133–143.
Ricketts, E. J., Bauer, C. C., van der Fluit, F., Capriotti, M. R., Espil, F. M., Snorrason, I., …
Woods, D. W. (2013). Behavior therapy for stereotypic movement disorders in typically
functioning children: A clinical case series. Cognitive and Behavioral Practice.
Robertson, M. M. (2008). The prevalence and epidemiology of Gilles de la Tourette syndrome.
Part 1: The epidemiological and prevalence studies. Journal of Psychosomatic Research, 65,
461–472. doi:10.1016/j.jpsychores.2008.03.006
Scahill, L., Bitsko, R. H., Visser, S. N., & Blumberg, S. J. (2009). Prevalence of diagnosed
Tourette syndrome in persons aged 6–17 years: United States, 2007. Morbidity and
Mortality Weekly Report, Centers for Disease Control and Prevention, 58, 581–585.
Scahill, L. D., Leckman, J. F., & Marek, K. L. (1995). Sensory phenomena in Tourette’s
syndrome. In A. E. Lang (Ed.), Behavioral neurology of movement disorders (pp. 273–280).
New York, NY: Raven Press.
Scotti, J. R., Schulman, D. E., & Hojnacki, R. M. (1994). Functional analysis and unsuccessful
treatment of Tourette’s syndrome in a man with profound mental retardation. Behavior
Therapy, 25, 721–738. doi:10.1016/S0005-7894(05)80206-0
Shapiro, A. K., & Shapiro, E. (1968). Treatment of Gilles de la Tourette’s syndrome with
haloperidol. British Journal of Psychiatry, 114, 345–350. doi:10.1192/bjp.114.508.345
Sheehan, D. V., Sheehan, K. H., Shytle, R. D., Janavs, J., Bannon, Y., Rogers, J. E., …
Wilkinson, B. (2010). Reliability and validity of the Mini International Neuropsychiatric
Interview for Children and Adolescents (MINI-KID). Journal of Clinical Psychiatry, 71,
313–326. doi:10.4088/JCP.09m05305whi
Silva, R. R., Muñoz, D. M., Daniel, W., Barickman, J., & Friedhoff, A. J. (1996). Causes
of haloperidol discontinuation in patients with Tourette’s disorder: Management and
alternatives. Journal of Clinical Psychiatry, 57 , 129–135.
Silverman, W. K., & Albano, A. M. (1996). Anxiety disorders interview schedule for DSM-IV:
Child and parent versions. San Antonio, TX: Psychological Corporation.
Singer, H. S. (2009). Motor stereotypies. Seminar of Pediatric Neurology, 16, 77–81. doi:
10.1016/j.spen.2009.03.008
Singer, H. S., Mink, J., Gilbert, D. L., & Jankovic, J. (2010). Movement disorders in childhood,
Philadelphia, PA: Saunders.
Specht, M. W., Woods, D. W., Piacenti, J., Scahill, L., Wilhelm, S., Peterson, A. L., … Walkup,
J. T. (2011). Clinical characteristics of children and adolescents with a primary tic disorder.
Journal of Developmental and Physical Disabilities, 23, 15–31. doi:10.1007/s10882-010-
9223-z
Varni, J. W., Boyd, E. F., & Cataldo, M. F. (1978). Self-monitoring, external reinforcement, and
timeout procedures in the control of high rate tic behaviors in a hyperactive child. Journal
of Behavior Therapy and Experimental Psychiatry, 9, 353–358. doi:10.1016/0005-
7916(78)90013-7
Verdellen, C. W. J., Hoogduin, C. A. L., & Keijsers, G. P. J. (2007). Tic suppression in
the treatment of Tourette’s syndrome with exposure therapy: The rebound phenomenon
reconsidered. Movement Disorders, 22, 1601–1606. doi:10.1002/mds.21577
Verdellen, C. W. J., Keijsers, G. P. J., Cath, D. C., & Hoogduin, C. A. L. (2004). Exposure
with response prevention versus habit reversal in Tourette’s syndrome: A controlled study.
Behaviour Research and Therapy, 42, 501–511. doi:10.1016/S0005-7967(03)00154-2
Wang, Z., Maia, T. V., Marsh, R., Colibazzi, T., Gerber, A., & Peterson, B. S. (2011). The
neural circuits that generate tics in Tourette syndrome. American Journal of Psychiatry,
168, 1326–1337.
Watson, T. S., & Sterling, H. E. (1998). Brief functional analysis and treatment of a vocal tic.
Journal of Applied Behavior Analysis, 31, 471–474. doi:10.1901/jaba.1998.31-471
Wilhelm, S., Deckersbach, T., Coffey, B. J., Bohne, A., Peterson, A. L., & Baer, L.
(2003). Habit reversal versus supportive psychotherapy for Tourette’s disorder: A
randomized controlled trial. American Journal of Psychiatry, 160, 1175–1177. doi:
10.1176/appi.ajp.160.6.1175
Wilhelm, S., Peterson, A. L., Piacentini, J., Woods, D. W., Deckersbach, T., Sukhodolsky,
D. G., … Scahill, L. (2012). Randomized trial of behavior therapy for adults with Tourette
syndrome. Archives of General Psychiatry, 69, 795–803.
Woods, D. W., Conelea, C. A., & Himle, M. B. (2010). Behavior therapy for Tourette’s
disorder: Utilization in a community sample and an emerging area of practice. Professional
Psychology: Research & Practice, 41, 518–525. doi:10.1037/a0021709
Woods, D. W., Miltenberger, R. G., & Lumley, V. A. (1996). Sequential application of major
habit-reversal components to treat motor tics in children. Journal of Applied Behavior
Analysis, 29, 483–493. doi:10.1901/jaba.1996.29-483
Woods, D. W., Piacentini, J. C., Chang, S. W., Deckersbach, T., Ginsberg, G. S., Peterson,
A. L., … Wilhelm, S. (2008). Managing Tourette syndrome: A behavioral intervention for
children and adult (therapist guide). New York, NY: Oxford University Press.
Woods, D. W., Piacentini, J., Himle, M. B., & Chang, S. (2005). Premonitory urge for
tics scale (PUTS): Initial psychometric results and examination of the premonitory urge
phenomenon in youths with tic disorders. Journal of Developmental and Behavioral
Pediatrics, 26, 397–403. doi:10.1097/00004703-200512000-00001
Woods, D. W., Twohig, M. P., Flessner, C. A., & Roloff, T. J. (2003). Treatment of vocal tics
in children with Tourette syndrome: Investigating the efficacy of habit reversal. Journal of
Applied Behavior Analysis, 36, 109–112. doi:10.1901/jaba.2003.36-109
46
Compulsive Hoarding
Sheila Woody
Gail Steketee
Hoarding has received considerable media attention in recent years, with reality
television shows devoted to peering into the homes of people who have so much
stuff they cannot use many, if not most or even all, of the rooms. Hoarding is a
fascinating topic for the general public, no doubt in part because everyone must
cope with objects, paper, and mail that come into their environment, and because
it conflicts with North American values of cleanliness and organization evident in
the many magazines and television shows depicting beautiful homes. Accordingly,
residents of hoarded homes are typically stigmatized and many become isolated due
to shame over the state of their home.
Epidemiological studies suggest that hoarding is a surprisingly common condition,
affecting 2–5% of the adult population in Western countries (Iervolino et al., 2009;
Mueller et al., 2009; Samuels et al., 2008). These statistics indicate that most city and
suburban neighborhoods have substantial numbers of individuals living in hoarded
homes (one in every 20–25 people), and that most people know someone who has
a hoarding problem, although they may not be aware of the extent of the problem
as it is commonly hidden from view. These epidemiological studies also suggest that
hoarding occurs in both men and women, perhaps even more frequently among
men, although women tend to volunteer for studies of hoarding and its treatment.
A substantial portion of people who hoard live alone and many are not married or
partnered (Grisham, Frost, Steketee, Kim, & Hood, 2006; Samuels et al., 2008).
The impairment due to hoarding is not simply related to social judgment about
“poor housekeeping” stemming from a misconception of hoarding as a lifestyle choice.
Due to dwellers’ unwillingness to let workers enter the home or their own inability to
access parts of their home, hoarded homes can be neglected, with mounting health
code violations and safety concerns. Of paramount concern is fire safety, which can
be compromised by blocked egress, high fuel load, or combustible materials piled

DOI: 10.1002/9781118528563.wbcbt46
near heat sources. The most commonly hoarded items are paper and clothing—both
highly combustible. As a result, 60% of fires in hoarded homes spread beyond the
room of origin, compared with just 10% for the general population. Most tragically,
over a 10-year period, hoarded homes accounted for 24% of preventable fire fatalities
in Melbourne, Australia (Lucini, Monk, & Szlatenyi, 2009).
The presence in the home of vulnerable persons such as children or frail elderly
raises special concerns about protection from harm. In high density communities,
neighbors may also be at risk, as fire or pests can spread quickly from one unit to
another. This risk to others can lead to eviction or nonconsensual clean-outs of the
home (Tolin, Frost, Steketee, Gray, & Fitch, 2008), especially for tenants, who have
fewer legal protections than do homeowners regarding the sanctity of their home.
Hoarding is also associated with strained family relationships and social isolation
(Frost, Steketee, Williams, & Warren, 2000; Steketee & Frost, 2003; Tolin, Frost,
Steketee, & Fitch, 2008).
The most obvious feature of compulsive hoarding is clutter that fills some or all of
the rooms of a home to a degree that prevents normal use of the rooms and their
furnishings. Clutter on its own, although it attracts attention and stigma, is not the
hallmark symptom of compulsive hoarding. A home can become extremely cluttered,
for example, when the resident has a condition such as depression or physical
impairment preventing normal daily maintenance. In these cases, clutter develops
because the individual lacks the energy or mobility to put things away, remove
garbage, and organize objects in the home. Compulsive hoarding, in contrast, is
characterized by difficulty parting with things due to emotions and beliefs about
discarding. In many cases, the problem is exacerbated by excessive acquiring and
failure to organize possessions, leading to a cluttered and chaotic environment.
Hoarding has historically been considered a manifestation of obsessive-compulsive
disorder (OCD) or a feature of obsessive-compulsive personality disorder, but hoard-
ing disorder is now under consideration as a distinct diagnostic category for the
DSM-5 (see American Psychiatric Association, 2012). Proposed criteria include: (a)
difficulty discarding or parting with possessions, even those that seem to others to
lack value, (b) failure to discard motivated by strong urges to save items or distress
about letting go of the items, and (c) accumulation of a large number of possessions
that clutter the home to the extent that rooms cannot be used for their intended
purpose. If all living areas are uncluttered, it is only because third parties (e.g., family
members, authorities) intervene. In addition, (d) the symptoms cause clinically sig-
nificant distress or impairment in social, occupational or other functioning, including
maintaining a safe environment for oneself and others.
The proposed criteria include a specifier for the presence of excessive acquisition
(collecting, buying, or stealing of items that are not needed or for which there is no
space). In addition, because the degree of insight among people who hoard has been
identified as problematic (e.g., Tolin, Fitch, Frost, & Steketee, 2010), insight is rated
“good or fair,” “poor,” or “absent,” with corresponding implications for treatment
planning (see below). The accumulation of belongings that are worthless or exceed
available space is not limited to hoarding disorder; alternatives such as organic
syndromes (e.g., Alzheimer’s disease, brain injury) must be ruled out before settling
on a diagnosis (see Pertusa, Frost, Fullana, et al., 2010, for a full discussion of the
Compulsive Hoarding 1089
boundaries of diagnostic features of compulsive hoarding). Particularly challenging

is determining whether hoarding disorder or another problem better accounts for
the excessive accumulation of belongings. Pertusa, Frost, and Mataix-Cols (2010)
provided clarification of cases in which OCD might account for excessive clutter
due to avoidance of contamination fears or excessive urges to checking. In addition,
during a major depressive episode, lethargy and apathy can affect functioning in ways
that result in failure to discard items that most people would discard (e.g., used food
containers, newspapers, advertising material delivered to the home). Smaller homes
can become overwhelmed relatively quickly if no routine discarding or housekeeping
is done. If the possessions are saved passively (i.e., failure to discard rather than
intention to save) and the individual does not exhibit distress about parting with the
objects, then compulsive hoarding is not the appropriate primary diagnosis.
Nordsletten et al. (2013) have prepared a Structured Interview for Hoarding
Disorder (SIHD) to diagnose hoarding disorder according to DSM-5 criteria. Mataix-
Cols, de la Cruz, Nakao, and Pertusa (2011) obtained Web survey data from over
200 experts in the field who were asked to provide diagnostic ratings of clinical case
descriptions. Findings indicated high sensitivity and specificity for hoarding diagnoses;
the experts also believed the diagnostic criteria would be acceptable to patients. Initial
indications from a clinical field trial suggest that the proposed diagnostic criteria for
hoarding disorder showed excellent sensitivity, specificity, and inter-rater reliability
for individual criteria and for specifiers (Mataix-Cols, Billotti, Fernández de la Cruz,
& Nordsletten, 2013). Further, nearly all clinical participants believed that the new
hoarding disorder was an acceptable and useful diagnosis, and a majority thought it
was not too stigmatizing.
Assessment
In the absence of adequate measures of hoarding developed during the past decade,
early researchers working in OCD or anxiety clinics utilized the Yale-Brown Obsessive
Compulsive Scale (YBOCS; Goodman et al., 1989) to determine whether hoarding
was present. Although the YBOCS symptom checklist contains two items that assess
the presence or absence of hoarding “obsessions” and hoarding “compulsions,” these
items are not descriptive enough to be useful in clinical or research assessments of
hoarding symptoms. An alternative OCD symptom measure that provides slightly
more information is the 18-item self-report Obsessive Compulsive Inventory-Revised
(OCI-R; Foa et al., 2002) which contains three items that form a subscale for
hoarding. Again, this instrument provides initial evidence of hoarding symptoms
that may merit further assessment, but the OCI-R alone provides too little detail to
determine symptom severity or to help guide treatment planning.
Several key features of compulsive hoarding should be considered in the initial
assessment for treatment planning and for measuring outcomes following treatment.
The three features included in the proposed diagnostic criteria (difficulty discard-
ing, excessive acquiring, and clutter) are obvious primary targets for intervention.
Treatment researchers have used several measures to assess these constructs, the most
common of which are described below.
The Saving Inventory-Revised (SI-R) is a 23-item self-report questionnaire with

three factor-analytically derived subscales to address the core features of compulsive
hoarding: acquisition problems, difficulty discarding, and clutter (Frost, Steketee, &
Grisham, 2004). This measure showed good internal and test-retest reliability and
good construct validity, correlating strongly with other measures of hoarding and
discriminating known groups.
The Hoarding Rating Scale (HRS) is a five-item scale that can be completed in
interview or self-report format (Tolin, Frost, & Steketee, 2010). The HRS assesses
the three key features as well as functional impairment. Each item uses a 0–8 scale.
Despite its brevity, the scale has high internal reliability and strong test-retest reliability
across settings of assessment (i.e., clinic vs. home). The HRS-I also demonstrates
strong evidence of validity, correlating well with self and observer ratings of hoarding
severity and showing good criterion-related validity.
Volume of clutter is frequently assessed using the Clutter Image Rating scale (CIR;
Frost, Steketee, Tolin, & Renaud, 2008). This unique scale presents nine photographs
that range from no clutter to extensive clutter for each of three rooms: living room,
bedroom, and kitchen. Clients, family members, clinicians, or other raters select the
photograph that most closely resembles the volume of clutter in each main room
of the home. The CIR shows strong reliability over time, good convergence across
assessment contexts and between raters (e.g., self and observer).
Functional impairment and safety concerns can be assessed using the Activities
of Daily Living-Hoarding (ADL-H; Frost, Hristova, Steketee, & Tolin, 2013). The
15-item ADL-H lists activities people ordinarily do in their home, such as sleeping
in the bed and using bathroom fixtures and kitchen appliances. Participants (or an
observer) rate the degree of difficulty clutter presents for engaging in each activity,
ranging from “can do it easily” to “unable to do.” The ADL-H demonstrated good to
excellent internal consistency, and test-retest and inter-rater reliability, as well as good
convergent and discriminant validity among individuals with hoarding, individuals
with OCD, and community controls. The ADL-H is especially useful in clinical
settings to understand the specific type and extent of impairment experienced by
hoarding clients.
In addition to determining the core diagnostic elements of compulsive hoarding,
other important targets of hoarding symptom assessment can include attachment
to possessions and beliefs about discarding. Toward this end, the Saving Cognitions
Inventory (SCI) is a 24-item self-report measure of beliefs related to discarding posses-
sions (Steketee, Frost, & Kyrios, 2003). The four factor-analytically derived subscales
assess emotional attachment, concerns about memory, control over possessions, and
responsibility toward possessions. Each item presents a thought, and participants rate
the degree to which each thought influences their decision about whether to throw
something away. The subscales have good internal consistency, criterion validity, and
convergent and discriminant validity.
Additional targets for assessment to help determine next steps with regard to
intervention include common comorbid conditions such as depression, social anxiety,
and generalized anxiety disorder (Frost et al., 2013). Social anxiety and depression
are especially important accompaniments to hoarding to consider in developing a
treatment plan. For example, social phobia may make some clients reluctant to
enter group treatment, and depression may interfere with motivation quite apart
from ambivalence about parting with items. These problems can be assessed via
various standard self-report or interview measures. Also important to assess are
cognitive deficits pertinent to attention, organizing, and decision making, the last
being considered a hallmark symptom of hoarding. Concerns about clients’ ability to
maintain attention and available skills for organizing and decision making are likely
to emerge during the treatment process itself. Specialized strategies for addressing
these problems are recommended in Steketee and Frost’s (2007) therapist guide to
treatment of hoarding. We now turn our attention to empirical studies of treatment
interventions for hoarding, beginning with psychosocial treatments before addressing
pharmacotherapy.
Initial efforts to examine the efficacy of cognitive and behavioral therapy (CBT)
for hoarding began with available data from studies treating clients with OCD
and examining the outcomes of those with hoarding symptoms. Several researchers
have retrospectively analyzed data from these studies in an effort to determine
whether particular OCD symptom profiles (subtypes) were associated with differential
outcomes. Hoarding is one profile that has reliably appeared in numerous independent
factor analyses of OCD symptoms (Baer, 1994; Calamari, Wiegartz, & Janeck, 1999;
Leckman et al., 1997; Mataix-Cols, Rauch, Manzo, Jenike, & Baer, 1999). Notably,
these studies recruited OCD patients with hoarding symptoms (typically assessed with
only two items on the YBOCS symptom checklist), rather than people for whom
hoarding was the primary problem.
Mataix-Cols, Marks, Greist, Kobak, and Baer (2002) analyzed data from a multisite
study that compared computer-based versus clinician-directed exposure and response
prevention (ERP) for 153 outpatients with OCD. ERP involved two major strategies:
exposure to fear-provoking stimuli (e.g., contaminants) and elimination of rituals (e.g.,
handwashing). Applied to hoarding, ERP was accomplished by exposing participants
to desired objects without acquiring them and to parting with objects via recycling,
donating, and discarding them. Mataix-Cols et al. reported a much higher rate of
treatment refusal among those with hoarding symptoms, with 27% discontinuing
before finishing the first session in contrast to 12% of participants without hoarding
symptoms. Among 20 patients with hoarding symptoms who completed at least one
session of ERP, only five (25%) responded with at least a 40% reduction in YBOCS
total score. The rate of treatment response was higher for participants with other
symptom dimensions (35– 40%), except sexual/religious obsessions (21%), but this
difference was not statistically significant with this sample size.
Two studies have examined OCD symptom profile dimensions as predictors of CBT
response in more traditional clinic settings (Abramowitz, Franklin, Schwartz, & Furr,
2003; Rufer, Fricke, Moritz, Kloss, & Hand, 2006). These two studies respectively
included 132 and 104 consecutive admissions to OCD specialty treatment centers.
Most patients in both studies also received pharmacological treatments. Although
both studies involved individual therapist-directed ERP, the details of the treatment
differed in some respects. The Abramowitz et al. study involved 15 outpatient sessions,
whereas the Rufer et al. study was conducted in an inpatient setting where patients
received CBT 4 days a week (mean duration = 9 weeks) plus participation in group
programs to develop social, stress management, and problem-solving skills. Despite
the protocol differences, results from these two studies were fairly consistent. Patients
with hoarding symptoms had more residual symptoms following treatment, with fewer
than 40% classed as treatment responders. In the Rufer et al. study, 37% of patients
with hoarding symptoms achieved at least 35% reduction in their YBOCS total score
compared with 63% of patients without hoarding symptoms. Using more stringent
criteria for treatment response, Abramowitz et al. reported 31% of hoarding patients
compared to 46–76% of patients with other symptom clusters showed clinically
significant change (Jacobson, Roberts, Berns, & McGlinchey, 1999).
Overall, these studies indicate that classic ERP treatment methods are effective for
a large portion of people with OCD symptoms that do not include hoarding, but
they are not very effective for those with hoarding problems. Unfortunately, these
studies did not have the advantage of our current understanding and assessment of
the symptoms and diagnostic criteria for hoarding, and therefore it is not clear how
many of the participants would have met proposed criteria for hoarding. Nonetheless,
these studies demonstrated that ERP methods did not improve hoarding problems
sufficiently compared to their benefit for OCD. New treatment methods were clearly
needed.
Specialized Cognitive Behavioral Therapy for Hoarding
In the wake of findings that ERP was inadequate to ameliorate hoarding symptoms,
Steketee and Frost (2007) developed a multicomponent approach to treating hoarding
that has undergone initial research testing of its efficacy using a variety of delivery
formats. The approach includes elements that are common to CBT approaches to
OCD, such as exposure and practice in reducing, acquiring, and removing clutter,
as well as cognitive strategies to facilitate these activities. In addition, the protocol
includes motivational interviewing methods to improve insight, reduce ambivalence
about making changes, and enhance clients’ involvement in establishing the treatment
goals, as well as cognitive skills training in organizing, decision-making, and problem-
solving skills. Much of the treatment can be conducted in the clinician’s office, but
the protocol also specifies monthly home-based sessions.
Individual Therapy
Tolin, Frost, and Steketee (2007a) conducted the first pre-post open (uncontrolled)
trial of this specialized CBT for compulsive hoarding. Of 14 clients enrolled in
the study, 10 completed 26 individual sessions over the course of 7–12 months.
Seventy-five percent of the sessions were held in the office, with the remaining 25%
(at least once a month) occurring in the client’s home or in places of excessive
acquisition. Tolin et al. reported roughly 25–30% reductions on subscales of the
SI-R, with six of 10 clients meeting Jacobson and Truax (1991) criteria for clinically
significant change. Changes on the CIR were statistically significant but not as large;
the effect size calculated via Cohen’s d was 0.8. Importantly, homework compliance
was strongly correlated with treatment gains, but clients generally completed only
25–50% of their between-session goals even with the motivational enhancement
strategies included in the protocol.
Following up on their initial pilot trial, Steketee, Frost, Tolin, Rasmussen, and
Brown (2010) conducted a somewhat larger but still small randomized controlled
trial comparing the specialized CBT for hoarding to a wait period without treatment
at two clinic sites. The wait-list and treatment groups were compared after 12 weeks,
at which point CBT participants continued their treatment for a total of 26 sessions,
while wait-listed participants were reassigned to CBT for 26 sessions. At the 12-week
comparison point, CBT patients showed an average 15% reduction in SI-R scores
(controlled d = 1.0) whereas wait-listed participants showed almost no improvement
(<2% change). Furthermore, at 12 weeks, therapists rated 43.5% of CBT patients
as “much” or “very much” improved, compared to 0% of the wait-list patients.
After the full 26 sessions of treatment for all patients (including those who began
treatment following their participation in the wait-list condition), effect sizes were
large (d > 1.2) for all measures of hoarding symptoms. Notably, the average duration
of the 26-session therapy was 44.8 weeks (range: 28–77) due to challenges with
patient scheduling and motivation.
Two studies have extended this intervention to older adults using case series
designs. In the Turner, Steketee, and Nauth (2010) study, trained community
clinicians provided the treatment. Although only six of 11 clients completed the
treatment, symptom reduction was similar in magnitude to that reported by Tolin
et al. (2007a), with 28% reduction in CIR and 24% improvement in functional use
of the home as measured by the ADL-H scale. Progress was notably uneven both
within and across clients. Ayers, Setherell, Golshan, and Saxena (2011) also tested the
Steketee and Frost (2007) version of CBT in a case series of 12 older adults. In an
effort to promote homework compliance and more rapid change, they scheduled the
first 20 sessions twice weekly and then tapered to once weekly for six final sessions.
Although the overall results showed approximately 20% reductions on two measures
of hoarding severity, only three of the clients were considered treatment responders.
Unfortunately, two of these three relapsed to baseline status during the 6-month
follow-up period, suggesting enhanced or alternative treatments may be necessary for
older adults who have problems with compulsive hoarding.
To date, we are not aware of other clinic settings that have tested this individual CBT
intervention for hoarding, despite its apparent efficacy. Ideally, future research will
also test how well this specialized intervention method compares to ERP treatment
or to group strategies for treating hoarding (which are described next in this chapter).
Group Therapy
Given the amount of therapist time invested in the specialized CBT protocol for
hoarding, cost and feasibility are obvious concerns. Using a group therapy format
for at least a portion of the treatment might help reduce the cost as well as address
issues of social isolation and poor motivation which are characteristic of clients with
hoarding problems. Steketee, Frost, Wincze, Greene, and Douglass (2000) described
the first specialized CBT for hoarding which was conducted mainly in a group therapy
format, although this early version of the treatment protocol did not yet contain
strategies for motivation enhancement or detailed cognitive therapy methods found
in the Steketee and Frost (2007) guide. In this initial study, seven clients engaged in
15 sessions of group therapy spaced over 20 weeks (weekly for the first 10 sessions
and every other week for the last five) plus individual home visits between most group
sessions; an eighth client received individual treatment only. Although the treatment
had positive effects, the magnitude of the gains was modest. Average scores on a
YBOCS adapted specifically for hoarding dropped from 22 to 19, but the overall level
of clutter showed little improvement.
In a next step of development of group approaches to CBT for hoarding, Muroff,
Steketee, Rasmussen, et al. (2009) reported pre-post data on a series of five treatment
groups with a total sample of 32 participants who met criteria for primary hoarding
problems. The first four groups involved 16 sessions of standard clinic care that
adapted the Steketee and Frost (2007) protocol for the group format (n = 27). Over
time, the researchers used their experiences to develop a manualized group treatment
protocol which was employed for 20 sessions for the fifth treatment group (n = 5).
The approach involved weekly 2-hour group sessions plus two 1.5-hour individual
home visits. Findings showed large reductions in hoarding symptoms (d = 1.57) and
depression, with the final manualized treatment group achieving better results than
the earlier ones (d = 1.88).
Picking up on the suggestion that a more formalized group CBT treatment protocol
could lead to better outcomes for hoarding clients, researchers at the Institute of
Living in Hartford conducted an open trial in which 16–20 group sessions were
delivered by the clinician without home visits (Gilliam et al., 2011). A modest fee
was charged for each session and home visits were eliminated in an effort to develop
a protocol that would be more feasible for community-based clinical settings. In data
collected with 35 patients, large effect sizes were observed for all subscales of the SI-R
(d ≥ 1.06) as well as social and occupational impairment (d = 1.12) and the ADL scales
(d = 0.82). Limitations of this study included the fact that all outcomes were self-
reported and lacked corroborative information from home visits. In addition, attrition
was a problem as only 67% of participants completed treatment. Nevertheless, these
results indicated that the development of group treatment protocols for hoarding was
progressing in a promising direction.
In a more recent small randomized controlled trial of group treatment, Muroff,
Steketee, Bratiotis, and Ross (2012) found even larger within-participant (i.e., uncon-
trolled pre-post) effect sizes. In this study, 38 participants who met criteria for
hoarding disorder were randomly assigned to receive one of three conditions: (a)
standard group CBT, (b) enhanced group CBT, and (c) bibliotherapy. The standard
group treatment (n = 14) involved 20 weekly 2-hour group sessions with two co-
therapists plus four 90-minute home visits by one of the therapists. The enhanced
format (n = 11) contained these features plus an additional four home visits by a
trained nonclinician home assistant. The bibliotherapy group was asked to read Buried
in Treasures (Tolin, Frost, & Steketee, 2007b) during the 20-week period. Although
the small sample size resulted in underpowered statistical tests, the group treatments
resulted in large effect sizes (1.19 ≤ d ≤ 3.36) for all outcome variables. No measure
of bibliotherapy outcomes showed changes of this magnitude (0.18 ≤ d ≤ 0.88).
Although the two group formats did not differ statistically at posttreatment, the home
assistant enhancement appears worthwhile to explore in future studies because the
effect sizes were substantially larger for some variables. For example, the SI-R clutter
subscale pre-post (uncontrolled) effect sizes were 3.03 for the enhanced format and
1.56 for the standard group CBT for hoarding, suggesting that additional home visits
may substantially improve clutter for some participants.
Enhanced Self-Help
The specialized CBT developed to treat compulsive hoarding has continued to
improve outcomes, with steadily increasing effect sizes. Nevertheless, most patients
remain symptomatic in spite of the sometimes lengthy and costly treatments, and
gaining access to a clinician with expertise in this specialized treatment is still extremely
difficult as few are trained in these methods for this complex syndrome. Partly in
response to these problems, Frost, Pekereva-Kochergina, and Maxner (2011) exam-
ined the feasibility and preliminary outcomes of carefully structured nonprofessional
support groups in an open trial. This study used trained undergraduate assistants to
facilitate the groups, which met in a university classroom for 2-hour sessions over 13
weeks. The facilitators had taken a seminar course on hoarding behavior and utilized
Buried in Treasures (Tolin et al., 2007b), a self-help book that served as a sort of
textbook for the group. An experienced psychologist supervised the facilitators and
provided clinical backup.
Results showed that 12 of 28 participants (43%) met criteria for clinically significant
change on the SI-R at the end of the group. Despite the small sample, all measures
of hoarding severity showed statistically significant reductions on self-report and
in-home clinician assessments. Nevertheless, at the conclusion of the groups, more
than half of participants continued to report hoarding symptoms above the clinical
cutoff score of 41 on the SI-R. These results suggest the potential utility of a stepped
care model whereby this type of group could be a cost-effective first step, resulting
in substantial improvements for some participants and potentially a motivation-
enhancing pretreatment step for those who need to make additional gains through
other treatment mechanisms.
Following on the demonstrated utility of self-help CBT for OCD participants
(for a review, see Mataix-Cols & Marks, 2006), Muroff, Steketee, Himle, and Frost
(2010) studied outcomes of an online CBT-based self-help community that has been
operating for more than 10 years. The online community is restricted to people
with self-identified problems with hoarding or cluttering (and explicitly excludes
researchers, professionals, and family members). The community has a maximum
size of 100 participants and a waiting list of another 100 individuals with hoarding,
with turnover ranging from three to 10 people per month. To remain in the group,
members are required to make regular postings about their behavioral goals and
progress toward those goals. Evidence-based resource materials are provided, and
community members and leaders provide CBT-style support in an online chat area.
Muroff et al. (2010) conducted a series of self-report surveys every 3 months to
document changes in hoarding symptoms for online community members who had
recently joined the group, as well as for those who had been members for a longer
period, and for those waiting for space to become available to join the group. Findings
indicated modest but significant improvement in active online members’ hoarding
symptoms over a 15-month period, with degree of engagement (i.e., number of
online posts) being a significant predictor of progress on hoarding. Effect sizes (0.35
≤ d ≤ 1.03) were comparable to those observed for the bibliotherapy condition in
the Muroff, Steketee, Bratiotis, and Ross (2012) study and somewhat smaller than
those observed in the Frost et al. (2011) in-person structured support groups.
Accordingly, it is clear that people with clinical hoarding problems benefit from self-
help groups that focus on CBT methods developed to treat hoarding problems. These
methods are derived from those described in Steketee and Frost’s (2007) therapy
manual and have been adapted for use by nonclinicians who have been trained or are
well-practiced in applying these methods. The extent of benefit from these guided
self-help groups ranges from modest to substantial, suggesting that further research
is needed to clarify the critical elements that produce the most change in hoarding
symptoms. It will be of value to determine whether these self-help methods affect
some symptoms more than others with regard to urges to acquire and save objects,
corresponding difficulty parting with possessions, and especially clutter in the home,
which may improve more slowly than other symptoms. To date, the CBT treatment
methods described above have not been combined with medications, as the literature
on effective medications for hoarding has been very limited and not particularly
promising. The research to date on this topic is described in the next section of this
chapter.
Pharmacotherapy
The earliest information on the value of medications for treating hoarding has emerged
in the context of efforts to identify prognostic indicators for OCD clients receiving
treatment. Several researchers have examined the degree to which factor-analytically
derived OCD symptom profiles (“symptom subtypes”) predicted response to phar-
macological treatments. As noted in the discussion of ERP treatment for OCD,
hoarding has emerged as a reliably distinct factor on the YBOCS symptom check-
list (e.g., Bloch, Landeros-Weisenberger, Rosario, Pittenger, & Leckman, 2008).
Retrospective studies of predictors of outcome provide hints about the potential
pharmacological treatment response for compulsive hoarding by examining patients
who participated in treatment studies for OCD.
Several studies indicate OCD patients with hoarding symptoms are less likely
to respond to serotonergic medications (e.g., paroxetine, fluvoxamine, fluoxetine,
citalopram) that have demonstrated effectiveness for OCD more broadly. In an early
study, Black et al. (1998) examined 38 nondepressed OCD patients who received 12
weeks of paroxetine (n = 20), CBT (n = 10), or pill placebo (n = 8). In spite of
the small sample, treatment responders were significantly less likely to have hoarding
symptoms (18% of responders in comparison to 67% of nonresponders). In a much
larger study, Mataix-Cols et al. (1999) analyzed data from 150 nondepressed OCD
patients drawn from six medication treatment trials. Ten patients reported hoarding
as their major problem, and 22 reported hoarding as a secondary symptom domain.
Hoarding dimension scores predicted worse outcome of medication treatment (but
not placebo responding).
In the last few years, other large retrospective studies have shown further evidence
that the hoarding symptom cluster of OCD does not respond as well to medication.
Stein’s research group conducted two multinational studies showing that hoarding
and symmetry symptoms (examined together as a single factor) predicted worse
treatment outcomes in response to several types and dosages of selective serotonin
reuptake inhibitors (SSRIs; Stein, Andersen, & Overo, 2007; Stein et al., 2008).
These very large studies (N = 867 patients across the two studies) included ample
numbers of patients with hoarding/symmetry as a primary symptom profile in the
analysis. Matsunaga et al. (2009) reported a similar result (N = 137) whereby patients
who failed to respond to 12 weeks of SSRI therapy were more likely to have hoarding
symptoms than were treatment responders. In the Matsunaga et al. study, symmetry
also emerged as a significant predictor of nonresponse to SSRI therapy, and, in
contrast to other studies reported here, other symptoms of ordering and repeating
also emerged as predictors of worse outcomes. Salomoni et al. (2009) examined 130
patients treated with 6 months of medication and/or behavior therapy. The overall
response rate (≥ 40% improvement in YBOCS score) in this open clinic-based study
was 53%, but only 28% of 18 patients with hoarding obsessions and 17% of 12 patients
with hoarding compulsions showed this level of response. Finally, using a different
design to study hoarding outcomes using retrospective data, Cullen et al. (2007)
analyzed medical history data gathered as part of two family studies of OCD and
reported hoarding symptoms predicted significantly lower odds of response to SSRIs.
On the other hand, some researchers have published evidence suggesting OCD
with hoarding is not predictive of poor response to medication. Some of these
studies are difficult to interpret because of small samples or inadequate description
of symptom profiles. For example, Alonso et al. (2001) described 60 OCD patients
who completed long-term treatment (1–5 years) with SSRIs plus behavior therapy.
Unfortunately, the sample included fewer than five patients with hoarding symptoms,
and only two reported hoarding compulsions as a major symptom. Alarcon, Libb,
and Spitler (1993) reported cleaning, but not hoarding, compulsions predicted poor
response to long-term clomipramine in an open study. Symptom profiles of the 45
OCD patients involved in this study were not presented, so it is not clear whether a
sufficient number of patients with hoarding symptoms were included.
Two larger studies are available. Erzegovesi et al. (2001) analyzed data from
159 nondepressed OCD patients who were randomly assigned to 12 weeks of
pharmacotherapy via SSRIs or clomipramine. Among responders, 8 of 90 (9%) had
hoarding symptoms, whereas 11 of 69 (16%) nonresponders had hoarding symptoms,
which was not a significant difference. Interestingly, only somatic obsessions were
significantly more frequent among the nonresponders. Shetti et al. (2005) reported
similar results in a study of 122 OCD patients who had previously received adequate
trials with at least two serotonin reuptake inhibitors (SRIs). Based on patient interview
and chart review, two psychiatrists independently rated patients as responder or
nonresponder to SRI therapy. Five of 13 (38%) patients with hoarding symptoms
were categorized as responders, and although the proportion of responders in the

total sample (including those with hoarding) appeared to be higher (67 of 122; 55%),
this difference was not statistically significant. Neither of these studies used empirically
derived symptom profiles, however, relying only on the semantic groupings of the
YBOCS symptom checklist. In contrast, nearly all of the studies showing hoarding
predicted poorer treatment response (cf. Matsunaga et al., 2009) used factor analysis
to derive symptom clusters.
These retrospective studies provide only hints about the degree to which hoarding
is responsive to pharmacotherapy. Most of these studies defined treatment response
on the basis of the YBOCS, the standard tool for assessing severity of OCD symptoms
in both research and clinical settings, but, as noted earlier, this instrument has serious
shortcomings in assessing hoarding. For example, the YBOCS involves clinician
ratings made on the basis of patient report during an interview. This is usually not
a problem for assessing OCD, as patients with this problem generally recognize
that their symptoms are unreasonable responses to anxious feelings. Individuals
with hoarding, however, often have fluctuating insight into the severity of their
problem, necessitating a home visit to obtain an assessment that is convincingly
reliable and valid. In addition, the YBOCS scale that indexes illness severity is based
on all OCD symptoms and therefore fails to reflect the severity of hoarding-specific
symptoms. Finally, as previously mentioned, these studies all examined patients who
were recruited for studies on OCD. This is problematic in two ways. As hoarding
differs from OCD in important respects (Pertusa, Frost, Fullana, et al., 2010), studies
specifically focusing on hoarding typically contain only a minority of participants who
display significant symptoms of OCD (see Frost, Steketee, & Tolin, 2011). Further,
clinical impression suggests that most people with primary hoarding problems do not
identify their symptoms as OCD-related and therefore do not seek treatment from
such clinic settings. Thus, studies of hoarding conducted in settings that recruit OCD
patients are unlikely to have representative samples of those who suffer from clinically
significant hoarding disorder.
In an effort to address some of the shortcomings of previous studies, Saxena,
Brody, Maidment, and Baxter (2007) conducted the first prospective study to
compare response of hoarding and nonhoarding OCD. This study involved 10–12
weeks of open treatment with paroxetine for 32 patients who met well-defined criteria
for compulsive hoarding (Frost, Krause, & Steketee, 1996) and 47 patients with
nonhoarding OCD. Patients in the two groups had very similar rates of improvement,
with 50% of those with hoarding and 47% of those with nonhoarding OCD showing
at least a partial response (defined as ≥ 25% decrease in YBOCS scores). Dropout rates
were 15% among nonhoarding OCD patients and 22% for the compulsive hoarding
group; this difference was not statistically significant. While this study was not as
large as some of the more recent retrospective studies, it clearly involved a sample
of patients for whom hoarding was their most prominent OCD symptom factor. In
addition, although treatment response was defined on the basis of YBOCS scores, this
study did implement a hoarding-specific interview assessment (without home visit)
partway through the study; response rates looked quite similar for this measure as
for the YBOCS. Still, the response rate in both treated groups was not particularly
impressive given the relatively low threshold used to indicate benefit according to
the YBOCS, and a substantial number of patients (n = 18) were unable to tolerate
the recommended full dose of medication. Clearly, this study requires replication and
extension to other serotonergic medications, given the promising findings.
Saxena (2011) reported preliminary findings from an open trial for hoarding that
used extended release venlafaxine (Effexor XR), a medication chosen because of its
tolerability for older adults and for nonresponders to SSRIs. Participants met DSM-5
proposed diagnostic criteria for hoarding disorder and were required to score 44 or
above on the SI-R and above threshold on another measure of hoarding. The sample
was more restricted in that only major depression and dysthymia were permitted as
comorbid conditions. Saxena reported preliminary results for 14 patients (12 women,
two men) enrolled to date, of whom only one had dropped out for reasons unrelated
to the medication. Nine of the 13 completers of the 12-week trial showed significant
improvements in hoarding (with an average 31% reduction on the SI-R), as well as on
measures of depression (51% reduction) and general functioning (21% improvement).
Among treatment completers, eight (61%) were classified as responders based on
30% reduction in hoarding symptoms and ratings of “much improved” or more on
the clinical global improvement scale. It appears that venlafaxine may be useful and
well tolerated for treating hoarding, although this sample size is very small and a
controlled trial will be needed to demonstrate clear efficacy over placebo or alternative
medications.
Overall, there are not yet sufficient data to indicate that any particular medication
is effective for treating hoarding symptoms. The retrospective findings from multiple
trials suggest that SRIs have not performed well in treatment for hoarding, although
there are exceptions to these findings. A major concern with these studies is their
recruitment methods through OCD clinics in which those with primary hoarding
problems may not be well represented in the samples. Only two prospective studies
that recruited for hoarding symptoms have been conducted, both by Saxena and
colleagues. While these are promising, the samples are small, and the research
designs are limited for drawing firm conclusions. Thus at this time, there is no
known medication treatment that can be recommended for hoarding symptoms.
Future studies will need to include larger samples recruited for hoarding as the
main problem, with common comorbid conditions allowed in order to adequately
represent this complex syndrome which is rarely found in isolation from other health
and mental health problems. Study of how medications affect the symptoms of
hoarding—acquiring, difficulty parting with objects, clutter, disorganization, and
difficulty making decisions—will be particularly helpful for understanding the specific
impact of medications on these problems.
Treatment Challenges
While the field now has a promising treatment for clinical hoarding problems in
the cognitive and behavioral methods described by Steketee and Frost and tested in
various modalities, perhaps the most serious challenge is achieving recovery from this
debilitating problem. While CBT is highly beneficial, the average treatment gains are
still modest and few treated clients have clutter-free homes. In fact, it seems that the
amount of clutter may be the slowest symptom to respond to treatment in contrast

to control over excessive acquiring which appears to show fairly rapid change (e.g.,
Steketee et al., 2010).
A particularly serious challenge in treating hoarding is the cost and time involved.
The Steketee et al. (2010) trial involved 26 sessions and took nearly a year for
the average patient to complete treatment. What takes so long? Many of the com-
plicating factors evident in the treatment of OCD are also apparent for hoarding.
Comorbid depression, for example, is common (Frost, Steketee, & Tolin, 2011)
and may interfere with treatment as for nonhoarding OCD (Muroff, Steketee, Frost,
& Tolin, 2012). Hoarding is accompanied by a variety of other comorbid mental
and physical health problems that impair the capacity to engage in CBT. Another
treatment challenge is the presence of other OCD symptoms, such as contamination
and checking compulsions. These can complicate CBT for hoarding as sorting disor-
ganized possessions often triggers these symptoms, generating additional discomfort
and sidetracking the therapy, at least for a time. Unfortunately, given the relatively
small samples treated in CBT trials so far, it is not surprising that comorbid depression,
OCD, and other symptoms have received very limited study to date.
Fluctuating insight is another treatment complication that is especially relevant in
the case of hoarding where awareness of the problem is more limited than for most
OCD patients. When anxious, OCD patients often show a sharp drop in insight into
the reasonableness of their concerns as the probability of terrible events (for example,
harm to a loved one) rises in their estimation, uncertainty is more difficult to tolerate,
and pressure to act to prevent feared events increases. This pattern is certainly apparent
in hoarding, and seems worse as insight is generally poorer in this population (Tolin,
Fitch, et al., 2010). Even during calm moments, hoarding sufferers are less likely to
recognize the extent of clutter and the problems it causes.
Delivering CBT for hoarding also presents some unique challenges that complicate
efforts to develop effective treatments. Home visits have become a common com-
ponent of protocols for delivering individual and group CBT for hoarding. Due to
the generally poor insight, completing a valid assessment can be difficult without at
least an initial home visit. At the same time, shame over the state of the home can
make it difficult for clients to agree to a clinician visit. To address this problem, CBT
protocols for hoarding often permit the initial visit to be delayed until the client has
had an opportunity to develop a therapeutic alliance with the clinicians in the first few
sessions of therapy. However, clients are asked to consent at the outset to periodic
home visits, beginning by the fourth session at the latest (Steketee & Frost, 2007).
The clinical practicality of treatment is an important problem—therapist time is
expensive, and adding travel costs may mean home visits are not feasible in many
settings. The high cost of home visits for assessment and therapy sessions prompted
Gilliam et al. (2011) to eliminate them from their group treatment protocol. In
practice, however, home visits seem extremely valuable, permitting the therapist to
make judgments about priority treatment targets (especially safety concerns) and how
to guide organizing skills, as well as facilitate in vivo exposure and cognitive skills
development. Nevertheless, no research has directly examined whether home visits
make a difference to outcome or the circumstances under which home visits are
necessary for progress.
Another complication with hoarding involves the multiple agencies that are some-
times involved in hoarding cases. Due to safety issues such as fire risk or child
protection, hoarding frequently comes to the attention of civil authorities because of
building code or property use violations. Addressing these hoarding-related problems
may require coordination of multiple agencies representing diverse disciplines such
as fire safety, building inspectors, housing providers or landlords, protective services
workers, and public health and mental health workers. Providing treatment within
the context of multiple agency involvement raises ethical challenges that are not faced
by clinicians engaged exclusively in office-based practice, such as managing confi-
dentiality concerns while advocating on a client’s behalf with enforcement officers.
Gibson, Rasmussen, Steketee, Frost, and Tolin (2010) provide a full discussion of
ethical concerns in treating hoarding.
Promising Future Directions
As is evident from a careful reading of the treatment literature, research on the

treatment of hoarding disorder is still in the early stages. Although hoarding has often
been conceptualized as a symptom profile or subtype of OCD, research increasingly
suggests that this is not accurate and that optimal treatment for hoarding requires a
different approach than standard treatment for OCD. Steketee and Frost (2007) have
made a good start with their specialized CBT model, and their approach continues to
improve with each study. With regard to pharmacotherapy, only Saxena and colleagues
(Saxena, 2011; Saxena et al., 2007) have prospectively examined medications for
hoarding using recruitment and assessment methods specifically focused on hoarding
symptoms. Research on psychosocial interventions initially began with retrospective
comparisons of symptom dimensions and then moved to innovative treatments that
targeted people suffering from primary hoarding. In parallel, researchers now need to
test pharmacological therapies aimed at hoarding symptoms based on physiological
models of how chosen medications might influence hoarding symptoms.
Developing innovative ways to achieve the benefits of home visits at lower cost
would be an important contribution. Muroff, Steketee, and Frost (2009) have begun
to test use of a webcam-based method that permits virtual home visits for every
session. Therapy takes place at a distance using the webcam (ideally on a laptop so
clients can move around the home and therapists can view different spaces in the
home). Results from the first few clients suggest fewer missed sessions and a good
therapeutic alliance comparable to in-office treatment. Two of the first three clients
treated with this method showed good improvement, while one client who was
working with an immovable desktop computer showed no change.
Family strain is an important problem that has received little research attention.
As with nonhoarding OCD, family members often must continually enforce limits
on how much they will accommodate the symptoms and where they draw the line.
Clutter can take over all available space in the home unless strong limits are imposed,
something not all family members are willing or able to do, especially as those who
hoard resist these limits with displays of strong emotion. Whether through conflict
over belongings and space in the home or through stigma and shame about living in a
cluttered (and sometimes neglected) home, hoarding places a burden on all members
of the family (Tolin, Frost, Steketee, & Fitch, 2008). Due to their frustration, some
family members engage in a misguided effort to reduce the problem by surreptitiously
removing things they perceive to be worthless; this is experienced as a violation and
betrayal by the person who hoards. Perhaps as a result, many people with hoarding
become isolated from family members and have impoverished social networks. Current
treatments do not address these family issues, although group treatments may help
provide social support that can be an important impetus for achieving and maintaining
treatment gains. Tompkins and Hartl (2009) have developed a compelling protocol
for family members in relation to a loved one’s hoarding, but its efficacy has not yet
been empirically tested.
More than 80 communities in the United States and Canada have formed
community-based task forces to coordinate multiagency interventions for hoard-
ing cases that come to public attention (Bratiotis, Sorrentino Schmalisch, & Steketee,
2011). In some cases, involvement of such agencies provides external pressure that
can increase the client’s motivation to address his or her hoarding behavior. Some of
these agencies can also provide helpful assistance—a well-trained home health aide,
for example, can help a client make substantial progress in sorting through accu-
mulated clutter. On the other hand, ill-conceived interventions from such agencies
can significantly interfere with treatment progress and threaten the client’s emotional
stability. Outcomes for both the individuals and communities involved have not yet
been studied.
Similarly, outcomes have not been studied for people who are not seeking treatment
but who come to agency attention involuntarily, for example, through a complaint to
one of the task force agencies. Such persons generally have much lower insight about
the severity of their problem and are often unwilling to engage with professionals
until the situation has reached a crisis (and sometimes not even then). Innovative
research strategies will be needed to establish interventions, such as harm-reduction
approaches, that would be useful for nonvoluntary cases of hoarding. Such inter-
ventions seem especially appropriate in cases of animal hoarding where the hoarded
animals themselves are also sufferers. Research on this problem is very limited to
date, and it is not yet clear how similar this problem is to object hoarding, or what
treatment approaches are most appropriate (see Steketee et al., 2011). To date, no
formal protocols have been developed or tested. This is obviously a topic in desperate
need of research.
Conclusions
It is clear that good progress has been made on developing specialized CBT methods
for treating hoarding, with somewhat less progress on medications that might prove
helpful. Still, research on hoarding remains in the early phases of development and it
is no surprise that treatment research is underdeveloped. More research is necessary to
learn how to maximize gains for specific hoarding symptoms, especially with regard to
reduction in clutter and to determine which elements of this multicomponent therapy
are most critical for what symptoms. Managing the cost of therapy is a continuing
area for future work, with a likely focus on group treatments and affordable in-home
services. Community interventions coordinated through organized task forces seem
a very promising strategy for helping clients who are not seeking treatment through
standard mental health services. Clients and providers can look forward to future
research that will shed light on the most effective and efficient methods for managing
this complex syndrome.
References
Abramowitz, J. S., Franklin, M. E., Schwartz, S. A., & Furr, J. M. (2003). Symptom presentation
and outcome of cognitive-behavioral therapy for obsessive-compulsive disorder. Journal of
Alarcon, R. D., Libb, J. W., & Spitler, D. (1993). A predictive study of obsessive-compulsive
disorder response to clomipramine. Journal of Clinical Psychopharmacology, 13, 210–213.
doi:10.1097/00004714-199306000-00010
Alonso, P., Menchon, J. M., Pifarre, J., Mataix-Cols, D., Torres, L., Salgado, P., & Vallejo, J.
(2001). Long-term follow-up and predictors of clinical outcome in obsessive-compulsive
patients treated with serotonin reuptake inhibitors and behavioral therapy. Journal of
Clinical Psychiatry, 62, 535–540. doi:10.4088/JCP.v62n07a06
American Psychiatric Association. (2012). Proposed criteria, hoarding disorder. Retrieved from
http://www.dsm5.org/ProposedRevisions/Pages/proposedrevision.aspx?rid=398
Ayers, C. R., Setherell, J. L., Golshan, S., & Saxena, S. (2011). Cognitive-behavioral therapy
for geriatric compulsive hoarding. Behaviour Research and Therapy, 49, 689–694. doi:
10.1016/j.brat.2011.07.002
Baer, L. (1994). Factor analysis of symptom subtypes of obsessive compulsive disorder and
their relation to personality and tic disorders. Journal of Clinical Psychiatry, 55(3, Suppl.),
18–23.
Black, D. W., Monahan, P., Gable, J., Blum, N., Clancy, G., & Baker, P. (1998). Hoarding
and treatment response in 38 nondepressed subjects with obsessive-compulsive disorder.
Bloch, M. H., Landeros-Weisenberger, A., Rosario, M. C., Pittenger, C., & Leckman,
J. F. (2008). Meta-analysis of the symptom structure of obsessive-compulsive disorder.
American Journal of Psychiatry, 165, 1532–1542. doi:10.1176/appi.ajp.2008.08020320
Bratiotis, C., Sorrentino Schmalisch, C., & Steketee, G. (2011). The hoarding handbook: A
guide for human service professionals, New York, NY: Oxford University Press.
Calamari, J. E., Wiegartz, P. S., & Janeck, A. S. (1999). Obsessive compulsive disorder
subgroups: A symptom-based clustering approach. Behaviour Research and Therapy, 37 ,
113–125. doi:10.1016/S0005-7967(98)00135-1
Cullen, B., Brown, C. H., Riddle, M. A., Grados, M., Bienvenu, O. J., Hoehn-Saric, R., …
Nestadt, G. (2007). Factor analysis of the Yale-Brown Obsessive Compulsive Scale in
a family study of obsessive-compulsive disorder. Depression and Anxiety, 24, 130–138.
doi:10.1002/da.20204
Erzegovesi, S., Cavallini, M. C., Cavedini, P., Diaferia, G., Locatelli, M., & Bellodi, L. (2001).
Clinical predictors of drug response in obsessive-compulsive disorder. Journal of Clinical
Psychopharmacology, 21, 488–492. doi:10.1097/00004714-200110000-00006
Foa, E. B., Huppert, J. D., Leiberg, S., Langner, R., Kichic, R., Hajcak, G., & Salkovskis, P.
M. (2002). The Obsessive-Compulsive Inventory: Development and validation of a short
version. Psychological Assessment, 14, 485–496. doi:10.1037/1040-3590.14.4.485
Frost, R. O., Hristova, V., Steketee, G., & Tolin, D. F. (2013). Activities of Daily Living in
hoarding disorder (ADL-H). Journal of Obsessive Compulsive and Related Disorders, 2,
85–90.
Frost, R. O., Krause, M. S., & Steketee, G. (1996). Hoarding and obsessive-compulsive
symptoms. Behavior Modification, 20, 116–132. doi:10.1177/01454455960201006
Frost, R. O., Pekereva-Kochergina, A., & Maxner, S. (2011). The effectiveness of a biblio-based
support group for hoarding disorder. Behaviour Research and Therapy, 49, 628–634. doi:
10.1016/j.brat.2011.06.010
Frost, R. O., Steketee, G., & Grisham, J. (2004). Measurement of compulsive hoard-
ing: Saving Inventory-Revised. Behaviour Research and Therapy, 42, 1163–1182. doi:
10.1016/j.brat.2003.07.006
Frost, R. O., Steketee, G., & Tolin, D. F. (2011). Comorbidity in hoarding disorder. Depression
and Anxiety, 28, 876–884. doi:10.1002/da.20861
Frost, R. O., Steketee, G., Tolin, D. F., & Renaud, S. (2008). Development and validation
of the clutter image rating. Journal of Psychopathology and Behavioral Assessment, 30,
193–203. doi:10.1007/s10862-007-9068-7
Frost, R. O., Steketee, G., Williams, L. F., & Warren, R. (2000). Mood, personality dis-
order symptoms and disability in obsessive compulsive hoarders: A comparison with
clinical and nonclinical controls. Behaviour Research and Therapy, 38, 1071–1081. doi:
10.1016/S0005-7967(99)00137-0
Gibson, A. K., Rasmussen, J., Steketee, G., Frost, R., & Tolin, D. (2010). Ethical considerations
in the treatment of compulsive hoarding. Cognitive and Behavioral Practice, 17 , 426–438.
doi:10.1016/j.cbpra.2009.06.008
Gilliam, C. M., Norberg, M. M., Villavicencio, A., Morrison, S., Hannan, S. E., & Tolin,
D. F. (2011). Group cognitive-behavioral therapy for hoarding disorder: An open trial.
Goodman, W. K., Price, L. H., Rasmussen, S. A., Mazure, C., Fleischmann, R. L., Hill, C. L., …
Charney, D. S. (1989). The Yale-Brown Obsessive Compulsive Scale: I. Development,
use, and reliability. Archives of General Psychiatry, 46, 1006–1011.
Grisham, J., Frost, R. O., Steketee, G., Kim, H.-J., & Hood, S. (2006). Age of
onset of compulsive hoarding. Journal of Anxiety Disorders, 20, 675–686. doi:
10.1016/j.janxdis.2005.07.004
Iervolino, A. C., Perroud, N., Fullana, M. A., Guipponi, M., Cherkas, L., Collier, D. A., …
Mataix-Cols, D. (2009). Prevalence and heritability of compulsive hoarding: A twin study.
Jacobson, N. S., Roberts, L. J., Berns, S. B., & McGlinchey, J. B. (1999). Methods for defining
and determining the clinical significance of treatment effects: Description, application,
and alternatives. Journal of Consulting and Clinical Psychology, 67 , 300–307. doi:
10.1037/0022-006X.67.3.300
Leckman, J. F., Grice, D. E., Boardman, J., Zhang, H., Vitale, A., Bondi, C., … Pauls, D. L.
(1997). Symptoms of obsessive-compulsive disorder. American Journal of Psychiatry, 154,
911–917.
Lucini, G., Monk, I., & Szlatenyi, C. (2009). An analysis of fire incidents involving hoarding
households (Unpublished Bachelor of Science thesis). Worcester Polytechnic Institute,
Worcester, MA.
Mataix-Cols, D., Billotti, D., Fernández de la Cruz, L., & Nordsletten, A. E. (2013). The
London field trial for hoarding disorder. Psychological Medicine, 43, 837–847.
Mataix-Cols, D., de la Cruz, L. F., Nakao, T., & Pertusa, A. (2011). Testing the validity and
acceptability of the diagnostic criteria for hoarding disorder: A DSM-5 survey. Psychological
Medicine, 41, 2475–2484. doi:10.1017/S0033291711000754
Mataix-Cols, D., & Marks, I. M. (2006). Self-help with minimal therapist contact
for obsessive-compulsive disorder: A review. European Psychiatry, 21, 75–80. doi:
10.1016/j.eurpsy.2005.07.003
Mataix-Cols, D., Marks, I. M., Greist, J. H., Kobak, K. A., & Baer, L. (2002). Obsessive-
compulsive symptom dimensions as predictors of compliance with and response to
behaviour therapy: Results from a controlled trial. Psychotherapy and Psychosomatics, 71,
255–262. doi:10.1159/000064812
Mataix-Cols, D., Rauch, S., Manzo, P. A., Jenike, M. A., & Baer, L. (1999). Use of factor-
analyzed symptom dimensions to predict outcome with serotonin reuptake inhibitors and
placebo in the treatment of obsessive-compulsive disorder. American Journal of Psychiatry,
156, 1409–1416.
Matsunaga, H., Nagata, T., Hayashida, K., Ohya, K., Kiriike, N., & Stein, D. J. (2009).
A long-term trial of the effectiveness and safety of atypical antipsychotic agents in
augmenting SSRI-refractory obsessive-compulsive disorder. Journal of Clinical Psychiatry,
70, 863–868. doi:10.4088/JCP.08m04369
Mueller, A., Mitchell, J. E., Crosby, R. D., Glaesmer, H., & de Zwaan, M. (2009). The
prevalence of compulsive hoarding and its association with compulsive buying in a
German population-based sample. Behaviour Research and Therapy, 47 , 705–709. doi:
10.1016/j.brat.2009.04.005
Muroff, J., Steketee, G., Bratiotis, C., & Ross, A. (2012). Group cognitive and behavioral
therapy and bibliotherapy for hoarding: A pilot trial. Depression and Anxiety, 29, 597–604.
doi:10.1002/da.21923
Muroff, J., Steketee, G., & Frost, R. (2009, November). Cognitive behavioral treatment
delivered via webcam. Paper presented at the Annual Meeting of the Association for
Behavioral and Cognitive Therapies, New York, NY.
Muroff, J. M., Steketee, G., Frost, R. O., & Tolin, D. F. (2012, January). Is cognitive behavioral
therapy for hoarding disorder durable? Follow-up outcomes and predictors from a randomized
controlled trial. Paper presented at the Annual Meeting of the Society for Social Work
Research, Washington, DC.
Muroff, J., Steketee, G., Himle, J., & Frost, R. (2010). Delivery of Internet treatment for
compulsive hoarding (DITCH). Behaviour Research and Therapy, 48, 79–85.
Muroff, J., Steketee, G., Rasmussen, J., Gibson, A., Bratiotis, C., & Sorrentino, C. (2009).
Group cognitive and behavioral treatment for compulsive hoarding: A preliminary trial.
Depression and Anxiety, 26, 634–640. doi:10.1007/s10615-010-0311-4
Nordsletten, A. E., Fernández de la Cruz, L., Pertusa, A., Reichenberg, A., Hotopf, M.,
Hatch, S. L., & Mataix-Cols, D. (2013). The Structured Interview for Hoarding Disorder
(SIHD): Development, usage and further validation. Journal of Obsessive-Compulsive and
Related Disorders, 2, 346–350.
Pertusa, A., Frost, R. O., Fullana, M. A., Samuels, J., Steketee, G., Tolin, D., … Mataix-
Cols, D. (2010). Refining the diagnostic boundaries of compulsive hoarding: A critical
review. Clinical Psychology Review, 30, 371–386. doi:10.1016/j.cpr.2010.01.007
Pertusa, A., Frost, R. O., & Mataix-Cols, D. (2010). When hoarding is a symptom of OCD: A
case series and implications for DSM-5. Behaviour Research and Therapy, 48, 1012–1020.
doi:10.1016/j.brat.2010.07.003
Rufer, M., Fricke, S., Moritz, S., Kloss, M., & Hand, I. (2006). Symptom dimensions in
obsessive-compulsive disorder: Prediction of cognitive-behavior therapy outcome. Acta
Psychiatrica Scandinavica, 113, 440–446. doi:10.1111/j.1600-0447.2005.00682.x
Salomoni, G., Grassi, M., Mosini, P., Riva, P., Cavedini, P., & Bellodi, L. (2009).
Artificial neural networks model for the prediction of obsessive-compulsive disor-
der treatment response. Journal of Clinical Psychopharmacology, 29, 343–349. doi:
10.1097/JCP.0b013e3181aba68f
Samuels, J. F., Bienvenu, O. J., Grados, M. A., Cullen, B., Riddle, M. A., Liang, K.-Y., …
Nestadt, G. (2008). Prevalence and correlates of hoarding behavior in a community-
based sample. Behaviour Research and Therapy, 46, 836–844. doi:10.1016/j.brat.2008.
04.004
Saxena, S. (2011). Pharmacotherapy of compulsive hoarding. Journal of Clinical Psychology: In
Session, 67 , 477–484. doi:10.1002/jclp.20792
Saxena, S., Brody, A. L., Maidment, K. M., & Baxter, L. R., Jr. (2007). Paroxetine
treatment of compulsive hoarding. Journal of Psychiatric Research, 41, 481–487.
doi:10.1016/j.jpsychires.2006.05.001
Shetti, C. N., Reddy, Y. C. J., Kandavel, T., Kashyap, K., Singisetti, S., Hiremath, A. S.,
… Raghunandanan, S. (2005). Clinical predictors of drug nonresponse in obsessive-
compulsive disorder. Journal of Clinical Psychiatry, 66, 1517–1523. doi:10.4088/
JCP.v66n1204
Stein, D. J., Andersen, E. W., & Overo, K. F. (2007). Response of symptom dimensions in
obsessive-compulsive disorder to treatment with citalopram or placebo. Revista Brasileira
de Psiquiatria, 29, 303–307. doi:10.1590/S1516-44462007000400003
Stein, D. J., Carey, P. D., Lochner, C., Seedat, S., Fineberg, N., & Andersen, E. W. (2008).
Escitalopram in obsessive-compulsive disorder: Response of symptom dimensions to
pharmacotherapy. CNS Spectrums, 13, 492–498.
Steketee, G., & Frost, R. O. (2003). Compulsive hoarding: Current status of the research.
Steketee, G., & Frost, R. O. (2007). Compulsive hoarding and acquiring: Therapist guide. New
Steketee, G., Frost, R. O., & Kyrios, M. (2003). Cognitive aspects of compulsive hoarding.
Cognitive Therapy and Research, 27 , 463–479. doi:10.1023/A:1025428631552
Steketee, G., Frost, R. O., Tolin, D. F., Rasmussen, J., & Brown, T. A. (2010). Waitlist-
controlled trial of cognitive behavior therapy for hoarding disorder. Depression and
Anxiety, 27 , 476–484. doi:10.1002/da.20673
Steketee, G., Frost, R. O., Wincze, J., Greene, K. A. I., & Douglass, H. (2000). Group and
individual treatment of compulsive hoarding: A pilot study. Behavioural and Cognitive
Psychotherapy, 28, 259–268. doi:10.1017/S1352465800003064
Steketee, G., Gibson, A., Frost, R. O., Alabiso, J., Arluke, A., Patronek, G., and the Hoarding of
Animals Research Consortium (HARC). (2011). Characteristics and antecedents of animal
hoarding: A comparative interview study. Review of General Psychology, 15, 114–124.
doi:10.1037/a0023484
Tolin, D. F., Fitch, K. E., Frost, R. O., & Steketee, G. (2010). Family informants’ perception
of insight in compulsive hoarding. Cognitive Therapy and Research, 34, 69–81. doi:
10.1007/s10608-008-9217-7
Tolin, D. F., Frost, R. O., & Steketee, G. (2007a). An open trial of cognitive-behavioral
therapy for compulsive hoarding. Behaviour Research and Therapy, 45, 1461–1470. doi:
10.1016/j.brat.2007.01.001
Tolin, D. F., Frost, R. O., & Steketee, G. (2007b). Buried in treasures: Help for compulsive
acquiring, saving, and hoarding, New York, NY: Oxford University Press.
Tolin, D. F., Frost, R. O., & Steketee, G. (2010b). A brief interview for assessing compulsive
hoarding: The Hoarding Rating Scale-Interview. Psychiatry Research, 178, 147–152. doi:
10.1016/j.psychres.2009.05.001
Tolin, D. F., Frost, R. O., Steketee, G., & Fitch, K. (2008). Family burden of compulsive
hoarding: Results of an Internet survey. Behaviour Research and Therapy, 46, 434–443.
doi:10.1016/j.brat.2007.12.008
Tolin, D. F., Frost, R. O., Steketee, G., Gray, K. D., & Fitch, K. E. (2008b). The economic
and social burden of compulsive hoarding. Psychiatry Research, 160, 200–211. doi:
10.1016/j.psychres.2007.08.008
Tompkins, M. A., & Hartl, T. L. (2009). Digging out: Helping your loved one manage clutter,
hoarding and compulsive acquiring. Oakland, CA: New Harbinger.
Turner, K., Steketee, G., & Nauth, L. (2010). Treating elders with compulsive hoard-
ing: A pilot program. Cognitive and Behavioral Practice, 17 , 449–457. doi:
10.1016/j.cbpra.2010.04.001
47
Body Dysmorphic Disorder
Jessica Rasmussen, Aaron J. Blashill,
Jennifer L. Greenberg, and Sabine Wilhelm
Introduction
Body dysmorphic disorder (BDD) is defined as a preoccupation with an imagined or

slight defect in appearance that frequently causes considerable distress and significant
functional impairment (American Psychiatric Association, 2000; Phillips, Menard,
Fay, & Weisberg, 2005). The disorder is characterized by a preoccupation with
several aspects of appearance (e.g., “My nose is too big”), as well as time-consuming
rituals (e.g., mirror checking, camouflaging, scrutinizing/comparing) and avoidance
behavior (e.g., avoidance of social situations). The distressing appearance related
thoughts and ritualistic behaviors are often present for up to several hours a day
(Phillips, McElroy, Keck, Pope, & Hudson, 1993).
The most common body areas of concern include skin, hair, stomach, nose, and
teeth (Phillips, Didie, et al., 2006). Individuals with BDD can become preoccupied
with virtually any body part. On average, patients with BDD report five to seven areas
of appearance concern (Phillips, Menard, Fay, & Weisberg, 2005). In response to
obsessive thoughts concerning body image, individuals with BDD perform ritualistic
behaviors. BDD related rituals often include camouflaging the perceived defect, com-
paring/scrutinizing self to others, mirror checking, reassurance seeking, and excessive
grooming behaviors (American Psychiatric Association, 2000). A significant propor-
tion of individuals with BDD have received dermatological (45.2%) or surgical treat-
ment (23.2%) for their perceived defect(s) and general response to these nonpsychiatric
treatments has been relatively poor (Phillips, Grant, Siniscalchi, & Albertini, 2001).
BDD has been associated with significant functional impairment in social activities
and academic/occupational performance (Didie, Menard, Stern, & Phillips, 2008;
Phillips, Menard, Fay, & Pagano, 2005). Patients with the disorder often report a
high number of missed work/school days (Phillips, Menard, Fay, & Pagano, 2005),

DOI: 10.1002/9781118528563.wbcbt47
and in one sample, 31.2% were completely unable to work within the past month
due to their symptoms (Didie et al., 2008). Partial or complete avoidance of social
situations is common (Phillips, Didie, et al., 2006) and if BDD symptoms are severe,
individuals can become housebound (Phillips, Didie, et al., 2006; Phillips et al.,
1993). Individuals with BDD report lower mental health-related quality of life scores
compared to the general U.S. population and compared to other medical populations
(e.g., patients with diabetes, depression, or myocardial infarction; Phillips, 2000).
Individuals with BDD often report severe or extreme distress due to their appearance
concerns and suicidal ideation and attempts are frequent. In a recent sample, 79.5%
of those with BDD reported having a lifetime history of suicidal ideation and 27.6%
reported a history of a suicide attempt (Phillips & Menard, 2006).
The prevalence of BDD has been reported as 1.7–2.4% in a series of community
samples (Buhlmann et al., 2010; Koran, Abujaoude, Large, & Serpe, 2008; Rief,
Buhlmann, Wilhelm, Borkenhagen, & Brahler, 2006) and has ranged anywhere from
5% (Bohne et al., 2002) to 13% (Biby, 1998) in student samples. Prevalence is even
higher in inpatient psychiatric populations (12–13%; Grant, Kim, & Crow, 2001).
Men and women both suffer from BDD and while one study found that BDD appears
to occur at a slightly higher rate in females (Buhlmann et al., 2010), other studies
have found no significant differences in occurrence rates by gender (Koran et al.,
2008; Rief et al., 2006). However, men and women do differ in their most frequent
areas of concern, with men being more preoccupied by body build, hair thinning,
and genitals, and women being more frequently distressed over their hips, stomach
area, and weight (Phillips & Diaz, 1997). In a sample of 183 individuals with BDD,
average age of onset was 16.5 years (Phillips, Pagano, Menard, & Stout, 2006). In
the same sample, 81.3% of individuals reported having had a continuous course of
the disorder and mean duration was 16.0 years (SD = 12.5; Phillips, Pagano, et al.,
2006).
It has been suggested that BDD be included with other disorders (e.g., obsessive-
compulsive disorder [OCD], trichotillomania) in an obsessive-compulsive spectrum
category in the upcoming DSM-5 (for a review, see Hollander, Kim, Braun, Simeon, &
Zohar, 2009). BDD, along with other disorders in the proposed obsessive-compulsive
spectrum, has been observed to share similarities with OCD in phenomenology (i.e.,
repetitive thoughts and behaviors; for a review, see Chosak et al., 2008; Wilhelm
& Neziroglu, 2002), family history (Bienvenu et al., 2000), and treatment response
(Eddy, Dutra, Bradley, & Westen, 2004; Hollander et al., 1999; Phillips & Hollander,
2008). OCD is also commonly comorbid in individuals with BDD (e.g., about
30%; Gunstad & Phillips, 2003). Despite an observed overlap between BDD and
OCD, the thought content in BDD is focused on appearance-based concerns as
opposed to the typical obsessional thought content seen in OCD (Chosak et al.,
2008).
It has also been proposed that BDD may fit into a broader affective spectrum
disorder category, grouped with major depression and other anxiety disorders, OCD
included (Phillips, McElroy, Hudson, & Pope, 1995; Phillips & Stout, 2006). BDD
patients have an increased rate of comorbid depressive and anxiety disorders including
major depressive disorder (75%) and social phobia (37%; Gunstad & Phillips, 2003).
Relatively high rates of BDD have been found in anxiety disorder samples, particularly
Body Dysmorphic Disorder 1111
in those with a principal diagnosis of social phobia (12%; Wilhelm, Otto, Zucker, &
Pollack, 1997). In addition to high rates of comorbid mood and anxiety disorders,
substance abuse disorders also commonly co-occur with BDD (48.9%; Grant, Menard,
Pagano, Fay, & Phillips, 2005).
Assessment
Regarding diagnostic assessment, the Body Dysmorphic Disorder Diagnostic Module

(BDDM) is an interview that is based on the diagnostic criteria for BDD found in the
DSM-IV, and is comparable to other modules of the Structured Clinical Interview
for DSM-IV Axis-I Disorders. Inter-rater reliability for the BDDM is high (κ = 0.96;
Phillips, 1996). A widely used instrument to assess BDD symptom severity is the BDD
modified Yale Brown Obsessive Compulsive Scale (BDD-YBOCS; Phillips, Hollander
et al., 1997). The BDD-YBOCS is a 12-item, semistructured, clinician-administered
interview, which assesses BDD-related cognitions, rituals, avoidance, and insight. The
BDD-YBOCS has demonstrated adequate psychometric properties, with a Cronbach’s
alpha of 0.80, and a 1-week test-retest reliability coefficient of 0.88. Further, a change
of 30% or greater has demonstrated 96% sensitivity and 93% specificity when compared
to Clinical Global Impression scores of “much” or “very much improved” (Phillips,
Hollander et al., 1997). Although the BDD-YBOCS has displayed adequate initial
reliability and validity, to date, no known studies have confirmed the factor structure
via advanced statistical analyses (e.g., structural equation modeling).
Another common clinician-administered interview is the Body Dysmorphic Dis-
order Examination (BDDE; Rosen & Reiter, 1996). The BDDE is a 34-item
instrument which assesses preoccupation with and negative evaluation of appear-
ance, self-consciousness and embarrassment, appearance investment, avoidance, and
compulsions. The BDDE has also displayed adequate psychometric properties, with
a Cronbach’s alpha of 0.81, a 2-week test-retest reliability coefficient of 0.87, and
interclass correlation coefficient of 0.86. Although the authors of the BDDE do
not recommend using a cutoff on the total score to determine the likelihood of a
BDD diagnosis, they do provide a nuanced algorithm for determining this based on
responses to individual items (cf. Rosen & Reiter, 1996). Unlike the BDD-YBOCS,
the BDDE’s factor structure has not been evaluated via exploratory factor analysis.
Examining the structural validity of the BDDE, both in exploratory and confirmatory
analyses, would prove a fruitful area of further inquiry.
Pharmacotherapy
Several serotonin reuptake inhibitors (SRIs) have been shown to be effective in the
treatment of BDD, including fluoxetine, clomipramine, fluvoxamine, citaprolam, and
escitaprolam (Hollander et al., 1999; Perugi et al., 1996; Phillips, 2006; Phillips,
Albertini, & Rasmussen, 2002; Phillips, Dwight, & McElroy, 1998; Phillips & Najjar,
2003). A 10-week open label trial of fluvoxamine for 15 individuals with BDD (Perugi
et al., 1996) found 10 of the individuals were much or very much improved on the
Clinical Global Impressions Scale and 10 of the 12 patients who completed the study
were responders (Perugi et al., 1996). In another open label trial of 30 BDD patients
treated with fluvoxamine for 16 weeks, 63% of patients were considered responders
(Phillips et al., 1998). Two 12-week open label trials of citalopram (Phillips & Najjar,
2003) and escitalopram (Phillips, 2006), both of which had 15 participants, found
that 73% of individuals responded and quality of life and functioning were significantly
improved.
Two randomized control trials have been conducted thus far, one of which
compared clomipramine to desipramine (Hollander et al., 1999) and another which
examined fluoxetine versus placebo (Phillips et al., 2002). Hollander et al. (1999)
found that in a 16-week randomized double-blind controlled cross-over study of
29 individuals with BDD, clomipramine was significantly more effective for the
reduction of BDD symptoms (65% vs. 35% response rate) and functional disability
than desipramine. The 12-week randomized double-blind, placebo controlled trial of
fluoxetine showed that fluoxetine was significantly more effective than placebo (53%
vs. 18% response rate; Phillips et al., 2002).
It has been clinically observed that BDD requires typically higher doses than are
used for depression (for a review, see Phillips & Hollander, 2008). Response time has
been shown to differ across various SRIs but mean response times for several studies
of fluoxetine and fluvoxamine have been between 6 and 9 weeks (Perugi et al., 1996;
Phillips et al., 2002; Phillips et al., 1998), whereas studies of citalopram (Phillips &
Najjar, 2003) and escitalopram (Phillips, 2006) have reported a mean response time
of 4.6 +/− 2.6 weeks and 4.7 +/− 3.7 weeks, respectively. Improvement with the
use of an SRI for BDD usually translates to lessened preoccupation with perceived
defects, a reduction of ritualistic behaviors, and better psychosocial functioning
(Hollander et al., 1999; Phillips et al., 2002). SRIs have also been shown in several
studies to improve insight concerning BDD appearance related beliefs (Hollander
et al., 1999; Phillips, McElroy, Dwight, Eisen, & Rasmussen, 2001; Phillips et al.,
2002).
Cognitive Behavioral Model of Body Dysmorphic Disorder
Cognitive behavioral models of BDD have been empirically supported and widely
accepted (e.g., Veale, 2004; Wilhelm, Buhlmann, Hayward, Greenberg, & Dimaite,
2010; Wilhelm & Neziroglu, 2002). Neurocognitive and neuroimaging studies, as
well as clinical observations, have shown that individuals with BDD have certain
biological predispositions that contribute to the development and maintenance of
BDD symptoms (Deckersbach et al., 2000; Feusner, Hembacher, Moller, & Moody,
2011; Feusner et al., 2010; Feusner, Townsend, Bystritsky, & Bookheimer, 2007).
Several neuroimaging studies have found that BDD patients have greater activation
in the left hemisphere (i.e., an area responsible for detail based processing) when
viewing pictures of their own and others’ faces (Feusner et al., 2010; Feusner et al.,
2007), as well as other objects (Feusner et al., 2011). In addition, neuropsychological
studies of BDD confirm a favored localized processing approach as opposed to a
global one (Deckersbach et al., 2000). Cognitive behavioral models of BDD theorize
that localized visual processing can cause individuals with the disorder to selectively
overattend to appearance details that lead to distortions concerning body image
(Veale, 2004; Wilhelm et al., 2010).
A distorted perception of body image along with selectively focused attention leads
patients with BDD to negatively interpret situations concerning the self and others
(Wilhelm et al., 2010). Several studies have demonstrated that patients with BDD have
heightened selective attention for BDD related perceived threat (Buhlmann, McNally,
Wilhelm, & Florin, 2002), are more likely to negatively interpret ambiguous body-
related and social scenarios (Buhlmann, Wilhelm, et al., 2002), and more often
misidentify pictures of facial expressions as angry or contemptuous (Buhlmann,
Etcoff, & Wilhelm, 2006). Early childhood experiences, cultural influences, and
psychological vulnerabilities are also thought to contribute to the development and
maintenance of negative appearance-related beliefs. Individuals with BDD report
more frequent childhood experiences of being teased (Buhlmann, Cook, Fama, &
Wilhelm, 2007). Cultural backgrounds in which the importance of appearance is
emphasized can also inflate beliefs about the importance of physical attractiveness
(e.g., the United States, where advertising and technology have placed an emphasis
on the “perfect” physical appearance; Neziroglu, Khelmani-Patel, & Veale, 2008;
Wilhelm, Phillips, & Steketee, 2013). Finally, certain psychological vulnerabilities
such as perfectionism (i.e., wanting the “perfect” appearance) and rejection sensitivity
have been proposed to influence negative appearance-related beliefs (Veale, 2004;
Wilhelm et al., 2010).
Patients with BDD frequently have automatic thoughts that other people are
negatively evaluating their appearance (Veale, 2004; Wilhelm et al., 2010). For
example, when walking into a store, a patient with BDD who has concerns about
his skin might think, “Everyone in the store is staring at me and thinking about
how red and ugly my skin is.” Patients may also be more likely to place a greater
level of importance on their appearance and interpret minor appearance concerns as
major personal flaws (e.g., “If my skin is red, I am worthless”), as well as confusing
physical attractiveness with happiness (e.g., “If my skin is too red, I will be alone
and unhappy for the rest of my life”; Wilhelm et al., 2010). In addition to automatic
interpretations of body image, individuals with BDD often hold deeper core beliefs
about the self and others that underlie their distorted perceptions of appearance
(Veale, 2004; Wilhelm, Phillips, Fama, Greenberg, & Steketee, 2011). For example,
a common core belief beneath appearance concerns may be “I am unlovable,”
and patients with BDD may also believe that other people will only like them if
they are perceived as attractive (e.g., “People only like attractive people”; Veale,
2004).
Maladaptive thinking leads to negative emotions in patients with BDD (e.g.,
anxiety, shame, sadness) that they then attempt to neutralize with ritualistic behaviors
(e.g., mirror checking) or avoidance of trigger situations (i.e., going to a party; Veale,
2004; Wilhelm et al., 2010). While avoidance of certain situations and engagement
in ritualistic behaviors may temporarily reduce unwanted emotions, these behaviors
negatively reinforce BDD-related thoughts, feelings, and behaviors in the long term
(Wilhelm et al., 2010).
Cognitive Behavioral Therapy for Body Dysmorphic Disorder
Cognitive behavioral therapy (CBT) for BDD has the most empirical support for
treatment of the disorder of all available psychosocial interventions (Ipser, Sander,
& Stein, 2009; Williams, Hadjistavropoulos, & Sharpe, 2006). At the core of CBT
for BDD are the identification, evaluation, and restructuring of maladaptive beliefs
surrounding appearance (e.g., “Everyone thinks that my hair is thin and ugly”), as
well as exposure to feared and avoided situations related to the disorder (e.g., going
out in public without wearing a hat; Rosen, Reiter, & Orosan, 1995; Veale et al.,
1996; Wilhelm et al., 2013). While cognitive restructuring and exposure and response
prevention (ERP) compose the core strategies used in CBT for BDD, there are a
number of other techniques that have been previously cited in the literature and
widely used. These techniques include psychoeducation, motivational enhancement,
and mindfulness/perceptual retraining (Rosen et al., 1995; Veale et al., 1996;
Wilhelm et al., 2013). In addition, several treatment modules aimed at addressing
specific concerns in BDD (e.g., skin picking, depression) are available to use flexibly
during the course of treatment (Wilhelm et al., 2013). Finally, a complete course of
treatment usually includes relapse prevention sessions.
Assessment
At the start of treatment, a comprehensive assessment of BDD symptoms should
be conducted (Wilhelm et al., 2013). Patients with BDD are often embarrassed
or ashamed of their body image concerns and are less likely to disclose them
openly. Additionally, some individuals with BDD may have poor insight into their
symptoms, believing that their problems are not psychiatric in nature and best
addressed through medical intervention alone (Wilhelm et al., 2013). Subsequently, a
focused assessment of BDD symptoms allows for a thorough evaluation of thoughts,
feelings, and behaviors related to appearance concerns, while at the same time helping
to build a therapeutic alliance between therapist and patient by beginning to address
specific fears or concerns related to treatment (e.g., talking about BDD symptoms,
psychiatric versus medical intervention; Wilhelm et al., 2013). The therapist can use
the assessment of a patient’s BDD symptoms to individualize therapeutic interventions
(e.g., psychoeducation, building of an individualized CBT model, ERP exercises).
Assessment can also inform future need for motivational interviewing techniques, as
well as modular interventions to address particular concerns (e.g., skin picking, muscle
dysmorphia; Wilhelm et al., 2013).
In the assessment of BDD symptoms, it is also important for the therapist to
differentiate BDD symptoms from other commonly co-occurring disorders (e.g.,
social phobia, OCD, eating disorders; Phillips, Didie, Feusner, & Wilhelm, 2008;
Rosen & Ramirez, 1998). BDD and social phobia share a fear of negative evaluation,
but BDD is focused on concerns about being judged for physical appearance (Phillips
et al., 2008). BDD and OCD are similar in being characterized by repetitive thoughts
and behaviors but the content of these thoughts differs widely (i.e., BDD is focused on
appearance whereas OCD is not; Wilhelm & Neziroglu, 2002). Body image concerns
typify both BDD and eating disorders, but research has shown that individuals with
BDD have a more diverse location of appearance dissatisfaction (e.g., nose, teeth, hair),
whereas those with eating disorders tend to be primarily focused on weight/shape
dissatisfaction (Rosen & Ramirez, 1998). In assessing and differentiating BDD
symptoms from other commonly co-occurring disorders, the therapist will ensure a
more accurate targeting of BDD symptoms during treatment (Phillips et al., 2008).
Psychoeducation
The first active treatment step in CBT for BDD is psychoeducation. To begin with,
therapists may provide patients with some initial information on BDD (i.e., typical
symptoms, common ways in which the disorder interferes, prevalence). Therapists
can then instill hope in patients by providing a brief overview of CBT for BDD
(i.e., helping patients to change maladaptive thoughts pertaining to appearance,
while reducing their distress and avoidance behaviors) and evidence-based support
for the treatment (Wilhelm et al., 2013). In explaining common manifestations of
the disorder and the manner in which it is treated, therapists can validate and engage
patients with the treatment process before it has fully begun (Wilhelm et al., 2013).
The other primary component of psychoeducation involves the therapist presenting
patients with the cognitive behavioral model of BDD (e.g., maladaptive thinking
surrounding appearance, selective attention to minor details of appearance, negative
emotions, and ritualistic behaviors/avoidance) and thoroughly explaining each com-
ponent to the patient. The therapist should collaborate with the patient to build
an individualized model based on the patient’s particular BDD symptoms (Veale
et al., 1996; Wilhelm et al., 2013). The creation of the patient’s individualized
cognitive behavioral model can be particularly helpful in providing the patient with
an understanding of the factors that may have contributed to the development of
the disorder (e.g., selective attention to detail, perfectionism, biological predispo-
sition), as well the current maladaptive thinking and behavioral patterns that are
maintaining the symptoms (Veale et al., 1996; Wilhelm et al., 2013). The therapist
and patient will most likely refer back to the model frequently during the course of
treatment as a method of tailoring intervention strategies that are most suitable for
the patient.
On a more general note, therapists can help patients maximize treatment by
establishing general session structure and flow from the outset of the process. Sessions
of CBT for BDD usually consist of a brief mood and symptom check at the beginning
of session followed by a review of homework assigned from the previous session
(Wilhelm et al., 2013). Homework between sessions is typically assigned during the
course of CBT (e.g., monitoring thoughts about appearance, ERP to feared situations
outside of session, reduction of behaviors such as ritualistic grooming) and can be
particularly helpful in assisting the patient with the practice of cognitive behavioral
strategies in a real-world context (e.g., social situations where the patient might be
concerned about his or her appearance being evaluated; Wilhelm et al., 2013). After
completing a homework review, the therapist and patient will collaboratively set the
agenda for a particular session (e.g., exposure where the patient walks into a store
without his or her hat on). The sessions typically end by the therapist and patient
deciding on the homework assignment for the week (e.g., to go into three public
spaces without a hat on), as well as giving the patient time to provide feedback to the
therapist on the session and the treatment (Wilhelm et al., 2013).
Motivational Strategies
Motivational strategies, including motivational interviewing techniques (Miller &
Rollnick, 2002), are frequently used during the course of CBT for BDD (Wilhelm
et al., 2010). Individuals with BDD are often relatively fixed in beliefs concerning
their appearance and patients with higher levels of delusionality may be completely
convinced that their appearance-related beliefs are true (e.g., “I am completely certain
that my nose is crooked”; Phillips, 2004). It is a common pitfall of therapists to
attempt to convince patients that their beliefs are incorrect (Phillips et al., 2008). This
strategy frequently ends in arguments and a poor therapeutic alliance that may result
in a lack of collaboration between the patient and therapist (Phillips et al., 2008).
In addition to rigidity of appearance-related beliefs, many patients with BDD are
ambivalent concerning therapeutic change (Wilhelm et al., 2013). For a significant
proportion of individuals with BDD, they may have tried numerous dermatological
or surgical strategies for their concerns (Crerand, Phillips, Menard, & Fay, 2005).
Subsequently, they may be uncertain or less willing to consider that CBT could be an
effective intervention for their distress (Wilhelm et al., 2013).
Motivational strategies for BDD are based on the principles of Miller and Rollnick
(2002) and are adapted to address disorder-specific concerns. Motivational strategies
can start with the therapist assessing possible barriers to change (i.e., lack of insight into
appearance-based concerns, desire for surgical/dermatological interventions; Wilhelm
et al., 2013). This information can be used to anticipate the need for motivational
strategies during the course of treatment. The therapist can also evaluate the extent
to which motivational techniques are needed and at what stage of treatment. For
example, patients who are ambivalent about the treatment process may need more
intensive motivational work at the beginning in order to engage with the treatment,
as compared to other patients who may need motivational strategies at specific time
points (e.g., ERP, homework adherence).
Motivational strategies for BDD emphasize a nonjudgmental, collaborative stance
in which the therapist attempts to guide the patient in exploring his or her willingness
and readiness for change surrounding his or her appearance-based concerns. The
therapist is encouraged to empathize with the patient around his or her body image
related distress as opposed to immediately challenging the validity of his or her
appearance related beliefs (e.g., “Your body image concerns seem to be causing
you a lot of distress; let’s try and work together to see if we can reduce your
distress”; Wilhelm et al., 2013). Another common motivational technique used in
BDD treatment is the use of nonjudgmental Socratic questioning to explore the
pros and cons of change (e.g., “What might be some of the benefits of participating
in CBT for BDD?”; Wilhelm et al., 2013). Similarly, the therapist may guide the
patient in developing a discrepancy between his or her BDD symptoms and his or
her goals and values; for instance, asking the patient to look forward (e.g., “What
would you like your life to be like in 5 years?”) or to look back (e.g., “Compared
to what your life was like at the beginning of treatment, what is different now?”).
This can be a particularly helpful technique when attempting to explore maladaptive
appearance-related beliefs into which some patients with BDD may have poor insight.
Instead of just considering the validity of a belief, it can also be helpful to consider the
usefulness of the belief (e.g., “Are your beliefs about your hair preventing you from
doing things that you would like, such as socializing or running errands?”; Wilhelm
et al., 2013).
The identification, evaluation, and restructuring of automatic maladaptive
appearance-based thoughts are techniques central to CBT for BDD. Therapists
can begin by introducing patients to common cognitive distortions seen in BDD,
such as “all-or-nothing thinking” (e.g., “I am either a model or monster”) or
‘‘discounting the positive (e.g., “She only complimented my appearance because she
feels sorry for me”; Wilhelm et al., 2013). This is usually followed by encouraging
patients to monitor their automatic appearance-based thoughts both in and outside
of session (e.g., “This scar on my chin makes me hideously ugly”) to identify
cognitive distortions (i.e., all-or-nothing thinking; Rosen et al., 1995; Veale et al.,
1996; Wilhelm et al., 2013). Patients may be aided in their identification of
these types of thoughts by learning to engage in their own Socratic questioning
surrounding situations in which they are experiencing significant distress or which
they are avoiding altogether (e.g., “Why do I feel so distressed about my appearance
when I go out with my friends?” “Is it possible that I am worried everyone will be
staring at the scar on my chin?”).
After the patient becomes comfortable with identifying automatic maladaptive
appearance related thoughts, the therapist can aid the patient in learning to evaluate
and (if indicated) modify these thoughts (e.g., Neziroglu, McKay, Todaro, & Yayura-
Tobias, 1996; Rosen et al., 1995; Veale et al., 1996; Wilhelm et al., 2013). While
it is often helpful to evaluate the validity of a maladaptive thought (“What is the
evidence that everyone is reacting negatively to my skin?”), it can also be beneficial
to examine its usefulness (e.g., “Is it really helpful for me to think that I can only
be happy if my skin changes?”; Wilhelm et al., 2013). The therapist may assist the
patient in examining the pros and cons of holding onto BDD related thoughts (e.g.,
“It may feel as though a potential benefit of holding onto this belief is that it feels as
though it is protecting you from harm [being laughed at], while a downside may be
that it interferes with socializing and going to work”).

The principal behavioral strategy in the treatment of BDD is ERP (McKay et al.,
1997; Neziroglu et al., 1996; Rosen et al., 1995; Wilhelm et al., 2013). Prior to
using ERP in treatment, it is prudent to obtain a thorough assessment of the patient’s
rituals (e.g., camouflaging) and avoidance behaviors (e.g., avoiding work-related
social functions) related to BDD symptoms (Wilhelm et al., 2013). When ritualistic
behavior has been identified, the therapist can work with the patient to set goals
around ritual prevention for homework. Various strategies on how to delay (e.g., wait
more time than usual before checking the mirror) or reduce rituals (e.g., only wear a
hat as opposed to hat and sunglasses when out in public) can be reviewed with the
patient, with the goal being eventual elimination of these behaviors (Wilhelm et al.,
2013).
In order to begin exposure-based treatment, the therapist and patient should
collaborate on the creation of a fear and avoidance hierarchy related to appearance-
based concerns (e.g., wearing a swimsuit at the beach, going to a party). The therapist
and patient can work together to identify appearance-related situations that provoke
the least anxiety while progressing up to situations that provoke the utmost anxiety
(Rosen et al., 1995; Wilhelm et al., 2013). The patient should also be encouraged to
use ritual prevention skills when engaging in exposure exercises.
The therapist then guides the patient in systematic completion of ERP based
on the hierarchy. The therapist can encourage the patient to view the exposure
as a “behavioral experiment” during which they evaluate the validity of negative
predictions based on maladaptive thinking (e.g., go to a party and make eye contact
with three people, evaluate whether their body language and eye contact appears
negative). The aim is that the patient will both practice tolerating the associated
distress that he or she feels, without intervening with the use of avoidance or rituals,
while at the same time properly evaluating negative predictions concerning appearance
(Wilhelm et al., 2013).
Advanced Cognitive Strategies

Once the patient has become adept at identifying, evaluating, and challenging auto-
matic appearance-related beliefs, therapists can use Socratic questioning to examine
more deeply held “core beliefs” as they relate to appearance concerns (Wilhelm et al.,
2013). Core beliefs related to maladaptive appearance-based thoughts might include
“I’m unlovable,” or “I’m a failure.” While core beliefs will often emerge naturally
during the course of therapy, they can also be elicited using the downward arrow
technique (e.g., if the thought is “People will think that my nose is too big,” the
downward arrow technique would involve asking the patient, “What would it mean if
people noticed your nose was too big?”). This technique involves the therapist asking
repetitiously what the worst consequences of a patient’s beliefs are, until the core
belief is reached (e.g., “If people noticed that my nose was too big, they wouldn’t
like me and this would mean that I would be unlovable”; Wilhelm et al., 2013).
The core belief can be addressed through cognitive restructuring as well as behavioral
experiments to test out the validity of the belief (e.g., having the patient approach
social situations that are regularly avoided to evaluate whether others will still be
interested in the patient regardless of his or her nose).
Mindfulness/Perceptual Retraining
Information processing studies have shown that individuals with BDD visually process
stimuli at a detail oriented level in lieu of the globalized picture (Deckersbach et al.,
2000; Feusner et al., 2010). Clinically, this style of visual processing seems to manifest
itself in the form of heightened selective attention to details of appearance, which

then lead to the maladaptive beliefs and behaviors seen in BDD (e.g., “Everyone can
see this spot on my face”). Cognitive behavioral treatments have recently included
mindfulness/perceptual retraining in order to address these information processing
difficulties and restructure the maladaptive beliefs and behaviors (e.g., Wilhelm et al.,
2010).
One of the primary mindfulness/perceptual retraining techniques is known as
mirror retraining (Wilhelm et al., 2013). Mirror retraining consists of having the
patient learn to observe him- or herself at a reasonable (i.e., arm’s length) distance from
the mirror using nonjudgmental descriptions regarding their appearance (example,
“My hair is mid-length to my shoulders and the color is dark brown”). Standing a
reasonable distance from the mirror is often a departure for patients with BDD, who
may often stand too close or too far away, or avoid mirrors entirely. A reasonable
distance from the mirror allows patients to see their entire image, as opposed to
limiting their viewpoint to one aspect of their appearance. When viewing their entire
image, patients with BDD may be less likely to focus on details and distort aspects
of their appearance and may be more likely to notice other positive aspects of their
appearance that they may have been overlooking (Wilhelm et al., 2013).
When viewing themselves in the mirror, individuals with BDD also tend to use
negative and judgmental language about their appearance (e.g., “My hair is so
ugly”), which is typically associated with strong negative affect (Wilhelm et al., 2013).
The use of a nonjudgmental stance toward appearance allows patients with BDD
to practice viewing themselves neutrally without descriptions laden with negative
emotion. Patients may be more likely to view their appearance in a less distorted
manner, as well as engage in healthier mirror-related behaviors (i.e., not avoiding the
mirror entirely, not getting too close to the mirror).
It is important to emphasize that when practicing mirror training techniques
the therapist should encourage patients to eliminate typical ritualistic or “safety”
behaviors they may typically use in front of the mirror, such as grooming or touching
certain body parts (e.g., elimination of repetitively touching one’s face in front of
the mirror). Outside of mirror retraining, attentional retraining can also be useful in
typical everyday environments in which the patient selectively attends to aspects of his
or her and others’ appearance (e.g., when out with others in a social situation, while
at work or in class). It can be helpful to have the patient practice attending to other
things in the environment (e.g., the conversation he or she is engaging in, what the
weather is like) as opposed to focusing on his or her or others’ appearance (Wilhelm
et al., 2013).
Modular Interventions
Several modular interventions can be applied as needed throughout CBT for BDD
treatment and include skin picking/hair plucking, muscularity and shape/weight,
cosmetic treatment, and mood management (Wilhelm et al., 2013). Compulsive skin
picking and hair plucking, designed to improve appearance, occurs in up to one-third
of BDD patients (Grant, Menard, & Phillips, 2006; Phillips & Taub, 1995) and
many BDD patients find it to be their most distressing symptom (O’Sullivan, Phillips,
Keuthen, & Wilhelm, 1999). This module uses habit reversal training to address
specific skin picking or hair pulling concerns. The muscularity and shape/weight
module is used to individualize treatment for individuals suffering from muscle
dysmorphia, a subtype of BDD in which patients are overly focused on and concerned
with the shape and size of their muscles (H. G. Pope, Gruber, Choi, Olivardia, &
Phillips, 1997; Wilhelm et al., 2013). The module can also be used for patients who
have concerns about their shape/weight in addition to specific body areas of concerns
(Wilhelm et al., 2013). Some patients with BDD seek dermatological or surgical
intervention for their concerns prior to seeking therapy, and despite starting CBT for
BDD may remain unconvinced or ambivalent that CBT is a better treatment option
than medical interventions (Wilhelm et al., 2013). The cosmetic module combines
motivational interviewing and psychoeducation techniques that allow therapists to
provide patients with information on the ineffectiveness of medical interventions
for BDD while at the same time helping the patient to explore the pros and cons
in a nonjudgmental environment (Wilhelm et al., 2013). The mood management
module addresses depressive symptoms which are commonly co-occurring with BDD
and may at times be treatment-interfering (Gunstad & Phillips, 2003; Phillips et al.,
2008). The module combines activity scheduling, as well as cognitive restructuring
techniques for patients with more severe symptoms of depression (Wilhelm et al.,
2013).
Relapse Prevention
Relapse prevention normally occurs in the final sessions of treatment (Wilhelm et al.,
2013). It typically consists of reviewing CBT skills, anticipating obstacles related to
BDD, and envisioning the application of skills to these problems (Wilhelm et al.,
2013). The therapist will often recommend to the patient that he or she sets time aside
weekly (often during the time that he or she came in for session) to review treatment
strategies and set upcoming goals related to BDD treatment. The therapist encourages
the patient to act as “his or her own therapist.” The therapist also suggests that the
patient find other, positive activities that he or she enjoys to fill the time gap left by
the reduction of BDD related symptoms (e.g., various hobbies or spending time with
friends; Wilhelm et al., 2013). Booster sessions can be offered after treatment ends
as a periodic way in which to assess progress, maintain gains, and review cognitive
behavioral skills as needed (Wilhelm et al., 2013).
Efficacy of Cognitive Behavioral Therapy for

Body Dysmorphic Disorder
Cognitive behavioral therapy has been shown to be efficacious in the treatment

of BDD (Ipser et al., 2009; Williams et al., 2006; for reviews, see Greenberg
& Wilhelm, 2011; Neziroglu & Khemlani-Patel, 2002). Initial single and multi-
ple case studies showed that behavioral (Gomez-Perez, Marks, & Gutierrez-Fisac,
1994; Marks & Mishan, 1988; Munjack, 1978) as well as cognitive and behavioral
strategies combined (Neziroglu & Yayura-Tobias, 1993; Schmidt & Harrington,
1995) could reduce symptoms of BDD. Two single-subject, multiple baseline studies
systematically demonstrated the separate use of ERP (Campisi, 1995) and of cog-
nitive therapy (Geremia & Neziroglu, 2001) for BDD. Campisi (1995) conducted
ERP with four individuals with BDD consisting of 7 weeks of 90-minute sessions,
three times a week. Study results showed that ERP was successful in decreasing
obsessions and compulsions related to body image concerns in three out of four
participants, although discomfort with appearance and body dissatisfaction remained.
Geremia and Neziroglu (2001) treated four individuals with BDD in a single-subject
multiple baseline design with cognitive therapy alone (consisting of twice-weekly 75-
minute sessions for 7 weeks) and found a significant reduction in obsessive thoughts
related to body image in three out of four patients, with two of the patients also
showing a significant reduction in BDD-related ritualistic behaviors. In addition,
three out of four patients showed a significant decrease in dissatisfaction with body
parts.
Uncontrolled and controlled treatment outcome studies for BDD in both individual
and group formats followed. An open trial group study using cognitive behavioral
techniques showed a significant reduction in BDD symptoms, as well as symptoms
of depression (Wilhelm, Otto, Lohr, & Deckersbach, 1999). Neziroglu et al. (1996)
conducted an open trial of intensive CBT for BDD and found significant improvement
in BDD symptoms for 12 of 17 patients. Two randomized controlled studies, one of
group CBT for BDD versus a wait-list control (Rosen et al., 1995) and another of
individual CBT versus a wait-list control (Veale et al., 1996), also showed a significant
reduction in BDD symptoms with large treatment effect sizes (d = 2.18, for the
BDDE, and d = 1.81, for the BDD-YBOCS, respectively). McKay et al. (1997)
conducted a standard treatment outcome study using only ERP techniques for 10
participants with BDD. At the end of treatment, a 6-month maintenance program
was instituted for five of the patients, while the other five served as controls. All of
the patients evidenced significant reductions in BDD related symptoms from pre- to
posttreatment, suggesting that ERP alone is effective for BDD.
While these studies have provided empirical evidence in support of CBT for BDD,
they should be interpreted with caution. Inconsistencies across studies including
widely varying session length (anywhere from seven to 30 sessions) and intensity of
session duration (with sessions varying from 1 to 3 hours at a time) could account
for differences in treatment outcome (Wilhelm et al., 2011; Williams et al., 2006).
Additionally, the majority of these treatments lacked a standardized manual with
the exception of Rosen et al.’s (1995) group treatment (which primarily focused on
weight and shape as opposed to other aspects of appearance) and Wilhelm et al.’s
(1999) group treatment study which used a preliminary standardized treatment
manual. More recently, Wilhelm et al. (2011) piloted a newly developed cognitive
behavioral modular treatment manual for BDD in a sample of 12 adults with primary
BDD. Treatment lasted between 18 and 22 weeks. At posttreatment, BDD (d = 3.82)
and related symptoms (depression symptoms as measured by the Beck Depression
Inventory [BDI]; d = 0.82) were significantly improved.
A meta-analysis conducted by Williams et al. (2006) analyzed the efficacy of phar-
macological versus CBT interventions for BDD through the use of randomized con-
trolled trials and case studies. While both pharmacotherapy (Md = +0.92) and CBT
(M d = +1.78) were shown to have large effect sizes, CBT was found to have signifi-
cantly greater effect sizes than pharmacotherapy in the treatment of BDD symptoms.
Special Populations
Adolescents
BDD typically onsets in early adolescence (Phillips & Diaz, 1997; Phillips, Didie, et al.,
2006) and has a chronic course without effective treatment (Phillips, Pagano, et al.,
2006). Adolescents with BDD have markedly poor psychosocial functioning and high
levels of morbidity, including high rates of school refusal/dropout and suicidality. The
psychosocial impact of BDD is particularly concerning during adolescence, a critical
period of developmental tasks and transitions characterized by significant physical,
psychological, and social changes (for a review, see Greenberg, Delinsky, Reese,
Buhlmann, & Wilhelm, 2009; Phillips & Rogers, 2011). BDD can interfere with
key tasks of adolescence, such as the development of a stable self-concept, increased
autonomy from parents, developing healthy social and romantic relationships, and
completing school. Thus, early intervention is critical.
Treatment research on adolescents with BDD is limited; however, CBT and
pharmacotherapy appear promising. High dose SRIs were effective for adolescents
with BDD in case reports (Albertini, Phillips, & Guevremont, 1996; Phillips, Atala, &
Albertini, 1995), and in a case series of 33 children and adolescents, 53% (n = 19) of
subjects treated with an SRI demonstrated significant improvement in BDD symptoms
(Albertini & Phillips, 1999). Notably, SRIs do not work for all individuals, and many
youth and their parents are not amenable to taking medication. CBT is the first-line
psychosocial treatment for adults with BDD, and preliminary data from case reports
(Braddock, 1982; Greenberg et al., 2010; Sobanski & Schmidt, 2000) suggest it may
be helpful for adolescents.
CBT for adolescents with BDD is delivered within a developmentally sensitive
framework (for a detailed description, see Greenberg et al., 2010). The clinician
should assess for potential interference in daily life, including home, school, and
social settings. The core treatment involves psychoeducation, cognitive strategies, and
exposure and ritual prevention; however, treatment strategies are influenced by age-
related and individual differences in developmental capacities (e.g., metacognition)
and should be age-appropriate and engaging for adolescents. Parents and schools
will likely be involved in the treatment; however, the extent of family and school
involvement will vary based on the developmental level of the child and his or
her specific treatment goals. After an initial assessment, providing the family with
psychoeducation—meaningful information about BDD and its prevalence—can help
to address feelings of shame, stigma, and embarrassment within the child as well as to
reduce feelings of blame, anger, or shamefulness within the family. For example, many
parents inadvertently reinforce BDD rituals and require guidance on how to reduce
accommodation (e.g., not paying for tanning, not driving to dermatologist visits)
or how to manage school refusal. Younger patients typically warrant more parent
involvement than do older adolescents (Greenberg et al., 2010; Phillips & Rogers,
2011). Parents of younger children may provide tangible rewards (e.g., a videogame or
gift card) for homework completion, whereas parents of older adolescents can provide
privileges (e.g., getting the car on the weekend) that also help foster independence.
Individually tailored metaphors and performance-based behavioral experiments are
cognitive strategies that can be used to test the accuracy or utility of cognitive
distortions and may be particularly helpful in addressing the overly rigid and present-
oriented thinking pattern characteristic of adolescence. Age-appropriate language
should be used to develop the ERP hierarchy (i.e., fear thermometer or ladder) as
well as to determine individual exposure tasks and the order in which they will be
attempted.
Motivational issues are common (Greenberg et al., 2010). Adolescents with BDD
are often brought in for treatment by parents, but do not believe their problems
can be fixed by a psychological treatment; many are severely depressed. Thus,
adolescents should be rewarded for session attendance and homework compliance.
Depression and suicidality should be monitored closely and addressed as needed
throughout treatment. By the time adolescents have been brought into treatment,
many have given up hobbies and experienced social (e.g., loss of friends, missed dating
opportunities) and academic losses (e.g., drop in grades, failed classes) due to BDD.
Information about the child’s strengths and interests should be collected early on so
that positive activities and hobbies can be cultivated through the treatment. Moreover,
as BDD can impede the normal trajectory toward self-directed skills and autonomy,
adolescents may struggle with basic problem-solving and social skills. Systematic skills
training (role play and modeling) can address deficits in problem-solving and social
skills throughout the treatment (Greenberg et al., 2010).
Surgery Seeking
Individuals with BDD commonly consider cosmetic surgery as a primary treatment
option. For instance, in one sample of BDD patients, 71% sought out and 64%
received cosmetic interventions (Crerand et al., 2005). Highly similar rates have also
been found in other independent samples of BDD patients (i.e., 76% seeking and
66% receiving cosmetic treatment; Phillips, Grant et al., 2001). Conversely, between
7% (Sarwer, Wadden, Pertschuk, & Whitaker, 1998) and 15% (Ishigooka et al.,
1998) of patients seeking cosmetic surgery meet criteria for BDD. It is of note that
cosmetic interventions rarely lead to a reduction in BDD symptoms, and in some
patients actually result in a worsening of symptomatology. Thus, BDD is viewed as
a contraindication for cosmetic surgery (e.g., Crerand et al., 2005; Phillips, Grant,
et al., 2001).
Given the propensity for patients with BDD to seek cosmetic surgery, in concert
with its contraindication for improved BDD symptomatology, explicit discussion of
this treatment option in therapy may prove effective. As is outlined in the modular
CBT for BDD (Wilhelm et al., 2011), a module on cosmetic treatment should
include psychoeducation on the strong likelihood that cosmetic procedures will not
reduce BDD symptoms, weighing the pros and cons of seeking this treatment, and
understanding that there are far more effective treatments for BDD (i.e., CBT) than
cosmetic procedures. It is important for clinicians to take a nonjudgmental stance,
and inform patients that cosmetics surgeries are not inherently “bad,” but rather, they
simply do not seem to be effective in treating BDD.
Muscle Dysmorphia
Muscle dysmorphia (MD) is considered a subtype of BDD, and is currently being
proposed for inclusion in the DSM-5 (Phillips et al., 2010). MD is characterized as
a pathological preoccupation that one’s body is not sufficiently lean and muscular
(H. G. Pope et al., 1997), and tends to disproportionally affect males (Olivardia,
2007). Among men with BDD, roughly 25% meet criteria for MD (C. G. Pope et al.,
2005). Core symptoms of MD include compulsive weightlifting, rigid adherence
to work-out and dietary schedules, use of appearance and performance-enhancing
substances, body and/or mirror checking, and avoidance of situations in which one’s
body is exposed, or endurance of these situations with great distress (Olivardia,
2007). Although there are a number of similarities between MD and other forms
of BDD, the symptomatology outlined above reveals important differences between
the two. For instance, dietary and exercise rigidity and use of anabolic-androgenic
steroids are not typically seen in other forms of BDD. Further, there is emerging
evidence that individuals with MD are more severely ill than those with other forms
of BDD (C. G. Pope et al., 2005). In a retrospective, archival study, C. G. Pope
et al. (2005) compared 49 men with other forms of BDD to 14 men with MD, on
several psychological variables. The MD group reported greater diagnoses of eating
disorders and substance use, as well as a greater number of past suicide attempts, and
worse quality of life, compared to the other BDD group. Given the differences noted
in phenomenology and symptomatology, traditional CBT interventions for BDD
may need modification when working with patients with a MD presentation. For
instance, given the higher levels of substance (including appearance and performance
enhancing substances) abuse, and eating pathology, an integrated CBT for BDD,
eating pathology, and substance use may be needed. However, given the paucity of
research conducted to date on MD, these suggestions remain tenuous and theoretical.
Additional research, sampling clinical populations, is needed to advance the study and
subsequent treatment of MD.
BDD is a debilitating disorder that causes significant distress and considerable impair-
ment in functioning (Phillips, Menard, Fay, & Pagano, 2005). The presence of shame
and embarrassment regarding body image concerns can prevent many individuals from
seeking psychiatric or psychological treatment for their symptoms (Buhlmann, Reese,
Renaud, & Wilhelm, 2008). In addition, low levels of insight can lead many patients
with BDD to seek surgical intervention as a first-line treatment with relatively low
levels of satisfaction (Crerand et al., 2005). The recent development of standardized
assessments and empirically supported psychiatric/psychological treatments for BDD
emphasizes the importance of proper screening and treatment for patients with this
impairing condition.
Cognitive behavioral models of BDD have provided a conceptualization of how

the disorder develops and is maintained (Veale, 2004; Wilhelm et al., 2010; Wilhelm
& Neziroglu, 2002). Recent insights into the neurobiology of BDD have further
advanced these models to include accurate and up-to-date information on the etiolog-
ical origins of the disorder (Feusner, Yayura-Tobias, & Saxena, 2008). Comprehensive
models have served as the foundation for efficacious interventions for BDD including
psychopharmacological agents (e.g., SRIs) and CBT. CBT for BDD, in both indi-
vidual and group formats, has been shown to effectively reduce symptoms of the
disorder in addition to treating symptoms of comorbid psychopathology (e.g., mood
and anxiety symptoms; Veale et al., 1996; Wilhelm et al., 1999; Wilhelm et al., 2011).
The core components of CBT for BDD consist of cognitively restructuring mal-
adaptive thoughts related to body image, as well as ERP to feared situations that
are BDD-related (Rosen et al., 1995; Veale et al., 1996; Wilhelm et al., 2011).
Additional CBT techniques for the disorder include psychoeducation, motivational
interviewing, and mindfulness/perceptual retraining, as well as flexible modular inter-
ventions (i.e., skin picking, muscle dysmorphia, depression; Wilhelm et al., 2013).
Certain patients with BDD (i.e., adolescents, those seeking surgery, patients with
MD) require specialized assessment and intervention. Future directions may include
expanding on the development and use of modular treatments for patients with BDD
as well as further study of interventions for special populations (e.g., children and
adolescents).
While CBT for BDD (both individual and group) has been established as an
efficacious intervention, only a handful of CBT treatment outcome studies for BDD
have demonstrated efficacy with the use of a standardized manual (Rosen et al.,
1995; Wilhelm et al., 1999; Wilhelm et al., 2011). Large sample trials of CBT for
BDD with the use of a standardized manual are needed. In addition, CBT for BDD
has yet to be compared in a randomized controlled trial against other treatments
for the disorder (e.g., pharmacotherapy). Finally, future efforts to deconstruct and
understand the active and most efficacious components of CBT for BDD could lead
to further advances in the understanding of etiology and intervention research.
References
Albertini, R. S., & Phillips, K. A. (1999). Thirty-three cases of body dysmorphic disorder
Psychiatry, 38, 453–459. doi:10.1097/00004583-199904000-00019
Albertini, R. S., Phillips, K. A., & Guevremont, D. (1996). Body dysmorphic disorder. Journal
of the American Academy of Child and Adolescent Psychiatry, 35, 1425–1426.
Biby, E. L. (1998). The relationship between body dysmorphic disorder and depression, self-
esteem, somatization and obsessive-compulsive disorder. Journal of Clinical Psychology,
54, 489–499.
Bienvenu, J. O., Samuels, J. F., Riddle, M. A., Hoehn-Saric, R., Liang, K. Y., Cullen, B. A.,
… Nedstat, G. (2000). The relationship of obsessive-compulsive disorder to possible
spectrum disorders: Results from a family study. Biological Psychiatry, 48, 287–293.
doi:10.1016/S0006-3223(00)00831-3
Bohne, A., Wilhelm, S., Keuthen, N. J., Florin, I., Baer, L., & Jenike, M. A. (2002). Prevalence
of body dysmorphic disorder in a German college student sample. Psychiatry Research,
109, 101–104. doi:10.1016/S0165-1781(01)00363-8
Braddock, L. E. (1982). Dysmorphophobia in adolescence: A case report. British Journal of
Buhlmann, U., Cook, L. M., Fama, J. M., & Wilhelm, S. (2007). Perceived teasing in body
dysmorphic disorder. Body Image, 4, 381–385. doi:10.1016/j.bodyim.2007.06.004
Buhlmann, U., Etcoff, N. L., & Wilhelm, S. (2006). Emotion recognition bias for contempt
and anger in body dysmorphic disorder. Journal of Psychiatric Research, 40, 105–111.
doi:10.1016/j.jpsychires.2005.03.006
Buhlmann, U., Glaesmer, H., Mewes, R., Fama, J. M., Wilhelm, S., Brahler, E., & Rief, W.
(2010). Updates of the prevalence of body dysmorphic disorder: A population-based
survey. Psychiatry Research, 178, 171–175. doi:10.1016/j.psychres.2009.05.002
Buhlmann, U., McNally, R. J., Wilhelm, S., & Florin, I. (2002). Selective processing of
emotional information in body dysmorphic disorder. Journal of Anxiety Disorders, 16,
289–298. doi:10.1016/S0887-6185(02)00100-7
Buhlmann, U., Reese, H. E., Renaud, S., & Wilhelm, S. (2008). Clinical considerations for the
treatment of body dysmorphic disorder with cognitive-behavioral therapy. Body Image, 5,
39–49. doi:10.1016/j.bodyim.2007.12.002
Buhlmann, U., Wilhelm, S., McNally, R. J., Tuschen-Caffier, B., Baer, L., & Jenike, M. A.
(2002). Interpretive biases for ambiguous information in body dysmorphic disorder. CNS
Spectrums, 7 , 435–436.
Campisi, T. A. (1995). Exposure and response prevention in the treatment of body dysmor-
phic disorder. Available from ProQuest Dissertation and Theses Database. (UMI No.
9611409).
Chosak, A., Marques, L., Greenberg, J. L., Jenike, E., Dougherty, D., & Wilhelm, S. (2008).
Body dysmorphic disorder and obsessive-compulsive disorder: Similarities, differences
and the classification debate. Expert Reviews in Neurotherapeutics, 8, 1209–1218. doi:
10.1586/14737175.8.8.1209
Crerand, C. E., Phillips, K. A., Menard, W., & Fay, C. (2005). Nonpsychiatric med-
ical treatment of body dysmorphic disorder. Psychosomatics, 46, 549–555. doi:
10.1176/appi.psy.46.6.549
Deckersbach, T., Savage, C. R., Phillips, K. A., Wilhelm, S., Bulhmann, U., Rauch, S. L., …
Jenike, M. A. (2000). Characteristics of memory dysfunction in body dysmorphic disorder.
Journal of the International Neuropsychological Society, 6, 673–681.
Didie, E. R., Menard, W., Stern, A. P., & Phillips, K. A. (2008). Occupational functioning
and impairment in adults with body dysmorphic disorder. Comprehensive Psychiatry, 49,
561–569. doi:10.1016/j.comppsych.2008.04.003
Eddy, K. T., Dutra, L., Bradley, R., & Westen, D. (2004). A multidimensional meta-analysis
of psychotherapy and psychopharmacotherapy for obsessive-compulsive disorder. Clinical
Feusner, J. D., Hembacher, E., Moller, H., & Moody, T. (2011). Abnormalities of object
visual processing in body dysmorphic disorder. Psychological Medicine, 41, 2385–2397.
doi:10.1017/S0033291711000572
Feusner, J. D., Moody, T., Hembacher, E., Townsend, J., McKinley, M., Moller, H.,
& Bookheimer, S. (2010). Abnormalities of visual processing and frontostriatal sys-
tems in body dysmorphic disorder. Archives of General Psychiatry, 67 , 197–205.
doi:10.1001/archgenpsychiatry.2009.190.
Feusner, J. D., Townsend, J., Bystritsky, A., & Bookheimer, S. (2007). Visual information
processing of faces in body dysmorphic disorder. Archives of General Psychiatry, 64,
1417–1425. doi:10.1001/archpsyc.64.12.1417
Feusner, J. D., Yayura-Tobias, J., & Saxena, S. (2008). The pathophysiology of body dysmor-
phic disorder. Body Image, 5, 3–12. doi:10.1016/j.bodyim.2007.11.002
Geremia, G. M., & Neziroglu, F. (2001). Cognitive therapy in the treatment of body dysmor-
phic disorder. Clinical Psychology and Psychotherapy, 8, 243–251. doi:10.1002/cpp.284
Gomez-Perez, J. C., Marks, I. M., & Gutierrez-Fisac, J. L. (1994). Dysmorphophobia: Clinical
features and outcome with behavioral therapy. European Psychiatry, 9, 229–235.
Grant, J. E., Kim, S. W., & Crow, S. J. (2001). Prevalence and clinical features of body
dysmorphic disorder in adolescent and adult psychiatric inpatients. Journal of Clinical
Grant, J. E., Menard, W., Pagano, M. E., Fay, C., & Phillips, K. A. (2005). Substance abuse
disorders in individuals with body dysmorphic disorder. Journal of Clinical Psychiatry, 66,
309–316.
Grant, J. E., Menard, W., & Phillips, K. A. (2006). Pathological skin picking in individ-
uals with body dysmorphic disorder. General Hospital Psychiatry, 28, 487–493. doi:
10.1016/j.genhosppsych.2006.08.009
Greenberg, J. L., Delinsky, S. S., Reese, H. E., Buhlmann, U., & Wilhelm, S. (2009). Body
image. In J. Grant and M. Potenza (Eds.), Young adult mental health (pp. 126–142).
Greenberg, J. L., Markowitz, S., Petronko, M. R., Taylor, C. E., Wilhelm, S., & Wilson, G. T.
(2010). Cognitive-behavioral therapy for adolescent body dysmorphic disorder. Cognitive
and Behavioral Practice, 17 , 248–258. doi:10.1016/j.cbpra.2010.02.002
Greenberg, J. L., & Wilhelm, S. (2011). Cognitive-behavioral therapy for body dysmorphic
disorder: A review and future directions. International Journal of Cognitive Therapy, 4,
349–362. doi:10.1521/ijct.2011.4.4.349
Gunstad, J., & Phillips, K. A. (2003). Axis I comorbidity in body dysmorphic disorder.
Comprehensive Psychiatry, 44, 270–276. doi:10.1016/S0010-440X(03)00088-9
Hollander, E., Allen, A., Kwon, J., Aronowitz, B., Schmeideler, J., Wong, C., & Simeon, D.
(1999). Clomipramine versus desipramine crossover trial in body dysmorphic disorder:
Selective efficacy of a serotonin reuptake inhibitor in imagined ugliness. Archives of General
Psychiatry, 56, 1033–1039.
Hollander, E., Kim, S., Braun, A., Simeon, D., & Zohar, J. (2009). Cross-cutting issues
and future directions for the OCD spectrum. Psychiatry Research, 170, 3–6. doi:
10.1016/j.psychres.2008.07.015
Ipser, J. C., Sander, C., & Stein, D. J. (2009). Pharmacotherapy and psychotherapy for
body dysmorphic disorder. Cochrane Database of Systematic Reviews, 21, CD005332.
doi:10.1002/14651858.CD005332.pub2
Ishigooka, J., Iwao, M., Suzuki, M., Fukuyama, Y., Murasaki, M., & Miura, S. (1998).
Demographic features of patients seeking cosmetic surgery. Psychiatry and Clinical
Neurosciences, 52, 283–287. doi:10.1046/j.1440-1819.1998.00388.x
Koran, L. M., Abujaoude, E., Large, M. D., & Serpe, R. T. (2008). The prevalence of body
dysmorphic disorder in the United States adult population. CNS Spectrums, 13, 316–322.
Marks, I., & Mishan, J. (1988). Dysmorphobic avoidance with disturbed bodily perception.
A pilot study of exposure therapy. British Journal of Psychiatry, 152, 674–678. doi:
10.1192/bjp.152.5.674
McKay, D., Todaro, J., Neziroglu, F., Campisi, T., Moritz, E. K., & Yaryura-Tobias, J. A.
(1997). Body dysmorphic disorder: A preliminary evaluation of treatment and maintenance
using exposure with response prevention. Behaviour Research and Therapy, 35, 67–70.
doi:10.1016/S0005-7967(96)00082-4
Munjack, D. (1978). Behavioral treatment of dysmorphophobia. Journal of Behavioral Therapy
and Experimental Psychiatry, 9, 53–56. doi:10.1016/0005-7916(78)90088-5
Neziroglu, F., & Khemlani-Patel, S. (2002). A review of cognitive behavioral treatment for
body dysmorphic disorder. CNS Spectrums, 7 , 464–471.
Neziroglu, F., Khemlani-Patel, S., & Veale, D. (2008). Social learning therapy and cog-
nitive behavioral models of body dysmorphic disorder. Body Image, 5, 28–38. doi:
10.1016/j.bodyim.2008.01.002
Neziroglu, F., McKay, D., Todaro, J., & Yayura-Tobias, J. A. (1996). Effect of cognitive
behavior therapy on persons with body dysmorphic disorder and comorbid Axis II
disorders. Behavior Therapy, 27 , 67–77. doi:10.1016/S0005-7894(96)80036-0
Neziroglu, F. A., & Yayura-Tobias, J. A. (1993). Exposure, response prevention and cognitive
therapy in the treatment of body dysmorphic disorder. Behavior Therapy, 24, 431–438.
doi:10.1016/S0005-7894(05)80215-1
Olivardia, R. (2007). Muscle dysmorphia: Characteristics, assessment, and treatment. In
J. K. Thompson & G. Cafri (Eds.), The muscular ideal: Psychological, social, and medical
perspectives (pp. 123–139). Washington, DC: American Psychological Association.
O’Sullivan, R. L., Phillips, K. A., Keuthen, N. J., & Wilhelm, S. (1999). Near-fatal skin picking
from delusional body dysmorphic disorder responsive to fluvoxamine. Psychosomatics, 40,
79–81. doi:10.1016/S0033-3182(99)71276-4
Perugi, G., Giannotti, D., Di Vaio, S., Frare, F., Saettoni, M., & Cassano, G. B. (1996). Fluvox-
amine in the treatment of body dysmorphic disorder (dysmorphophobia). International
Clinical Psychopharmacology, 11, 247–254.
Phillips, K. A. (1996). The broken mirror, New York, NY: Oxford University Press.
Phillips, K. A. (2000). Quality of life for patients with body dysmorphic disorder. Journal of
Phillips, K. A. (2004). Psychosis in body dysmorphic disorder. Journal of Psychiatric Research,
38, 63–72. doi:10.1016/S0022-3956(03)00098-0
Phillips, K. A. (2006). An open-label study of escitalopram in body dysmorphic disorder.
International Clinical Psychopharmacology, 21, 177–179.
Phillips, K. A., Albertini, R. S., & Rasmussen, S. A. (2002). A randomized placebo-controlled
trial of fluoxetine in body dysmorphic disorder. Archives of General Psychiatry, 59,
381–388.
Phillips, K. A., Atala, K. D., & Albertini, R. S. (1995). Case study: Body dysmorphic disorder
in adolescents. Journal of the American Academy of Child and Adolescent Psychiatry, 34,
1216–1220. doi:10.1097/00004583-199509000-00020
Phillips, K. A., & Diaz, S. F. (1997). Gender differences in body dysmorphic disorder. Journal
of Nervous & Mental Disease, 185, 570–577.
Phillips, K. A., Didie, E. R., Feusner, J., & Wilhelm, S. (2008). Body dysmorphic disorder:
Treating an underrecognized disorder. American Journal of Psychiatry, 165, 1111–1118.
doi:10.1176/appi.ajp.2008.08040500
Phillips, K. A., Didie, E., Menard, W., Pagano, M. E., Fay, C., & Weisberg, R. B. (2006).
Clinical features of body dysmorphic disorder in adolescents and adults. Psychiatry
Research, 3, 305–314. doi:10.1016/j.psychres.2005.09.014
Phillips, K. A., Dwight, M. M., & McElroy, S. L. (1998). Efficacy and safety of fluvoxamine in
body dysmorphic disorder. Journal of Clinical Psychiatry, 59, 165–171.
Phillips, K. A., Grant, J., Siniscalchi, J., & Albertini, R. S. (2001). Surgical and nonpsychiatric
medication treatment of patients with body dysmorphic disorder. Psychosomatics, 42,
504–510. doi:10.1176/appi.psy.42.6.504
Phillips, K. A., & Hollander, E. (2008). Treating body dysmorphic disorder with medica-
tion: Evidence, misconceptions and a suggested approach. Body Image, 5, 13–27. doi:
10.1016/j.bodyim.2007.12.003
Phillips, K. A., Hollander, E., Rasmussen, S. A., Arnowitz, B. R., DeCaria, C., & Goodman,
W. K. (1997). A severity rating scale for body dysmorphic disorder: Development,
reliability, and validity of a modified version of the Yale-Brown Obsessive Compulsive
Scale. Psychopharmacology Bulletin, 33, 17–22.
Phillips, K. A., McElroy, S. L., Dwight, M. M., Eisen, J. L., & Rasmussen, S. A. (2001).
Delusionality and response to open-label fluvoxamine in body dysmorphic disorder.
Phillips, K. A., McElroy, S. L., Hudson, J. I., & Pope, H. G., Jr. (1995). Body dysmorphic
disorder: An obsessive-compulsive disorder, a form of spectrum disorder, or both? Journal
of Clinical Psychiatry, 56, 41–51.
Phillips, K. A., McElroy, S. L., Keck, P. E., Pope, H. G., & Hudson, J. I. (1993). Body
dysmorphic disorder: 30 cases of imagined ugliness. American Journal of Psychiatry, 150,
302–308.
Phillips, K. A. & Menard, W. (2006). Suicidality in body dysmorphic disorder: A prospective
study. American Journal of Psychiatry, 163, 1280–1282. doi: 10.1176/appi.ajp163.7.
1280
Phillips, K. A., Menard, W., Fay, C., & Pagano, M. E. (2005). Psychosocial functioning and
quality of life in body dysmorphic disorder. Comprehensive Psychiatry, 46, 254–280. doi:
10.1016/j.comppsych.2004.10.004
Phillips, K. A., Menard, W., Fay, C., & Weisberg, R. (2005). Demographic characteristics,
phenomenology, comorbidity, and family history in 200 individuals with body dysmorphic
disorder. Psychosomatics, 46, 317–356. doi:10.1176/appi.psy.46.4.317
Phillips, K. A., & Najjar, F. (2003). An open-label study of citalopram in body dysmorphic
disorder. Journal of Clinical Psychiatry, 64, 715–720.
Phillips, K. A., Pagano, M. E., Menard, W., & Stout, R. L. (2006). A 12-month follow-up
study of the course of body dysmorphic disorder. American Journal of Psychiatry, 163,
907–912. doi:10.1176/appi.ajp.163.5.907
Phillips, K. A., & Rogers, J. (2011). Cognitive-behavioral therapy for youth with body
dysmorphic disorder: Current status and future directions. Child and Adolescent Psychiatric
Clinics of North America, 20, 287–304. doi:10.1016/j.chc.2011.01.004
Phillips, K. A., & Stout, R. L. (2006). Associations in the longitudinal course of body dys-
morphic disorder with major depression, obsessive-compulsive disorder and social phobia.
Journal of Psychiatric Research, 40, 360–269. doi:10.1016/j.jpsychires.2005.10.001
Phillips, K. A., & Taub, S. L. (1995). Skin picking as a symptom of body dysmorphic disorder.
Psychopharmacology Bulletin, 31, 279–288.
Phillips, K. A., Wilhelm, S., Koran, L. M., Didie, E. R., Fallon, B. A., Feusner, J., & Stein, D.
(2010). Body dysmorphic disorder: Some key issues for DSM-V. Depression and Anxiety,
27 , 573–591. doi:10.1002/da.20709
Pope, H. G., Jr., Gruber, A. J., Choi, P. Y., Olivardia, R., & Phillips, K. A. (1997). Muscle
dysmorphia: An underrecognized form of body dysmorphic disorder. Psychosomatics, 38,
548–557. doi:10.1016/S0033-3182(97)71400-2
Pope, C. G., Pope, H. G., Menard, W., Fay, C., Olivardia, R., & Phillips, K. A. (2005). Clinical
features of muscle dysmorphia among males with body dysmorphic disorder. Body Image,
2, 395–400. doi:10.1016/j.bodyim.2005.09.001
Rief, W., Buhlmann, U., Wilhelm, S., Borkenhagen, B., & Brahler, E. (2006). The prevalence
of body dysmorphic disorder: A population-based survey. Psychological Medicine, 36,
877–885. doi:10.1017/S0033291706007264
Rosen, J. C., & Ramirez, E. (1998). A comparison of eating disorders and body dysmorphic
disorder on body image and psychological adjustment. Journal of Psychosomatic Research,
44, 441–449. doi:10.1016/S0022-3999(97)00269-9
Rosen, J. C., & Reiter, J. (1996). Development of the Body Dysmorphic Disorder Examination.
Behaviour Research and Therapy, 34, 755–766. doi:10.1016/0005-7967(96)00024-1
Rosen, J. C., Reiter, J., & Orosan, P. (1995). Cognitive-behavioral body image therapy for
body dysmorphic disorder. Journal of Consulting and Clinical Psychology, 63, 263–269.
Sarwer, D. B., Wadden, T. A., Pertschuk, M. J., & Whitaker, L. A. (1998). Body image
dissatisfaction and body dysmorphic disorder in 100 cosmetic surgery patients. Plastic and
Reconstructive Surgery, 101, 1644–1649.
Schmidt, N. B., & Harrington, P. (1995). Cognitive-behavioral treatment of body dysmorphic
disorder: A case report. Journal of Behavior Therapy and Experimental Psychiatry, 26,
161–167.
Sobanski, E., & Schmidt, M. H. (2000). “Everybody looks at my pubic bone”: A case report
of a patient with body dysmorphic disorder. Acta Psychiatrica Scandinavica, 101, 80–82.
doi:10.1034/j.1600-0447.2000.101001080.x
Veale, D. (2004). Advances in a cognitive behavioural model of body dysmorphic disorder.
Body Image, 1, 113–125. doi:10.1016/S1740-1445(03)00009-3
Veale, D., Gournay, K., Dryden, W., Boocock, A., Shah, F., Willson, R., & Walburn, J.
(1996). Body dysmorphic disorder: A cognitive behavioural model and pilot randomized
control trial. Behaviour Research and Therapy, 34, 717–729. doi:10.1016/0005-
7967(96)00025-3
Wilhelm, S., Buhlmann, U., Hayward, L., Greenberg, J., & Dimaite, R. (2010). A cognitive-
behavioral treatment approach for body dysmorphic disorder. Cognitive and Behavioral
Practice, 17 , 241–247. doi:10.1016/j.cbpra.2010.02.001
Wilhelm, S. N., & Neziroglu, F. (2002). Cognitive theory of body dysmorphic disorder.
In R. O. Frost & G. S. Steketee (Eds.), Cognitive approaches to obsessions and compul-
sions: Theory, assessment and treatment (pp. 203–214). Amsterdam, The Netherlands:
Pergamon/Elsevier Science Inc.
Wilhelm, S., Otto, M. W., Lohr, B., & Deckersbach, T. (1999). Cognitive behavior group
therapy for body dysmorphic disorder: A case series. Behaviour Research and Therapy, 37 ,
71–75. doi:10.1016/S0005-7967(98)00109-0
Wilhelm, S., Otto, M. W., Zucker, B., & Pollack, M. H. (1997). Prevalence of body dysmorphic
disorder in patients with anxiety disorders. Journal of Anxiety Disorders, 5, 499–502. doi:
10.1016/S0887-6185(97)00026-1
Wilhelm, S., Phillips, K. A., Fama, J. M., Greenberg, J. L., & Steketee, G. (2011). Mod-
ular cognitive-behavioral therapy for body dysmorphic disorder. Behavior Therapy, 42,
624–633. doi:10.1016/j.beth.2011.02.002
Wilhelm, S., Phillips, K. A., & Steketee, G. (2013). A cognitive behavioral treatment manual
for body dysmorphic disorder. New York, NY: Guilford Press.
Williams, J., Hadjistavropoulos, T., & Sharpe, D. (2006). A meta-analysis of psychological
and pharmacological treatments for body dysmorphic disorder. Behaviour Research and
48
Major Depressive Disorder
Jeffrey R. Vittengl
Truman State University, United States
Robin B. Jarrett
University of Texas Southwestern Medical Center, United States
Focus of the Chapter
The ideal treatment for major depressive disorder (MDD) would quickly eliminate
depressive symptoms, fully restore psychosocial functioning, and wholly prevent return
of depression for all patients. Further, interventions would exist to reliably prevent
first onsets of depressive episodes. No treatment approaches these ideals currently, but
cognitive therapy (CT) offers considerable progress and lays the foundation for future
research questions, potential improvement in outcomes, and emerging innovation.
In this chapter we summarize research on CT applied to MDD in persons aged 18
years and older. We first review the nature, prevalence, course, and consequences
of MDD. We then distinguish goals, timing, forms, and delivery methods of CT
for depression. We consider what is known, and what is not known, about the
efficacy of CT in reducing depressive symptoms, preventing relapse and recurrence,
and improving psychosocial functioning. We comment on best practice processes to
promote competence in CT and to make decisions when treating depressed patients.
Finally, we consider the increasing need for effectively disseminating CT to depressed
elderly patients given their predictable increase in numbers.
What Is Major Depressive Disorder?
Major depressive disorder (MDD) is defined by prolonged disturbances in mood with

attendant changes in cognition and behavior that produce significant life interference
(American Psychiatric Association [APA], 2000). Persons with MDD experience one
or more major depressive episode (MDE). The MDEs last a minimum of 2 weeks by
definition (APA, 2000) but often several months or more, especially among patients

DOI: 10.1002/9781118528563.wbcbt48
with empirically-established risk factors including higher neuroticism, borderline

personality disorder, negative cognitive content, longer prior episodes, and low social
support (e.g., Scott, Williams, Brittleband, & Ferrier, 1995; Skodol et al., 2011;
Spijker et al., 2002). Persons with MDD suffer from depressed mood and/or loss of
pleasure or interest in life’s activities, as well as four or more additional symptoms
including significant changes in body weight, sleep quantity, and psychomotor
behavior, fatigue, feelings of guilt and worthlessness, diminished concentration and
difficulty making decisions, and suicidal thoughts, plans, or actions (APA, 2000). Such
symptoms must impair functioning or prompt help seeking and cannot be attributed
to another medical disorder to be diagnosed.
The prevalence of MDD is high, with estimates of about 13–17% over the lifetime
and 5–7% over the past year in U.S. national samples (Hasin, Goodwin, Stinson, &
Grant, 2005; Kessler, Berglund, et al., 2005; Kessler, Chiu, et al., 2005). However,
the lifetime prevalence of MDD may be higher in the United States than in many other
nations, including Japan (3%), Canada (8%), Chile (9%), and Germany (12%; Andrade
et al., 2003). MDD is more common in women than in men, and in younger than
older persons (Byers, Yaffe, Covinsky, Friedman, & Bruce, 2010; Kessler et al., 2003).
Although most people with MDD have a moderate or serious (80%) rather than mild
(20%) illness (Kessler, Chiu, et al., 2005), many people with MDD (43%) report
receiving no treatment in any form during the past year (Wang et al., 2005). Among
MDD patients who do receive treatment, less than half (38%) receive minimally
adequate treatment, defined as (a) at least 2 months of appropriate medication and
at least four physician visits, or (b) at least eight psychotherapy visits of 30 or more
minutes delivered by a trained professional (Wang et al., 2005).
The course of MDD is variable. Most people who experience depressive episodes
eventually return to normal or near-normal mood, with or without treatment, but
perhaps 15–25% display chronic depression (Eaton et al., 2008; Satyanarayana,
Enns, Cox, & Sareen, 2009). (Chronic depression is addressed more extensively in
Chapter 49, “Dysthymia and Chronic Major Depression”.) Among the majority with
non-chronic MDD, many people show an episodic course with one or more additional
MDEs during the lifetime (recurrences). Although there is general agreement that
MDD recurrence is common, estimates vary by method of assessment, time period
assessed, and population sampled. Persons’ lifetime retrospective recall (e.g., during
a brief diagnostic interview) may substantially underestimate the number of prior
episodes (e.g., Patten, 2009), calling into question estimates derived from cross-
sectional studies. Prospective studies with repeated assessment of patients show high
recurrence rates, including an average of about 0.2 MDE per year and 85% of
patients experiencing at least one recurrence within 15 years (Solomon et al., 2000).
Moreover, the chance of another recurrence increases with each MDE (Mueller et al.,
1999; Solomon et al., 2000). On the other hand, MDD recurrence in the general
population, in contrast to patients at specialized mental health treatment centers,
may only be 35% over 15 years (Hardeveld, Spijker, De Graaf, Nolen, & Beekman,
2010). Further, among patient samples, most research fails to differentiate patients in
their first episode who may have a lower lifetime recurrence rate of about 50–60%
(Monroe & Harkness, 2011).
Major Depressive Disorder 1133
People suffering from MDD show poor psychosocial functioning and increased
mortality. For example, workers with MDD miss an average of 9 days of work per
year due to MDD, plus the equivalent of 18 additional missed days due to reduced
productivity, resulting in 225 million days lost from the U.S. workforce per year
(Kessler et al., 2006). In addition to reduced work performance, persons with MDD
demonstrate impaired role functioning in social and family relationships, even more
so than patients with other chronic medical conditions including congestive heart
failure, diabetes, and hypertension. Similarly, depressed persons’ physical capacity is
reduced comparably to patients with diabetes and arthritis (K. Wells et al., 1989).
Depressed persons show increased mortality from both suicide and “natural” causes
including comorbid heart disease, hypertension, and diabetes (e.g., Angst, Stassen,
Clayton, & Angst, 2002; Cassano & Fava, 2002; Thomson, 2011). Risk of suicide
can be an immediate concern for cognitive therapists since lifetime estimates include
16% of persons with MDD attempting (Chen & Dilsaver, 1996) and 7% completing
(Brådvik, Mattisson, Bogren, & Nettelbladt, 2008) suicide. However, suicide rates
vary greatly by population sampled (e.g., inpatients’ rates are several times higher than
the general population of persons with MDD; Blair-West & Mellsop, 2001; Angst
et al., 2002).
When and with What Goals Is Major Depressive

Disorder Treated?
Because MDD is often episodic, both pharmacotherapies and psychotherapies may

be staged to satisfy different goals (Frank, Prien, Jarrett, & Keller, 1991; Rush et al.,
2006). Figure 48.1 depicts each phase of CT in relation to the change points in the
course of depressive illness. Acute phase treatments (including traditional CT; e.g.,
Symptom levels in a hypothetical patient with MDD

30
Major Recurrence
depressive Relapse
(before (after
25 episode
recovery) recovery)
20
HRSD score
15
Response Recovery
(without
10
relapse)
Remission
5
0
0
4
8
12
16
20
24
28
32
36
40
44
48
52
56
60
64
68
72
76
80
84
88
92
96
100
104
Week
A-CT C-CT M-CT
Figure 48.1 Stages of treatment and events in major depressive disorder. HRSD = Hamilton
Rating Scale for Depression. CT = cognitive therapy. A-CT = acute phase CT. C-CT =
continuation phase CT. M-CT = maintenance phase CT. Dotted lines represent relapse and
recurrence events that CT aims to prevent.
Beck, Rush, Shaw, & Emery, 1979) are applied during MDEs to reduce depressive
symptom severity by a clinically meaningful amount resulting in an initial treatment
response. A response signals that a treatment may be effective for the presenting
patient. For example, when 17-item Hamilton Rating Scale for Depression (HRSD;
Hamilton, 1960) scores decrease by ≥ 50% of their pretreatment values (e.g., from
20 to 10) and/or reach some absolute threshold (e.g., HRSD ≤ 9), we may infer
that the patient has responded. The term response implies that the acute phase
treatment, rather than extra-treatment processes (e.g., life events or “spontaneous”
changes), caused the reduction in symptoms; however, when treating individual
patients it is typically impossible to demonstrate cause and effect definitely. After
response, remission is defined as more than one (e.g., ≥ 3) continuous weeks of
reduced symptoms when the patient no longer meets criteria for an MDE. Remission
may be qualified as full remission when patients have very low or no remaining
depressive symptoms (e.g., HRSD ≤ 6) or partial remission when residual depressive
symptoms persist (e.g., HRSD 7–9). Acute phase treatments often stop after some
level of response or remission but may be followed by continuation phase treatments.
Continuation phase treatments (e.g., C-CT; Jarrett, 1989, 1992) aim to prevent
relapse and to promote remission and may produce recovery for some. Recovery refers
to several (e.g., ≥ 8) months of reduced symptoms and no MDE. As in remission,
recovery may include residual depressive symptoms that are important predictors of
relapse and recurrence (e.g., Fava, Ruini, & Belaise, 2007). After remission, patients
relapse before recovery, but recur after recovery, if they again meet criteria for an
MDE. Conceptually, relapse refers to return of the prior unresolved MDE whereas
recurrence marks a new MDE. Finally, maintenance phase treatments (e.g., Blackburn
& Moore, 1997; Klein et al., 2004) are applied after recovery to reduce recurrence
and promote persistent recovery.
Are There Different Types of Cognitive Therapy?
Various forms of CT for depression share a focus on changing patients’ cognition

correlated with distress as an entry point toward improving mood and psychosocial
functioning. Conceptual and technical distinctions are possible among several tradi-
tional and newer (sometimes called “third wave”) forms of CT, but data on differential
efficacy are limited or absent. Consequently, empirically-based recommendations for
one type of CT over another for a given patient often are impossible at this time.
The evidence base tends to be stronger for traditional forms of CT (e.g., Hofmann,
Sawyer, & Fang, 2010; Öst, 2008), perhaps due to its larger volume. Moreover, CT
can be delivered in person by a therapist, remotely (e.g., by Internet), individually, or
in groups. The following are examples of several implementations of CT.
Traditional Forms of Cognitive Therapy

Beck et al.’s (1979) individual, in-person treatment arguably is prototypical and the
most commonly researched and practiced form of CT. Beck’s CT first emphasizes
behavioral activation (increasing the patient’s engagement with sources of reinforce-

ment and improving functioning), followed by cognitive assessment and restructuring
of negative automatic thoughts, and finally efforts to identify and change broader
negative assumptions or schema about the self, world, and future. Similarly, Lewin-
sohn et al.’s (1984) Coping with Depression treatment aims to teach relaxation skills,
increase pleasant activities, change negative and irrational cognition, and improve
social skills, but is delivered in a group format. Finally, bibliotherapy as described in
such manuals as Burns’s (1980) Feeling Good or Greenberger and Padesky’s (1995)
Mind over Mood may be used in conjunction with in-person sessions delivered by
a therapist (e.g., Burns & Nolen-Hoeksema, 1991) or prescribed to patients to
promote skill building and understanding of the cognitive model. Some patients may
rely on these tools for “self-help” (e.g., Scoggin, Jamison, & Gochneaur, 1989). The
mechanism of change and the active ingredients responsible for outcomes within CT
remain hypothesized rather than conclusively identified.
Newer Forms of Cognitive Therapy

Whereas traditional forms of CT (e.g., Beck et al., 1979) aim to challenge and
change unrealistically negative cognitive content (e.g., about the self, world, and
future), metacognitive therapy (meta-CT) focuses primarily on changing how negative
thoughts are monitored and regulated (A. Wells, 2008, 2009). For patients with
MDD, meta-CT goals include reducing time-consuming rumination (e.g., past-
oriented thoughts such as, “Why do I feel so depressed?”), worry (e.g., future-oriented
thoughts such as, “What should I do about my depression?”), threat-monitoring
(e.g., focusing attention on depressive symptoms and their implications for effective
functioning), and maladaptive coping behaviors (e.g., avoiding social activities and
work to spend the time ruminating and worrying).
Mindfulness-based cognitive therapy (MBCT) was first developed for patients with
recurrent MDD and implemented after acute phase treatment response (following
pharmacotherapy) to prevent relapse and recurrence (Teasdale et al., 2000). In an
8-week group format, MBCT patients learn mindfulness meditation to gain awareness
of, and detachment from, negative thoughts and feelings when risk of relapse and
recurrence is high. In some ways similar to meta-CT, and different from traditional CT,
MBCT is not focused on changing the content of negative thoughts but instead on
changing patients’ reactions to negative thoughts to prevent escalation of depressive
symptoms. Preliminary data also suggest that MBCT reduces depressive symptoms as
an acute phase treatment (van Aalderen et al., 2012), but additional study is required.
Cognitive behavioral analysis system of psychotherapy (CBASP) is designed to treat
patients with chronic depression by improving their rational thinking and social-
interpersonal functioning (McCullough, 2003). For example, situational analysis is
designed to improve patients’ understanding of the consequences of their interper-
sonal behavior (e.g., differentiating between actual and desired outcomes). Based
in psychodynamic and developmental theories, interpersonal discrimination exercise
aims to improve the accuracy of patients’ views of the therapist by differentiating
patients’ historical reactions to influential persons (e.g., parents). Finally, behav-

ioral skills training and rehearsal build on patients’ improved understanding of the
consequences of their interpersonal behavior to reach desired outcomes.
Acceptance and commitment therapy (ACT) seeks to teach patients to accept their
negative emotional and cognitive experiences, rather than attempting to resist or
change them, while simultaneously working toward “valued goals” (Hayes, Strosahl,
& Wilson, 1999). In this sense, ACT is similar to MBCT and meta-CT. For example,
ACT patients practice “cognitive diffusion” to become nonjudgmentally mindful
of themselves and their external circumstances. ACT is often delivered as a group
treatment (e.g., Forman, Herbert, Moitra, Yeomans, & Geller, 2007) or as a self-help
program (e.g., Fledderus, Bohlmeijer, Pieterse, & Schreurs, 2012).
Behavioral activation (BA) can be conceptualized as a component of traditional CT
(Beck et al., 1979) or behavior therapy but has been expanded more recently as a
free-standing intervention (e.g., Martell, Addis, & Jacobson, 2001). Some argue that
the conceptual distinctions are important (as suggested by the findings of Dimidjian
et al., 2006). As in traditional CT, BA reduces avoidance/withdrawal behaviors and
promotes patients’ (re)engagement with reinforcing activities consistent with positive
long-term functioning (e.g., social, vocational). Traditional cognitive interventions
are deemphasized in BA, and instead patients are taught to shift attention away from
ruminative thoughts to immediate experiences and behaviors that are associated with
positive consequences.
Computerized and Internet-Based Cognitive Therapy

Partly addressing calls for treatment models scalable to the high prevalence of MDD
(Kazdin & Blase, 2011), several forms of CT can be delivered through electronic
media. A meta-analysis of six randomized controlled trials of Internet- and computer-
based CT for MDD showed a statistically significant, moderate advantage of CT
(effect size g = 0.78; note that g is very similar to d described in more detail later)
compared to control groups (Andrews, Cuijpers, Craske, McEvoy, & Titov, 2010),
which is consistent with a more recent clinical trial (Levin et al., 2011).
An important issue in this literature is identifying the conditions under which
ongoing contact, of some type, with a live therapist is helpful or necessary. A meta-
analysis of both anxiety and depression treatments suggested that computer- and
Internet-based CT programs including contacts with a live therapist (e.g., a brief
weekly email or telephone conversations) produce better outcomes (d = 0.61) than
entirely preprogrammed treatments (d = 0.25; Andersson & Cuijpers, 2009). This
general finding was replicated in a more recent randomized trial comparing therapist-
guided (d = 1.14 vs. wait-list control) with unguided (d = 0.66 vs. wait-list control)
Internet-based CT for patients with depression (MDD or dysthymic disorder; Berger,
Hämmerli, Gubser, Andersson, & Caspar, 2011). Related unanswered questions are
for which types of patients with varying degrees of symptom severity, or number
of comorbid disorders or types of underlying risk factors, contact with a therapist is
necessary.
Another issue requiring additional research is which patients fare better or worse
in computerized or Internet-based CT versus other treatments (e.g., in-person CT
or pharmacotherapy). Two studies included in the Andrews et al. (2010) meta-

analysis compared computerized CT to traditional face-to-face CT with a trivial (and
nonsignificant) difference favoring computerized treatments (g = 0.09). Similarly, a
recent clinical trial found no difference through one year of follow-up. On average, for
depressed patients (N = 303; scoring ≥ 16 on the Beck Depression Inventory (BDI)
[Beck et al., 1961], but not necessarily meeting criteria for MDD) randomized to
computerized CT, treatment as usual with the patient’s general medical practitioner,
or their combination, all groups improved during treatment (e.g., within-group
decrease in BDI ds = 1.1–1.3, or about 10–11 raw scale points; de Graaf, Hollon,
& Huibers, 2010). There were, however, some indications that patients higher in
optimism fared better in computerized CT alone versus treatment as usual, whereas
patients with more severe illness (MDD diagnosis and parental psychiatric history)
had better outcomes in CT plus treatment as usual versus treatment as usual (de Graaf
et al., 2010).
How Much Do Depressive Symptoms Decrease during

Acute Phase Cognitive Therapy?
A substantial literature supports acute phase CT’s efficacy in treating MDD. The
literature includes comparisons of patients from pre- to post-CT, and, more rigorously,
randomized clinical trials comparing CT to inactive (e.g., placebo, wait-list) and active
(e.g., medication, behavior therapy, interpersonal psychotherapy) control conditions
(e.g., Butler, Chapman, Forman, & Beck, 2006; Craighead, Sheets, Brosse, & Ilardi,
2007; Cuijpers et al., 2012). In this section, we consider depressive symptoms and
psychosocial functioning levels at the end of acute phase CT, as well as prevention of
relapse and recurrence of MDD after the end of the acute phase.
On average from pre- to post-CT, MDD patients experience a large average decline
in depressive symptom scores, usually on the order of 1–3 standard deviations. For
example, mean scores on the BDI typically decrease from about 26–30 to 6–12,
mean scores on the HRSD typically decrease from about 18–25 to 5–11, and about
50–70% of patients who complete CT no longer meet criteria for MDD post-CT
(Craighead et al., 2007). A patient’s initial substantial reduction in symptoms (e.g.,
≥ 50% from pretreatment) is often called a response, whereas several weeks of reduced
symptoms mark remission. On the other hand, at least 10–20% of patients start but
do not complete acute phase CT (e.g., DeRubeis et al., 2005; Dimijian et al., 2006;
Jarrett et al., 2001), many of whom likely fare more poorly. Consequently, a somewhat
lower estimate that 50–60% of patients who begin CT will no longer meet criteria for
MDD post-CT may be more informative to patients and therapists deciding whether
or not to begin CT (e.g., DeRubeis et al., 2005; Dimidjian et al., 2006; Hollon
et al., 2005). It is also important to note that the degree and consistency of change in
symptoms varies among CT patients, with the majority experiencing residual (partial
remission; e.g., Fava et al., 2002) and/or fluctuating (unstable remission; e.g., Jarrett
et al., 2001; Jarrett & Thase, 2010) symptoms at the end of CT.
The rate of patients’ symptom decreases in CT is sometimes steady (i.e., linear) but
often nonlinear. In particular, the average symptom curve is roughly log-linear with
Mean depressive symptom scores among completers of acute-phase

cognitive therapy for major depressive disorder
50
45
Inventory for depressive symptomatology--self-report (30 items)
40
Beck depressive inventory (21 items)
35 Hamilton rating scale for depression (17 items)
Mean score
30
25
20
15
10
0
Intake W1 W2 W3 W4 W5 W6 W7 W8 W9 W10 W11 W12 Post
Assessment
Figure 48.2 Mean depressive symptom scores among patients (N = 489) completing acute
phase cognitive therapy for major depressive disorder in two clinical trials (Jarrett et al., 2001;
Jarrett & Thase, 2010). W = week in CT.
larger, quicker decreases in symptoms over the first few CT sessions, and smaller,
slower decreases in symptoms over the last half of CT (e.g., Lutz, Martinovich,
Howard, & Leon, 2002; Vittengl, Clark, Kraft, & Jarrett, 2005). Figure 48.2 shows
average symptom scores on the BDI and HRSD from among patients completing
acute phase CT with proficient therapists in two large trials (Jarrett et al., 2001; Jarrett
& Thase, 2010). The symptom curves in Figure 48.2 allow benchmarking individual
patients’ progress in a “dose–response” model of treatment. It is possible to calculate
whether patients are above, at, or significantly below average at a particular point in
treatment (Hansen, Lambert, & Forman, 2002; Lutz et al., 2002). Some therapists
may conclude that CT is not working well enough if a patient is not meeting or
exceeding expectation based on the average symptom curve or some percent reduction
in change compared to baseline.
However, average symptom curves are much smoother than most individual
patients’ changes. Recent research shows that only a minority of patients in acute
phase CT follow log-linear change patterns, whereas others follow linear (steady
decreases in symptoms throughout CT) and “one-step” (a quick, large drop in
symptoms) patterns, and all three change patterns are associated with roughly similar
acute phase outcomes (e.g., response rate and levels of psychosocial functioning;
Vittengl, Clark, Thase, & Jarrett, 2013). For example, clinicians should consider the
three patients in Figure 48.3 to have made equivalent progress during acute phase CT.
Similarly, symptom levels late in CT for MDD (Vittengl, Clark, Kraft, & Jarrett, 2005;
Vittengl et al., 2013) and other psychotherapies (Percevic, Lambert, & Kordy, 2006)
are not well predicted from symptom levels early in treatment. Consequently, some
patients may miss opportunities for substantial improvement if a 12- to 14-week acute
Individual patients showing three symptom change patterns

40
Beck depression inventory score

35 Linear (ID 217)
Log-linear (ID 2045)
30
One-step (ID 2130)
25
20
15
10
0
Intake W1 W2 W3 W4 W5 W6 W7 W8 W9 W10 W11 W12 Post
Assessment
Figure 48.3 Three patients with different change trajectories in acute phase cognitive therapy
(CT) in a clinical trial dataset (Jarrett & Thase, 2010). W = week in CT.
phase CT protocol is discontinued early due to less-than-average progress during the

first few weeks.
How Well Does Acute Phase Cognitive Therapy Work

Compared to Other Treatments?
Patients’ improvements in CT sometimes are “spontaneous” (i.e., not due to CT),

and randomized clinical trials are needed to establish CT’s efficacy compared to
nonactive (e.g., wait-list, placebo) and active (e.g., interpersonal psychotherapy,
behavior therapy, pharmacotherapy) controls during which patients may also improve
spontaneously. For treatments such as CT with multiple clinical trials completed,
treatments’ effects can be summarized quantitatively by averaging results from many
studies via meta-analysis. Here, the d effect size metric captures the difference in
outcome means (e.g., depressive symptom levels) between treatments divided by the
pooled or control group standard deviation. In the absence of more context-specific
interpretations, effect sizes of 0.2, 0.5, and 0.8 mark “small,” “moderate,” and “large”
effects (Cohen, 1988).
A frequently cited meta-analysis favored CT with effect sizes of 0.82 compared to
nonactive control (large effect), 0.38 compared to pharmacotherapy (small effect),
and 0.24 compared to a mix of other psychotherapies (small effect; Gloaguen, Cot-
traux, Cucherat, & Blackburn, 1998). Later researchers have concluded that these
estimates of CT’s efficacy may be somewhat inflated due to the inclusion of studies
with suboptimal comparison treatments, especially for CT compared to pharma-
cotherapy (e.g., low doses, early discontinuation) and other psychotherapies (e.g.,
some treatments not commonly recognized as adequate for depression; Butler et al.,
2006). More recent and more conservative meta-analytic estimates for CT include
effect sizes of 0.67 compared to nonactive control (moderate effect), 0.03 compared
to pharmacotherapy (trivial effect), and 0.03 compared to all other psychotherapies

(trivial effect; Cuijpers et al., 2012). Some of the most rigorous and conservative
data supporting acute phase CT come from randomized, pill placebo controlled
trials using blinded assessment (i.e., clinicians assessing depressive symptoms who do
not know whether patients are receiving pill placebo or CT). Four such trials have
been conducted to date (DeRubeis et al., 2005; Dimidjian et al., 2006; Elkin, Shea,
Watkins, & Imber, 1989; Jarrett et al., 1999) and their small-to-moderate average
effect size (0.41) indicates that CT reduced depressive symptoms modestly more
than pill placebo (Lynch, Laws, & McKenna, 2010). Comparisons of antidepressant
medications to pill placebo, albeit with larger samples, have yielded similar effect sizes
(e.g., Turner, Matthews, Linardatos, Tell, & Rosenthal, 2008).
Transformations of effect size d may clarify CT’s practical value. For example, U3 is
a transformation of d that gives the approximate proportion of treated patients who
are better off than the average patient in the comparison group (Cohen, 1988). Effect
sizes of 0.82 and 0.67 yield U3 estimates of 79% and 75%, respectively. Thus, roughly
three-quarters of patients treated with CT are better off than the average patient
receiving no treatment. The other quarter of CT patients have short-term outcomes
that are the same or worse than the average control patient in the meta-analyses
(Cuijpers et al., 2012; Gloaguen et al., 1998).
One limitation of U3 is the definition of “better off” used in its computation.
Because effect size d represents continuous symptom scores on measures like the
BDI and HRSD, individual patients who achieve scores only one point lower than
the average comparison patient are categorized as “better off.” But a single-point
advantage on the BDI or HRSD may be due to measurement error, and even if
real, not a worthwhile payoff for the time and money spent on CT. Consequently,
Jarrett and Vittengl (in press) proposed a correction to U3 based on Jacobson’s
reliable change index (Jacobson, Roberts, Berns, & McGlinchey, 1999; Jacobson &
Truax, 1991). Patients exceeding the reliable change threshold are significantly, not
just nominally, improved. The reliable change threshold is smaller for measures
that are more stable over time (higher retest reliability). Reliable change thresholds
(p < .05) for the BDI and HRSD are about 8–9 points (Grundy, Lambert, & Grundy,
1996; Seggar, Lambert, & Hansen, 2002). Assuming reliabilities of .80–.90, which
are representative of depressive symptom measures including the BDI and HRSD
(Grundy et al., 1996; Seggar et al., 2002), effect sizes of 0.82 and 0.67 yield reliable-
change-corrected U3 estimates of 34–48% and 28–42%, respectively, indicating that
roughly four out of 10 patients treated with CT are reliably improved compared to
the average patient receiving no treatment.
Although acute phase CT’s effects are well-replicated and robust, some meta-
analysts see indirect evidence of publication bias in the CT literature (Cuijpers, Smit,
Bohlmeijer, Hollon, & Andersson, 2010). A similar issue may characterize studies of
pharmacotherapy for depression, but for pharmacotherapy the evidence of publication
bias is much clearer because the U.S. Food and Drug Administration requires
registration of clinical trials whether they are published ultimately or not (Turner
et al., 2008). For CT, smaller studies with results less favorable to CT (lower effect
sizes) appear less often than expected in the published literature (Cuijpers et al., 2010).
The expectation of studies with lower effect sizes rests on statistical assumptions such
as a symmetrical distribution of effect sizes (e.g., Duval & Tweedie, 2000). Post hoc
statistical procedures have been applied to adjust CT’s mean effect size downward
by filling in assumed “missing” studies. Cuijpers et al. (2010) adjusted CT’s effect
size of 0.67 compared to nonactive control down to 0.42 assuming publication
bias.
However, other meta-analysts have cautioned against conclusions of publication
bias because many processes, including treatment effect moderators, instead may be
responsible for observed patterns in published studies’ results (e.g., Egger et al., 1997;
Petticrew, Gilbody, & Sheldon, 1999; Sterne, Egger, & Smith, 2001). For example,
suppose that CT is more effective when provided by expert versus novice therapists,
who from study to study produce effect sizes that vary normally (mean dexpert =
1.0, SD = 0.3; mean dnovice = 0.5, SD = 0.2). If these two populations of studies
are unknowingly pooled in a meta-analysis, their pooled effect size distribution is
positively skewed and might be viewed wrongly as missing low effect size studies due
to publication bias. For example, in a computer simulation of 100 “studies” drawn
randomly from the expert and novice therapist distributions (50 studies from each),
the mean effect size d was 0.78 (SD = 0.35), but the distribution was skewed to
the right (skewness = 0.58) and not normal (Shapiro-Wilk W = 0.96, p < .01). Of
course, studies are not missing and there is no bias because the pooled distribution of
effect sizes is naturally asymmetrical.
With only indirect evidence of publication bias for CT, we suggest that it is
more fruitful to search for moderators of CT’s effects so that we understand for
whom (e.g., MDD subtypes, severity, comorbidity) and under what conditions (e.g.,
protocols, therapist competence, delivery methods) CT works better. In sum, instead
of attempting to estimate the effect size of CT, the field may advance by knowing
the effect sizes of CT (cf. Aguinis, Pierce, Bosco, Dalton, & Dalton, 2011). Thus, we
consider evidence of CT moderators later in this chapter.
How Much Does Psychosocial Functioning Improve during

Acute Phase Cognitive Therapy?
Because MDD is defined by life interference in addition to depressive symptoms

(APA, 2000), the measurement of changes in psychosocial functioning is essential for
understanding CT’s efficacy. Psychosocial functioning reflects the level of success ver-
sus impairment in important domains including social relationships, work, and leisure.
Common measures include the Social Adjustment Scale–Self-Report (Weissman &
Bothwell, 1976), the Inventory of Interpersonal Problems (Horowitz, Rosenberg,
Baer, Ureño, & Villaseñor, 1988), the Dyadic Adjustment Scale (for patients who are
married or in similar relationships; Spanier, 1976), the Range of Impaired Functioning
Tool (Leon et al., 1999), and the Short-Form Health Survey (Ware & Sherbourne,
1992).
Compared to improvements in depressive symptoms, psychosocial functioning
tends to improve more slowly and less overall during acute phase treatment, although
researchers have paid less attention to psychosocial functioning and measured it less
often (Kennedy, Foy, Sherazi, McDonough, & McKeon, 2007; Papakostas et al.,
2004). For example, in four recent studies measuring both constructs, the mean
pre-/post-CT effect size for improvement in psychosocial functioning (1.0, range
0.8–1.2) was little more than half of the level of improvement in depressive symptoms
(1.8, range 1.3–2.4; Dunn et al., 2012; Hirschfeld et al., 2002; Matsunaga et al.,
2010; Vittengl, Clark, & Jarrett, 2004). Although changes in depressive symptoms
and psychosocial function correlate moderately highly (i.e., patients who improve in
one area tend to improve in the other), the extent and direction of causal relations
is unclear currently (Dunn et al., 2012; Hirschfeld et al., 2002; Vittengl et al.,
2004).
Residual and recurring psychosocial impairment after acute phase treatment are
important risk factors for MDD relapse and recurrence. Perhaps 60–65% of patients
show normative psychosocial functioning after completing acute phase CT, whereas
the remaining 35–40% show significantly impaired functioning (Vittengl et al., 2004).
Impairment in diverse areas of functioning, including interpersonal relationships,
work, and recreation, all predict recurrence of MDD (Rodriguez, Bruce, Pagano,
& Keller, 2005). Among currently euthymic patients with a history of MDD,
moderate psychosocial impairment (vs. very good functioning) may increase the risk
of recurrence by over 300% (Solomon et al., 2004). Further, after acute phase CT,
psychosocial functioning may deteriorate in the month before relapse and recurrence
events (Vittengl, Clark, & Jarrett, 2009a). Much like residual depressive symptoms
(Fava, Ruini, Rafanelli, & Grandi, 2002), we suggest that psychosocial impairment
is an emerging and important therapeutic target in CT for MDD and a potential
psychosocial marker of illness course.
Does Acute Phase Cognitive Therapy Prevent

Return of Depression?
In addition to reducing depressive symptoms and improving psychosocial functioning,

acute phase CT offers an important preventive effect relative to antidepressant medi-
cation. Meta-analytic estimates are that remitted patients who discontinue acute phase
treatment experience a relapse/recurrence rate of 39% for CT versus 61% for pharma-
cotherapy during an average follow-up period of 68 weeks (Vittengl, Clark, Dunn, &
Jarrett, 2007). This 22% advantage of CT versus pharmacotherapy is very similar to the
23% reduction in relapse/recurrence for acute phase CT plus pharmacotherapy dis-
continued versus pharmacotherapy alone discontinued. However, studies comparing
relapse/recurrence after acute phase CT versus other psychotherapies (interpersonal,
psychodynamic, BA) on average do not show significant differences (Vittengl et al.,
2007). Whether CT’s preventive effects are due to the reduction of processes that
produce depression or to the addition of compensatory strategies is unclear (Hol-
lon, Stewart, & Strunk, 2006). Nonetheless, many patients presenting with MDD
who remit on acute phase CT eventually will experience relapse/recurrence (29%
within 1 year, 54% within 2 years; Vittengl et al., 2007), highlighting the need
for continuation and maintenance phase treatments for patients with this recurrent
course.
For Which Patients Does Acute Phase Cognitive Therapy

Work Best?
Understanding for whom and under what conditions CT works best informs the
treatment’s theory and application. In considering demographic, clinical, psychoso-
cial, and other variables, it is useful to distinguish predictors from moderators of CT’s
efficacy (e.g., Kraemer, Wilson, Fairburn, & Agras, 2002). Predictors are baseline
variables that indicate which patients tend to fare better or worse, on average, regard-
less of comparison condition (e.g., CT versus pharmacotherapy or nontreatment).
Predictors are main effects in statistical models that do not provide the information
needed to recommend one treatment over another. Moderators, in contrast, are
baseline variables that predict outcomes differently in one condition versus another.
Moderators are interaction effects in statistical models that do provide information
needed to recommend (or to advise against) CT as a treatment for a particular patient.
Although the research literature is at times inconsistent, predictors of poor response
to acute phase CT often include markers of more severe illness and fewer personal
resources, whereas predictors of good outcomes include the opposite. For example,
in an open trial of acute phase CT, Jarrett et al. (2013) reported that patients who
showed more skill in CT, worked for pay, had a history of three or fewer depressive
episodes, had less pretreatment social impairment and evidenced a 50% or greater
reduction in pretreatment HRSD scores at midtreatment were more likely to respond.
On the other hand, chronic depression, more severe depressive symptoms, a longer
current MDE, younger age of onset, family history of mood disorder, personality
pathology, dysfunctional attitudes, being unmarried, older age, and lower intelligence
predicted poor CT outcomes in some studies (Driessen & Hollon, 2010; Hollon et al.,
2005). As predictors, these variables color expectations for a patient’s improvement
in CT (and often other treatments, too) but they do not inform preferences for CT
versus another treatment.
Different than predictors that give a general sense of a patient’s chances of success
in CT, moderators are variables that indicate differential response to acute phase
CT versus a comparison treatment. Moderators are prescriptive because they inform
choices among competing treatments (e.g., “Should this patient be treated with CT or
with medication?”). Unfortunately, replicated moderators are relatively uncommon
in the research literature. Consequently, it is also instructive to note commonly
assumed moderators that are not well supported empirically. As summarized in
recent reviews (Driessen & Hollon, 2010; Hollon et al., 2005), patients likely
to fare better in CT than in pharmacotherapy are often married (vs. unmarried).
Conversely, patients likely to fair more poorly in pharmacotherapy than in CT have
a history of failed trials of pharmacotherapy. On the other hand, CT’s benefits may
be tempered by the presence of personality disorders and high levels of dysfunctional
attitudes but pharmacotherapy’s effects are not. Conventional wisdom holds that
pharmacotherapy should be preferred over CT for depressions that some argue are
more likely “biological”—e.g., severe, melancholic, vegetative—but this pattern is
not strongly supported by the literature. The caveat is that CT may be more effective
for severely depressed patients when delivered by expert versus less experienced
cognitive therapists (Driessen & Hollon, 2010; Hollon et al., 2005).
How Well Does Continuation Phase Cognitive

Therapy Work?
Roughly half of patients with MDD who respond to acute phase CT (and perhaps
three-quarters of responders to acute phase pharmacotherapy) will experience relapse
or recurrence within 2 years without continuation treatment. After response to an
acute phase treatment, continuation phase CT can help prevent relapse and may
prevent recurrence and promote recovery in some adults with MDD (e.g., Vittengl
et al., 2007; Vittengl, Clark, & Jarrett, 2009b). The research literature addresses
several sequences of treatment modalities (e.g., CT vs. pharmacotherapy) across
phases (e.g., acute vs. continuation), and we summarize key examples in the rest of
this section.
Continuation Phase Cognitive Therapy Following Acute Phase

Cognitive Therapy
Jarrett developed continuation phase CT (Jarrett, 1989, 1992; Jarrett, Vittengl, &
Clark, 2008b) to reduce the rate of relapse in adults with MDD who responded
to acute phase CT. Initial cohort comparisons (Jarrett et al., 1998) suggested that
patients in continuation phase CT (n = 15) had a lower relapse rate (20%) over
8 months compared to a control cohort (n = 27; 45%). A second small sample
of patients with atypical MDD also suggested that continuation phase CT reduces
relapse rates (Jarrett et al., 2000).
Given these promising pilot results, a randomized clinical trial of continuation
phase CT versus an assessment-only control condition was conducted (Jarrett et al.,
2001). Outpatients (N = 156) with MDD were first treated with 20 sessions of acute
phase CT in a 12-week protocol. Acute phase CT responders (N = 84) were then
randomized to 10 sessions of continuation phase CT (n = 41) or to assessment-only
control (n = 43) conducted over the 8-month continuation phase. Continuation
phase CT reduced the 8-month relapse rate to 10% compared to 31% among patients
who received only assessment after acute phase CT. Among patients with “unstable”
remission in acute phase CT (one or more HRSD scores above 6 during the final
6 weeks), continuation phase CT reduced the 24-month relapse/recurrence rate
to 37% compared to 62% in assessment control. Moreover, continuation phase CT
increased the rate of recovery (84% of patients had no MDD and Psychiatric Status
Ratings [Keller, Shapiro, Lavori, & Wolfe, 1982] of 2 or less for 8 consecutive
months) compared to assessment control (62%) in the 24 months after the end
of the acute phase (Vittengl et al., 2009b). In particular, continuation phase CT
increased the recovery rate among younger patients with higher residual depressive
symptoms, unstable remission in acute phase CT, personality traits marking low
positive activation, more dysfunctional attitudes, and lower self-efficacy (Vittengl,
Clark, & Jarrett, 2010). Additionally, results are pending from a two-site randomized
clinical trial comparing continuation phase CT to clinical management plus fluoxetine
or matched pill placebo in CT responders at high risk for relapse and recurrence of
MDD (Jarrett & Thase, 2010).
Continuation Phase Cognitive Therapy Following

Acute Phase Pharmacotherapy
Paykel et al. (1999) showed that augmenting continuation phase pharmacotherapy
with continuation phase CT can reduce relapse rates. Patients (N = 158) on
antidepressant pharmacotherapy with partially-remitted MDD (i.e., they had residual
symptoms) were randomized to 20 weeks of continuation phase pharmacotherapy plus
clinical management without or with the addition of 16 CT sessions (plus two booster
sessions 6 and 14 weeks later). Study treatments were then withdrawn and patients
were assessed for an additional 48 weeks. Over 68 weeks, the cumulative relapse
rate was lower (29%) among patients who received CT compared to 47% among
patients who did not receive CT. A follow-up study suggested that a detectable
relapse-reducing benefit of CT persisted for 3.5 years after the end of CT (Paykel
et al., 2005).
Among patients with recurrent MDD, Fava and colleagues (Fava, Rafanelli, Grandi,
Conti, & Belluardo, 1998; Fava et al., 2004) also showed benefits of CT after response
to acute phase antidepressant pharmacotherapy. In the 20-week continuation phase,
patients (N = 40) were randomized to either clinical management or CT; pharma-
cotherapy was tapered and discontinued in both groups. The CT aimed to reduce
residual symptoms, improve lifestyles (e.g., time and stress management), and enhance
well-being. Patients were assessed regularly for several years after the end of contin-
uation treatment. At both 2 (25% vs. 80%) and 6 (40% vs. 90%) years, the CT group
experienced a lower relapse/recurrence rate than the clinical management group.
MBCT has also been tested after acute phase pharmacotherapy response. Teasdale
et al. (2000) randomized 145 recovered patients with recurrent MDD to treatment
as usual (TAU) or to TAU plus MBCT. For the majority of the sample (n = 105)
with a history of three or more prior depressive episodes, MBCT produced a lower
relapse/recurrence rate (40%) than did TAU alone (66%) through 60 weeks of study.
Ma and Teasdale (2004) replicated the protective effect of MBCT compared to TAU
for patients with at least three depressive episodes (36% vs. 78% relapse/recurrence
rate over 60 weeks), as well as the lack of a preventive MBCT effect for patients with
fewer episodes.
Replication trials conducted by other research groups have widened the evidence
base for MBCT. In a trial of remitted MDD patients (N = 60) with a history of three
or more prior depressive episodes, there was no significant difference in the 14-month
relapse rates of patients randomized either to TAU alone (34%) or TAU plus MBCT
(29%). However, MBCT significantly lengthened time-to-relapse compared to TAU
alone (medians of 204 vs. 69 days; Bondolfi et al., 2010). In a second trial of
MDD patients who achieved remission on acute phase pharmacotherapy (N = 103),
patients randomized to continue pharmacotherapy did not differ significantly in their
15-month relapse/recurrence rate (60%) compared to patients who received MBCT
combined with antidepressant medication tapering (47%). However, MBCT patients

showed significantly fewer residual symptoms, reduced psychiatric comorbidity, and
improved quality of life compared to pharmacotherapy continuation (Kuyken et al.,
2008). Finally, a randomized trial compared TAU to TAU plus MBCT for patients
with recurrent MDD either currently remitted or in a depressive episode (van Aalderen
et al., 2012). Patients receiving MBCT experienced greater decreases in depressive
symptoms than patients receiving only TAU (d = 0.5), and, interestingly, decreases in
depressive symptoms were similar whether patients were remitted or depressed when
starting the study. MBCT patients also had increased mindfulness skills (e.g., accep-
tance) and decreased negative cognition (e.g., rumination) compared to TAU alone.
Maintenance Phase Cognitive Therapy after Continuation Phase

Cognitive Therapy or Pharmacotherapy
The CT literature is also developing on preventing recurrence of MDD in the main-
tenance phase. Blackburn and Moore (1997) randomized outpatients (N = 75)
with recurrent depression to an acute treatment (16 weeks) followed by a continua-
tion/maintenance treatment (2 years) in one of three sequences: (a) pharmacotherapy
→ pharmacotherapy, (b) pharmacotherapy → CT, or (c) CT→CT. Depressive symp-
toms decreased significantly during all acute phase treatments, and relapse/recurrence
rates did not differ significantly among the three groups (26% pooled across mainte-
nance CT groups; 31% in maintenance pharmacotherapy). Similar to the Kuyken et al.
(2008) comparison of continuation phase MBCT to pharmacotherapy, the Blackburn
and Moore (1997) study suggests that continuation/maintenance phase CT may
yield preventive effects comparable to pharmacotherapy.
Bockting et al. (2005, 2009) randomized patients (N = 187) with recurrent
depression, currently in remission for 10–108 weeks and receiving TAU (chosen
naturalistically by patients; e.g., pharmacotherapy, psychotherapy, no treatment),
to maintenance TAU or to TAU plus 8 weekly sessions of group CT. The
relapse/recurrence rate among patients receiving CT (75%) was lower compared
to only TAU (95%) during a 5.5-year follow-up period. The same research group
is currently comparing three “maintenance” treatments (maintenance pharmacother-
apy; brief CT with pharmacotherapy tapering; brief CT combined with maintenance
pharmacotherapy) among patients remitted on pharmacotherapy (Bockting et al.,
2011). The results of this study can provide important guidance for patients and
clinicians.
Finally, a pilot study compared treatments of relapse/recurrence during mainte-
nance pharmacotherapy (Fava et al., 2002). Patients with recurrent MDD (N = 10)
who remitted but then relapsed/recurred on pharmacotherapy were randomly
assigned to a pharmacotherapy dose increase or to CT while taking the same dose of
pharmacotherapy. In both groups 80% (four of five) patients responded. All respon-
ders to increased pharmacotherapy subsequently relapsed/recurred (100%), whereas
only one responder to CT relapsed/recurred (25%), during a year of follow-up.
Replication is necessary.
For Which Patients Does Continuation Phase Cognitive

Therapy Work Best?
After remission of depression, consideration of predictors and moderators focuses

on preventing relapse and recurrence. Several intake, clinical, and remission-quality
variables predict relapse and recurrence of MDD. Earlier age of onset of MDD, a
history of more MDEs, comorbid dysthymia, family history of depression, negative
cognitive content, personality (e.g., high neuroticism), and poorer social support
are risk factors for relapse and recurrence (Burcusa & Iacono, 2007). Although
remission typically is coded categorically, patients who remit vary in important ways.
In particular, higher residual depressive symptoms in remission are a strong risk for
relapse and recurrence (Fava, Fabbri, & Sonino, 2002; Jarrett et al., 2008a) and relate
to negative cognitive content and psychosocial dysfunction (Fava, Ruini, & Belaise,
2007; Vittengl et al., 2010). In addition, some remissions are unstable because
patients experience moderate, transient elevations in depressive symptoms. Unstable
remission also predicts relapse and recurrence (Jarrett et al., 2001; Thase, Simons,
McGeary, & Cahalane, 1992).
Replicated moderators of continuation phase CT’s effects are scarce in the literature.
One moderator deserving attention is a patient’s number of MDEs. Continuation
phase CT (compared to no additional treatment) may prevent relapse/recurrence
only for patients with more prior MDEs, although the number varies from three
(Ma & Teasdale, 2004; Teasdale et al., 2000) to five (Bockting et al., 2005) among
studies. Vittengl et al. (2010) did not replicate number of MDEs as a moderator, but
did find that continuation phase CT worked better for patients with an earlier age
of MDD onset, which correlates with a history of more MDEs (Burcusa & Iacono,
2007). Other potential moderators include greater benefits of continuation CT (vs. no
additional treatment) for patients with higher residual symptoms (Jarrett et al., 2008a);
greater dysfunctional attitudes, lower self-efficacy, and personality traits suggesting
low positive activation (e.g., reduced energy, enthusiasm, gregariousness; Vittengl
et al., 2010); and patients who discontinue antidepressant medication (Bockting
et al., 2008) and do not experience stressful life events (Bockting et al., 2006).
Specifically for residual symptoms, Jarrett et al. (2008a) found preventive benefits for
continuation phase CT for patients with HRSD scores of 4 and over and BDI scores
of 5 and over, which is higher than average for patients completing acute phase CT
(Jarrett & Vittengl, in press).
How Can Clinicians Become Cognitive Therapists?
Through our experience in three randomized controlled trials (Jarrett et al., 1999;
Jarrett et al., 2001; Jarrett & Thase, 2010) spanning more than two decades, we
have observed the importance of ongoing consultation and/or supervision in order
to foster both competence and “best practices” within the cognitive model and
for therapists to maintain adherence. We hypothesize that if cognitive therapists
engage in weekly peer supervision, they will produce better and safer outcomes for
patients. An advantage of this routine consultation or supervision is that the cognitive

therapist is “embedded” in a supportive context before and as difficulties arise in the
clinical process. As patient difficulty, severity of symptoms, and number of comorbid
disorders increase, so does the importance of supervision. Such supervision groups
can be professionally enriching when therapists share information on new directions
the field is taking after attending sessions in continuing education and best and ethical
practices.
The most helpful supervision groups are likely to consist of professionals who have
already developed competence in CT through graduate level education consisting of
formal didactics as well as supervised clinical experience involving direct observation
of sessions in CT. In supervision, the therapists and “trainer” share randomly-selected
videotaped therapy sessions and rate these for adherence to and competence in the
cognitive model, using a tool such as the Cognitive Therapy Scale (CTS; Young &
Beck, 1980). In peer supervision, the therapists meet weekly and longitudinally, and
provide honest competence ratings and supportive feedback when a demographic
or life circumstance of the therapist may be influencing the process of therapy. We
maintain that clinical supervision is an ongoing process in the best practice of cognitive
therapy from which therapists never “graduate.”
We are excited about the opportunities that Web-based training offers for increasing
the number of experienced and competent cognitive therapists worldwide in order to
disseminate evidence-based practices. We note that a frequent criticism is that “CT is
not readily available” (i.e., the demand for services exceeds the supply of therapists).
We speculate that as training programs in mental health evolve and as professional
organizations learn to exploit existing “virtual” technologies for education, this
problem will decrease and perhaps disappear.
How Well Does Acute Phase Cognitive Therapy Work for

Older Adults?
The current population of older adults (≥ 60 years) has a lower lifetime prevalence
of MDD than the general population (e.g., 11% vs. 17% for U.S. adults; Kessler,
Berglund, et al., 2005). However, currently younger persons are likely to carry
their increased prevalence (and recurrence) of MDD forward as they age, rates of
depression are substantially higher in sub-populations of older adults (e.g., with
medical problems, living in extended-care facilities), and the older population is
growing substantially (e.g., Administration on Aging, 2011; Feliciano, Segal, & Vair,
2011). Consequently, the need for treatment of depression among older adults is also
large and expanding.
Although the literature is smaller in older than in younger adults, research supports
CT’s efficacy in depressed older adults (e.g., Feliciano et al., 2011; Kiosses, Leon,
& Areán, 2011; Mackin & Areán, 2005; Pinquart, Duberstein, & Lyness, 2007;
Wilson, Mottram, & Vassilas, 2008). Meta-analytic estimates include an effect size d
of 0.76 for patients with MDD (or 1.26 including both MDD and other unipolar
disorders; Pinquart et al., 2007) and a mean difference of about 10 HRSD points
(including both MDD and other unipolar disorders; Wilson et al., 2008) favoring
CT over no-treatment control groups at the end of acute phase treatment. Similar
to estimates above for younger adult populations, the geriatric effect size of 0.76
yields U3 estimates of 78%, and reliable-change U3 estimates of 32–45% (assuming
measurement reliabilities of .80–.90). That is, roughly 78% of older adults treated
with CT will be nominally better, and 40% reliably better, than the average untreated
control patient.
Data addressing CT’s effects on relapse/recurrence in older adults are limited.
In general, relapse/recurrence of depression may be more common in older than
younger adults (Areán & Ayalon, 2010), highlighting the need for research on
acute and continuation phase CT’s effects (e.g., effects relative to pharmacotherapy;
which patients benefit most). In Pinquart et al.’s (2007) meta-analysis, cognitive
and behavioral therapies’ mean effect size relative to control for unipolar depressive
disorders at an average of 7–8 months of follow-up (0.79) was about 75% as large as
at the immediately postacute phase (1.06), but direct estimates of relapse/recurrence
were not available. More direct relapse/recurrence estimates vary widely from study to
study (e.g., from 11% at 1 year to 100% at 3 months; Koder, Brodaty, & Anstey, 1996)
perhaps due to small samples and the operation of uncertain moderators (e.g., varying
patient populations, cross-sectional versus longitudinal assessment methods). Clearly,
understanding the extent and duration of CT’s benefits will become increasingly
important in an aging population with increased prevalence of depression among
currently-younger cohorts.
Parallel to goals held by researchers and clinicians focusing on other chronic illnesses
(e.g., diabetes, heart disease, cancer), we continue to assert that prevention and
cure (versus reduction of symptoms, and delay of relapse and recurrence) are the
ultimate goals for MDD. CT has pushed treatment of MDD forward and continues
to provoke new research questions and hypotheses; some have been mentioned and
reviewed in this chapter. It will be important to determine the extent to which
findings originating from largely white samples (such as those cited herein) will
generalize to nonwhite samples with differing ethnic and cultural backgrounds (cf.
U.S. Census Bureau, 2012). Other critical unanswered questions include: How
are new onsets of depression best prevented? How and for whom does CT work
best across acute, continuation, and maintenance phases? Which patients do not
need each or all of these phases? Which patients will fare better in CT versus
other available treatments during each phase and to what extent do preferences
affect outcomes? Which form of CT will work best for which patients during
each phase? What are the best platforms of delivery to improve course of illness?
How can emergent technologies be used to effect best practices and behavioral
change, not only in patients’ suffering, but also in the clinicians and health care
systems responsible for treating them? How can we reduce health disparities for
depressed patients and make CT more readily available to those who can benefit?
Which patients can safely stop treatment after acute or continuation phase treatment,
and which patients need continuation and/or maintenance CT to avoid relapse and
recurrence and to promote recovery? What sequences of treatments across phases (e.g.,
pharmacotherapy, CT) produce the best outcomes for the most patients (e.g., Fava
& Tomba, 2010)? Continued search for causal mechanisms and replicable sequences
of longitudinal change in symptoms and correlates (e.g., psychosocial functioning),
as well as enhanced connections with neuroscience and basic psychology (e.g., Beck,
2008), may offer advancements in technology and practice to bridge gaps in care
and reduce disparities. We look forward to research-driven advances in identifying
mechanisms of change, the dissemination and practice of CT, as well as new evidence-
based treatments focused on prevention and cure of mood disorders across the lifespan
in patients of all demographics.
References
Administration on Aging. (2011). A profile of older Americans: 2011. Washington, DC: U.S.
Department of Health and Human Services.
Aguinis, H., Pierce, C. A., Bosco, F. A., Dalton, D. R., & Dalton, C. M. (2011). Debunking
myths and urban legends about meta-analysis. Organizational Research Methods, 14,
306–331. doi:10.1177/1094428110375720
Andersson, G., & Cuijpers, P. (2009). Internet-based and other computerized psychologi-
cal treatments for adult depression: A meta-analysis. Cognitive Behaviour Therapy, 38,
196–205. doi:10.1080/16506070903318960
Andrade, L., Caraveo-Anduaga, J. J., Berglund, P., Bijl, R. V., De Graaf, R., Vollebergh, W.,
… Wittchen, H. (2003). The epidemiology of major depressive episodes: Results from
the International Consortium of Psychiatric Epidemiology (ICPE) Surveys. International
Journal of Methods in Psychiatric Research, 12, 3–21. doi:10.1002/mpr.138
Andrews, G., Cuijpers, P., Craske, M. G., McEvoy, P., & Titov, N. (2010). Computer therapy
for the anxiety and depressive disorders is effective, acceptable and practical health care: A
meta-analysis. PLoS ONE, 5. doi: 10.1371/journal.pone.0013196
Angst, F. F., Stassen, H. H., Clayton, P. J., & Angst, J. J. (2002). Mortality of patients
with mood disorders: Follow-up over 34–38 years. Journal of Affective Disorders, 68,
167–181. doi:10.1016/S0165-0327(01)00377-9
Areán, P. A., & Ayalon, L. (2010). Preventing depression relapse in older adults. In C. Richards
& M. G. Perri (Eds.), Relapse prevention for depression (pp. 157–176). Washington, DC:
American Psychological Association. doi:10.1037/12082-006
Beck, A. T. (2008). The evolution of the cognitive model of depression and its neurobio-
logical correlates. American Journal of Psychiatry, 165, 969–977. doi:10.1176/appi.ajp.
2008.08050721
Beck, A. T., Ward, C. H., Mendelson, M., Mock, J., & Erbaugh, J. (1961). An inventory for
measuring depression. Archives of General Psychiatry, 4, 561–571.
Berger, T., Hämmerli, K., Gubser, N., Andersson, G., & Caspar, F. (2011). Internet-based
treatment of depression: A randomized controlled trial comparing guided with unguided
self-help. Cognitive Behaviour Therapy, 40, 251–266. doi:10.1080/16506073.2011.
616531
Blackburn, I. M., & Moore, R. G. (1997). Controlled acute and follow-up trial of cognitive
therapy and pharmacotherapy in out-patients with recurrent depression. British Journal of
Blair-West, G. W., & Mellsop, G. W. (2001). Major depression: Does a gender-based down-
rating of suicide risk challenge its diagnostic validity? Australian and New Zealand Journal
of Psychiatry, 35, 322–328. doi:10.1046/j.1440-1614.2001.00895.x
Bockting, C. L., Kok, G., van der Kamp, L., Smit, F., van Valen, E., Schoevers, R., …
Beck, A. (2011). Disrupting the rhythm of depression using mobile cognitive therapy for
recurrent depression: Randomized controlled trial design and protocol. BMC Psychiatry,
11. doi:10.1186/1471-244X-11-12
Bockting, C. L., Schene, A. H., Spinhoven, P., Koeter, M. J., Wouters, L. F., Huyser, J.,
& Kamphuis, J. H. (2005). Preventing relapse/recurrence in recurrent depression with
cognitive therapy: A randomized controlled trial. Journal of Consulting and Clinical
Psychology, 73, 647–657. doi:10.1037/0022-006X.73.4.647
Bockting, C. L., Spinhoven, P., Koeter, M., Wouters, L., Visser, I., & Schene, A. (2006).
Differential predictors of response to preventive cognitive therapy in recurrent depression:
A 2-year prospective study. Psychotherapy and Psychosomatics, 75, 229–236.
Bockting, C. L., Spinhoven, P., Wouters, L. F., Koeter, M. J., & Schene, A. H. (2009). Long-
term effects of preventive cognitive therapy in recurrent depression: A 5.5-year follow-up
study. Journal of Clinical Psychiatry, 70, 1621–1628. doi:10.4088/JCP.08m04784blu
Bockting, C. L., ten Doesschate, M. C., Spijker, J., Spinhoven, P., Koeter, M. J., & Schene, A.
H. (2008). Continuation and maintenance use of antidepressants in recurrent depression.
Psychotherapy and Psychosomatics, 77 , 17–26. doi:10.1159/000110056
Bolton, J., Pagura, J., Enns, M., Grant, B., & Sareen, J. (2010). A population-based longitudinal
study of risk factors for suicide attempts in major depressive disorder. Journal of Psychiatric
Research, 44, 817–826.
Bondolfi, G., Jermann, F., Van der Linden, M., Gex-Fabry, M., Bizzini, L., Rouget, B., …
Bertschy, G. (2010). Depression relapse prophylaxis with mindfulness-based cognitive
therapy: Replication and extension in the Swiss health care system. Journal of Affective
Disorders, 122, 224–231. doi:10.1016/j.jad.2009.07.007
Brådvik, L., Mattisson, C., Bogren, M., & Nettelbladt, P. (2008). Long-term suicide risk of
depression in the Lundby cohort 1947–1997: Severity and gender. Acta Psychiatrica
Scandinavica, 117 , 185–191.
Burcusa, S. L., & Iacono, W. G. (2007). Risk for recurrence in depression. Clinical Psychology
Review, 27 , 959–985. doi:10.1016/j.cpr.2007.02.005
Burns, D. D. (1980). Feeling good: The new mood therapy. New York, NY: William Morrow.
Burns, D. D., & Nolen-Hoeksema, S. (1991). Coping styles, homework compliance, and
the effectiveness of cognitive-behavioral therapy. Journal of Consulting and Clinical
Psychology, 59, 305–311. doi:10.1037/0022-006X.59.2.305
17–31.
Byers, A. L., Yaffe, K., Covinsky, K. E., Friedman, M. B., & Bruce, M. L. (2010). High
occurrence of mood and anxiety disorders among older adults. Archives of General
Psychiatry, 67 , 489–496. doi:10.1001/archgenpsychiatry.2010.35
Cassano, P., & Fava, M. (2002). Depression and public health: An overview. Journal of
Psychosomatic Research, 53, 849–857. doi:10.1016/S0022-3999(02)00304-5
Chen, Y., & Dilsaver, S. C. (1996). Lifetime rates of suicide attempts among subjects with
bipolar and unipolar disorders relative to subjects with other axis I disorders. Biological
Psychiatry, 39, 896–899. doi:10.1016/0006-3223(95)00295-2
Cohen, J. (1988). Statistical power analysis for the behavioral sciences (2nd ed.). Hillsdale, NJ:
Erlbaum.
Craighead, W. E., Sheets, E. S., Brosse, A. L., & Ilardi, S. S. (2007). Psychosocial treatments
for major depressive disorder. In P. E. Nathan & J. M. Gorman (Eds.), A guide to
treatments that work (3rd ed., pp. 289–307). New York, NY: Oxford University Press.
Cuijpers, P., Smit, F., Bohlmeijer, E., Hollon, S. D., & Andersson, G. (2010). Efficacy of
cognitive-behavioural therapy and other psychological treatments for adult depression:
Meta-analytic study of publication bias. British Journal of Psychiatry, 196, 173–178. doi:
10.1192/bjp.bp.109.066001
Cuijpers, P., van Straten, A., Driessen, E., van Oppen, P., Bockting, C. L., & Andersson,
G. (2012). Depression and dysthymic disorders. In M. Hersen & P. Sturmey (Eds.),
Handbook of evidence-based practice in clinical psychology. Vol. II: Adult disorders (pp.
243–284). Hoboken, NJ: John Wiley & Sons, Inc.
de Graaf, L. E., Gerhards, S. H., Arntz, A. A., Riper, H. H., Metsemakers, J. M., Evers,
S. A., … Huibers, M. H. (2011). One-year follow-up results of unsupported online
computerized cognitive behavioural therapy for depression in primary care: A ran-
domized trial. Journal of Behavior Therapy and Experimental Psychiatry, 42, 89–95.
doi:10.1016/j.jbtep.2010.07.003
de Graaf, L. E., Hollon, S. D., & Huibers, M. H. (2010). Predicting outcome in computerized
cognitive behavioral therapy for depression in primary care: A randomized trial. Journal
of Consulting and Clinical Psychology, 78, 184–189. doi:10.1037/a0018324
DeRubeis, R. J., Hollon, S. D., Amsterdam, J. D., Shelton, R. C., Young, P. R.,
Salomon, R. M., … Gallop, R. (2005). Cognitive therapy vs medications in the treat-
ment of moderate to severe depression. Archives of General Psychiatry, 62, 409–416.
doi:10.1001/archpsyc.62.4.409
Dimidjian, S., Hollon, S. D., Dobson, K. S., Schmaling, K. B., Kohlenberg, R. J., Addis,
M. E., … Jacobson, N. S. (2006). Randomized trial of behavioral activation, cognitive
therapy, and antidepressant medication in the acute treatment of adults with major depres-
sion. Journal of Consulting and Clinical Psychology, 74, 658–670. doi:10.1037/0022-
006X.74.4.658
Driessen, E., & Hollon, S. D. (2010). Cognitive behavioral therapy for mood disorders:
Efficacy, moderators and mediators. Psychiatric Clinics of North America, 33, 537–555.
doi:10.1016/j.psc.2010.04.005
Dunn, T. W., Vittengl, J. R., Clark, L. A., Carmody, T., Thase, M. E., & Jarrett, R. B.
(2012). Change in psychosocial functioning and depressive symptoms during acute-
phase cognitive therapy for depression. Psychological Medicine, 42, 317–326. doi:
10.1017/S0033291711001279
Duval, S., & Tweedie, R. (2000). Trim and fill: A simple funnel-plot-based method of testing
and adjusting for publication bias in meta-analysis. Biometrics, 56, 455–463.
Eaton, W. W., Shao, H., Nestadt, G., Lee, B., Bienvenu, O., & Zandi, P. (2008). Population-
based study of first onset and chronicity in major depressive disorder. Archives of General
Egger, M., Davey Smith, G., Schneider, M., & Minder, C. (1997). Bias in meta-analysis
detected by a simple, graphical test. BMJ (Clinical Research Ed.), 315, 629–634.
Elkin, I., Shea, M., Watkins, J. T., & Imber, S. D. (1989). National Institute of Mental
Health Treatment of Depression Collaborative Research Program: General effectiveness
of treatments. Archives of General Psychiatry, 46, 971–982.
Fava, G. A., Fabbri, S., & Sonino, N. (2002). Residual symptoms in depression: An emerging
therapeutic target. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 26,
1019–1027. doi:10.1016/S0278-5846(02)00226-9
Fava, G. A., Rafanelli, C., Grandi, S., Conti, S., & Belluardo, P. (1998). Prevention of recurrent
depression with cognitive behavioral therapy: Preliminary findings. Archives of General
Fava, G. A., Ruini, C., & Belaise, C. (2007). The concept of recovery in major depression.
Fava, G. A., Ruini, C., Rafanelli, C., Finos, L., Conti, S., & Grandi, S. (2004). Six-year
outcome of cognitive behavior therapy for prevention of recurrent depression. American
Fava, G. A., Ruini, C., Rafanelli, C., & Grandi, S. (2002). Cognitive behavior approach to
loss of clinical effect during long-term antidepressant treatment: A pilot study. American
Fava, G. A., & Tomba, E. (2010). New modalities of assessment and treatment plan-
ning in depression: The sequential approach. CNS Drugs, 24, 453–465. doi:
10.2165/11531580-000000000-00000
Feliciano, L., Segal, D. L., & Vair, C. L. (2011). Major depressive disorder. In K. Sorocco, S.
Lauderdale, K. Sorocco, & S. Lauderdale (Eds.), Cognitive behavior therapy with older
adults: Innovations across care settings (pp. 31–64). New York, NY: Springer.
Fledderus, M. M., Bohlmeijer, E. T., Pieterse, M. E., & Schreurs, K. G. (2012). Acceptance
and commitment therapy as guided self-help for psychological distress and positive mental
health: A randomized controlled trial. Psychological Medicine, 42, 485–495.
Forman, E. M., Herbert, J. D., Moitra, E., Yeomans, P. D., & Geller, P. A. (2007). A
randomized controlled effectiveness trial of acceptance and commitment therapy and
cognitive therapy for anxiety and depression. Behavior Modification, 31, 772–799.
Frank, E., Prien, R. F., Jarrett, R. B., & Keller, M. B. (1991). Conceptualization and rationale
for consensus definitions of terms in major depressive disorder: Remission, recovery,
relapse, and recurrence. Archives of General Psychiatry, 48, 851–855.
Gloaguen, V., Cottraux, J., Cucherat, M., & Blackburn, I. (1998). A meta-analysis of the
effects of cognitive therapy in depressed patients. Journal of Affective Disorders, 49,
59–72. doi:10.1016/S0165-0327(97)00199-7
Greenberger, D., & Padesky, C. A. (1995). Mind over mood: A cognitive therapy treatment
manual for clients. New York, NY: Guilford Press.
Grundy, C. T., Lambert, M. J., & Grundy, E. M. (1996). Assessing clinical significance:
Application to the Hamilton Rating Scale for Depression. Journal of Mental Health, 5,
25–33. doi:10.1080/09638239650037162
Hamilton, M. (1960). A rating scale for depression. Journal of Neurology, Neurosurgery, and
Hansen, N. B., Lambert, M. J., & Forman, E. M. (2002). The psychotherapy dose-response
effect and its implications for treatment delivery services. Clinical Psychology: Science and
Practice, 9, 329–343. doi:10.1093/clipsy/9.3.329
Hardeveld, F., Spijker, J., De Graaf, R., Nolen, W., & Beekman, A. (2010). Prevalence
and predictors of recurrence of major depressive disorder in the adult population. Acta
Psychiatrica Scandinavica, 122, 184–191.
Hasin, D. S., Goodwin, R. D., Stinson, F. S., & Grant, B. F. (2005). Epidemiology of
major depressive disorder: Results from the National Epidemiologic Survey on Alco-
holism and Related Conditions. Archives of General Psychiatry, 62, 1097–1106. doi:
10.1001/archpsyc.62.10.1097
An experiential approach to behavior change. New York, NY: Guilford Press.
Hirschfeld, R., Dunner, D., Keitner, G., Klein, D., Koran, L., Kornstein, S., … Keller, M.
(2002). Does psychosocial functioning improve independent of depressive symptoms? A
comparison of nefazodone, psychotherapy, and their combination. Biological Psychiatry,

51, 123–133.
Hofmann, S. G., Sawyer, A. T., & Fang, A. (2010). The empirical status of the “new wave”
of cognitive behavioral therapy. Psychiatric Clinics of North America, 33, 701–710. doi:
10.1016/j.psc.2010.04.006
Hollon, S. D., Jarrett, R. B., Nierenberg, A. A., Thase, M. E., Trivedi, M., & Rush, A.
(2005). Psychotherapy and medication in the treatment of adult and geriatric depression:
Which monotherapy or combined treatment? Journal of Clinical Psychiatry, 66, 455–468.
doi:10.4088/JCP.v66n0408
Hollon, S. D., Stewart, M. O., & Strunk, D. (2006). Enduring effects for cognitive behavior
therapy in the treatment of depression and anxiety. Annual Review of Psychology, 57 ,
285–315. doi:10.1146/annurev.psych.57.102904.190044
Horowitz, L. M., Rosenberg, S. E., Baer, B. A., Ureño, G., & Villaseñor, V. S. (1988). Inventory
of interpersonal problems: Psychometric properties and clinical applications. Journal of
Jacobson, N. S., Roberts, L. J., Berns, S. B., & McGlinchey, J. B. (1999). Methods for defining
and determining the clinical significance of treatment effects: Description, application,
and alternatives. Journal of Consulting and Clinical Psychology, 67 , 300–307.
Jarrett, R. B. (1989, 1992). Cognitive therapy for recurrent unipolar major depressive disorder:
The continuation/maintenance phase. Unpublished treatment manuals.
Jarrett, R. B., Basco, M. R., Risser, R., Ramanan, J., Marwill, M., Kraft, D., & Rush, A.
(1998). Is there a role for continuation phase cognitive therapy for depressed outpatients?
Journal of Consulting and Clinical Psychology, 66, 1036–1040. doi:10.1037/0022-
006X.66.6.1036
Jarrett, R. B., Kraft, D., Doyle, J., Foster, B. M., Eaves, G., & Silver, P. C. (2001). Preventing
recurrent depression using cognitive therapy with and without a continuation phase.
Archives of General Psychiatry, 58, 381–388. doi:10.1001/archpsyc.58.4.381
Jarrett, R. B., Kraft, D., Schaffer, M., Witt-Browder, A., Risser, R., Atkins, D. H., & Doyle,
J. (2000). Reducing relapse in depressed outpatients with atypical features: A pilot study.
Psychotherapy and Psychosomatics, 69, 232–239. doi:10.1159/000012401
Jarrett, R. B., Minhajuddin, A., Kangas, J., Friedman, E., Callan, J., & Thase, M. (2013).
Acute phase cognitive therapy for recurrent major depressive disorder: Who drops out
and how much do patient skills influence response? Behaviour Research and Therapy, 51,
221–230.
Jarrett, R. B., Schaffer, M., McIntire, D., Witt-Browder, A., Kraft, D., & Risser, R. C.
(1999). Treatment of atypical depression with cognitive therapy or phenelzine: A
double-blind, placebo-controlled trial. Archives of General Psychiatry, 56, 431–437.
doi:10.1001/archpsyc.56.5.431
Jarrett, R. B., & Thase, M. E. (2010). Comparative efficacy and durability of continuation
phase cognitive therapy for preventing recurrent depression: Design of a double-blinded
fluoxetine- and pill placebo-controlled randomized trial with 2-year follow-up. Contem-
porary Clinical Trials, 31, 355–377.
Jarrett, R. B., & Vittengl, J. R. (in press). Efficacy of cognitive-behavioral therapy for
depression. In P. L. Fisher & A. Wells (Eds.), Innovations in treating depres-
sion: Metacognition, acceptance, behavioural activation and mindfulness. Hoboken, NJ:
John Wiley & Sons, Inc.
Jarrett, R. B., Vittengl, J. R., & Clark, L. (2008a). How much cognitive therapy, for which
patients, will prevent depressive relapse? Journal of Affective Disorders, 111, 185–192.
doi:10.1016/j.jad.2008.02.011
Jarrett, R. B., Vittengl, J. R., & Clark, L. (2008b). Preventing recurrent depression. In
M. A. Whisman (Ed.), Adapting cognitive therapy for depression: Managing complexity and
comorbidity (pp. 132–156). New York, NY: Guilford Press.
Kazdin, A. E., & Blase, S. L. (2011). Rebooting psychotherapy research and practice to
reduce the burden of mental illness. Perspectives on Psychological Science, 6, 21–37. doi:
10.1177/1745691610393527
Keller, M. B., Shapiro, R. W., Lavori, P. W., & Wolfe, N. (1982). Recovery in major depressive
disorder: Analysis with the life table and regression models. Archives of General Psychiatry,
39, 905–910.
Kennedy, N., Foy, K., Sherazi, R., McDonough, M., & McKeon, P. (2007). Long-term
social functioning after depression treated by psychiatrists: A review. Bipolar Disorders, 9,
25–37. doi:10.1111/j.1399-5618.2007.00326.x
Kessler, R. C., Berglund, P., Demler, O., Jin, R., Koretz, D., Merikangas, K. R., … Wang,
P. S. (2003). The epidemiology of major depressive disorder: Results from the National
Comorbidity Survey Replication (NCS-R). Journal of the American Medical Association,
289, 3095–3105. doi:10.1001/jama.289.23.3095
doi:10.1001/archpsyc.62.6.593
Kessler, R. C., Chiu, W., Demler, O., & Walters, E. E. (2005). Prevalence, severity, and comor-
bidity of 12-month DSM-IV disorders in the National Comorbidity Survey Replication.
Archives of General Psychiatry, 62, 617–627. doi:10.1001/archpsyc.62.6.617
Kessler, R. C., Akiskal, H. S., Ames, M., Birnbaum, H., Greenberg, P., Hirschfeld, R. A., &
… Wang, P. S. (2006). Prevalence and effects of mood disorders on work performance in
a nationally representative sample of U.S. workers. The American Journal Of Psychiatry,
163, 1561–1568. doi:10.1176/appi.ajp.163.9.1561
Kiosses, D. N., Leon, A. C., & Areán, P. A. (2011). Psychosocial interventions for late-life
major depression: Evidence-based treatments, predictors of treatment outcomes, and
moderators of treatment effects. Psychiatric Clinics of North America, 34, 377–401. doi:
10.1016/j.psc.2011.03.001
Klein, D. N., Santiago, N. J., Vivian, D., Blalock, J. A., Kocsis, J. H., Markowitz, J. C., … Keller,
M. B. (2004). Cognitive-behavioral analysis system of psychotherapy as a maintenance
treatment for chronic depression. Journal of Consulting and Clinical Psychology, 72,
681–688. doi:10.1037/0022-006X.72.4.681
Koder, D., Brodaty, H., & Anstey, K. J. (1996). Cognitive therapy for depression in the elderly.
International Journal of Geriatric Psychiatry, 11, 97–107. doi: 10.1002/(SICI)1099-
1166(199602)11:2<97::AID-GPS310>3.0.CO;2-W
Kraemer, H., Wilson, G., Fairburn, C. G., & Agras, W. (2002). Mediators and moderators of
treatment effects in randomized clinical trials. Archives of General Psychiatry, 59, 877–883.
doi:10.1001/archpsyc.59.10.877
Kuyken, W., Byford, S., Taylor, R. S., Watkins, E., Holden, E., White, K., … Teasdale, J. D.
(2008). Mindfulness-based cognitive therapy to prevent relapse in recurrent depression.
Journal of Consulting and Clinical Psychology, 76, 966–978. doi:10.1037/a0013786
Leon, A. C., Solomon, D. A., Mueller, T. I., Turvey, C. L., Endicott, J. J., & Keller,
M. B. (1999). The Range of Impaired Functioning Tool (LIFE-RIFT): A brief mea-
sure of functional impairment. Psychological Medicine, 29, 869–878. doi:10.1017/
S0033291799008570
Levin, W. W., Campbell, D. R., McGovern, K. B., Gau, J. M., Kosty, D. B., Seeley, J. R., &
Lewinsohn, P. M. (2011). A computer-assisted depression intervention in primary care.
Psychological Medicine, 41, 1373–1383. doi:10.1017/S0033291710001935
Lewinsohn, P. M., Antonuccio, D., Stemmetz. J., & Teri, L. (1984). The coping with
depression course: A psychoeducational intervention for unipolar depression. Eugene, OR:
Castalia.
Lutz, W., Martinovich, Z., Howard, K. I., & Leon, S. C. (2002). Outcomes manage-
ment, expected treatment response, and severity-adjusted provider profiling in outpatient
psychotherapy. Journal of Clinical Psychology, 58, 1291–1304. doi:10.1002/jclp.10070
Lynch, D. D., Laws, K. R., & McKenna, P. J. (2010). Cognitive behavioural therapy for major
psychiatric disorder: Does it really work? A meta-analytical review of well-controlled trials.
Psychological Medicine, 40, 9–24. doi:10.1017/S003329170900590X
Ma, S., & Teasdale, J. D. (2004). Mindfulness-based cognitive therapy for depression: Repli-
cation and exploration of differential relapse prevention effects. Journal of Consulting and
Mackin, R., & Areán, P. A. (2005). Evidence-based psychotherapeutic interventions for
geriatric depression. Psychiatric Clinics of North America, 28, 805–820. doi:10.1016/
j.psc.2005.09.009
Martell, C. R., Addis, M. E., & Jacobson, N. S. (2001). Depression in context: Strategies for
guided action. New York, NY: Norton.
Matsunaga, M., Okamoto, Y., Suzuki, S., Kinoshita, A., Yoshimura, S., Yoshino, A., …
Yamawaki, S. (2010). Psychosocial functioning in patients with treatment-resistant depres-
sion after group cognitive behavioral therapy. BMC Psychiatry, 10. doi:10.1186/1471-
244X-10-22
McCullough, J. P. (2003). Treatment for chronic depression: Cognitive behavioral analysis
system of psychotherapy (CBASP). Journal of Psychotherapy Integration, 13, 241–263.
doi:10.1037/1053-0479.13.3-4.241
Monroe, S. M., & Harkness, K. L. (2011). Recurrence in major depression: A conceptual
analysis. Psychological Review, 118, 655–674. doi:10.1037/a0025190
Mueller, T. I., Leon, A. C., Keller, M. B., Solomon, D. A., Endicott, J., Coryell, W., … Maser,
J. D. (1999). Recurrence after recovery from major depressive disorder during 15 years
of observational follow-up. American Journal of Psychiatry, 156, 1000–1006.
Öst, L.-G. (2008). Efficacy of the third wave of behavioral therapies: A systematic review
and meta-analysis. Behaviour Research and Therapy, 46, 296–321. doi:10.1016/
j.brat.2007.12.005
Papakostas, G. I., Petersen, T., Mahal, Y., Mischoulon, D., Nierenberg, A. A., & Fava, M.
(2004). Quality of life assessments in major depressive disorder: A review of the literature.
General Hospital Psychiatry, 26, 13–17. doi:10.1016/j.genhosppsych.2003.07.004
Patten, S. B. (2009). Accumulation of major depressive episodes over time in a prospective
study indicates that retrospectively assessed lifetime prevalence estimates are too low.
BMC Psychiatry, 9, 19. doi:10.1186/1471-244X-9-19
Paykel, E. S., Scott, J. J., Cornwall, P. L., Abbott, R. R., Crane, C. C., Pope, M. M.,
& Johnson, A. L. (2005). Duration of relapse prevention after cognitive therapy in
residual depression: Follow-up of controlled trial. Psychological Medicine, 35, 59–68.
doi:10.1017/S003329170400282X
Paykel, E. S., Scott, J., Teasdale, J. D., Johnson, A. L., Garland, A., Moore, R., … Pope, M.
(1999). Prevention of relapse in residual depression by cognitive therapy: A controlled
trial. Archives of General Psychiatry, 56, 829–835. doi:10.1001/archpsyc.56.9.829
Percevic, R., Lambert, M. J., & Kordy, H. (2006). What is the predictive value of responses to
psychotherapy for its future course? Empirical explorations and consequences for outcome
monitoring. Psychotherapy Research, 16, 364–373. doi:10.1080/10503300500485524
Petticrew, M., Gilbody, S., & Sheldon, T. (1999). Relation between hostility and coronary heart
disease: Evidence does not support link. BMJ (Clinical Research Ed.), 319, 917–918.
Pinquart, M. M., Duberstein, P. R., & Lyness, J. M. (2007). Effects of psychotherapy and
other behavioral interventions on clinically depressed older adults: A meta-analysis. Aging
& Mental Health, 11, 645–657. doi:10.1080/13607860701529635
Rodriguez, B. F., Bruce, S. E., Pagano, M. E., & Keller, M. B. (2005). Relationships among
psychosocial functioning, diagnostic comorbidity, and the recurrence of generalized
anxiety disorder, panic disorder, and major depression. Journal of Anxiety Disorders, 19,
752–766. doi:10.1016/j.janxdis.2004.10.002
Rush, A., Kraemer, H. C., Sackeim, H. A., Fava, M., Trivedi, M. H., Frank, E., … Schatzberg,
A. F. (2006). Report by the ACNP Task Force on response and remission in major depres-
sive disorder. Neuropsychopharmacology, 31, 1841–1853. doi:10.1038/sj.npp.1301131
Satyanarayana, S., Enns, M. W., Cox, B. J., & Sareen, J. (2009). Prevalence and correlates
of chronic depression in the Canadian Community Health Survey: Mental health and
well-being. Canadian Journal of Psychiatry/La Revue Canadienne de Psychiatrie, 54,
389–398.
Scoggin, F., Jamison, C., & Gochneaur, K. (1989). Comparative efficacy of cognitive and
behavioral bibliotherapy for mildly and moderately depressed older adults. Journal of
Consulting and Clinical Psychology, 57 , 403–407. doi:10.1037/0022-006X.57.3.403
Scott, J., Williams, J. G., Brittleband, A., & Ferrier, I. (1995). The relationship between premor-
bid neuroticism, cognitive dysfunction and persistence of depression: A 1-year follow-up.
Journal of Affective Disorders, 33, 167–172. doi:10.1016/0165-0327(94)00085-N
Seggar, L. B., Lambert, M. J., & Hansen, N. B. (2002). Assessing clinical significance: Appli-
cation to the Beck Depression Inventory. Behavior Therapy, 33, 253–269. doi:10.1016/
S0005-7894(02)80028-4
Skodol, A. E., Grilo, C. M., Keyes, K. M., Geier, T., Grant, B. F., & Hasin, D. S. (2011).
Relationship of personality disorders to the course of major depressive disorder in a nation-
ally representative sample. American Journal of Psychiatry, 168, 257–264. doi:10.1176/
appi.ajp.2010.10050695
Solomon, D. A., Keller, M. B., Leon, A. C., Mueller, T. I., Lavori, P. W., Shea, M., …
Endicott, J. (2000). Multiple recurrences of major depressive disorder. American Journal
of Psychiatry, 157 , 229–233. doi:10.1176/appi.ajp.157.2.229
Solomon, D. A., Leon, A. C., Endicott, J., Mueller, T. I., Coryell, W., Shea, M., & Keller, M.
B. (2004). Psychosocial impairment and recurrence of major depression. Comprehensive
Psychiatry, 45, 423–430. doi:10.1016/j.comppsych.2004.07.002
Spanier, G. B. (1976). Measuring dyadic adjustment: New scales for assessing the qual-
ity of marriage and similar dyads. Journal of Marriage & the Family, 38, 15–28.
doi:10.2307/350547
Spijker, J., De Graaf, R., Bijl, R. V., Beekman, A. F., Ormel, J., & Nolen, W. A. (2002).
Duration of major depressive episodes in the general population: Results from the
Netherlands Mental Health Survey and Incidence Study (NEMESIS). British Journal of
Sterne, J., Egger, M., & Smith, G. (2001). Systematic reviews in health care: Investigating and
dealing with publication and other biases in meta-analysis. BMJ (Clinical Research Ed.),
323, 101–105.
Teasdale, J. D., Segal, Z. V., Williams, J. G., Ridgeway, V. A., Soulsby, J. M., & Lau, M. A.
(2000). Prevention of relapse/recurrence in major depression by mindfulness-based cog-
nitive therapy. Journal of Consulting and Clinical Psychology, 68, 615–623. doi:10.1037/
0022-006X.68.4.615
Thase, M. E., Simons, A. D., McGeary, J., & Cahalane, J. F. (1992). Relapse after cognitive
behavior therapy of depression: Potential implications for longer courses of treatment.
Thomson, W. (2011). Lifting the shroud on depression and premature mortality: A 49-
year follow-up study. Journal of Affective Disorders, 130, 60–65. doi:10.1016/j.jad.
2010.09.028
Turner, E., Matthews, A., Linardatos, E., Tell, R., & Rosenthal, R. (2008). Selective publication
of antidepressant trials and its influence on apparent efficacy. New England Journal of
Medicine, 358, 252–260.
U.S. Census Bureau. (2012). Most children younger than age 1 are minorities, Census
Bureau reports. Retrieved from http://www.census.gov/newsroom/releases/archives/
population/cb12-90.html
van Aalderen, J., Donders, A., Giommi, F., Spinhoven, P., Barendregt, H., &
Speckens, A. A. (2012). The efficacy of mindfulness-based cognitive therapy in recur-
rent depressed patients with and without a current depressive episode: A randomized
controlled trial. Psychological Medicine, 42, 989–1001.
Vittengl, J. R., Clark, L. A., Dunn, T. W., & Jarrett, R. B. (2007). Reducing relapse and recur-
rence in unipolar depression: A comparative meta-analysis of cognitive-behavioral therapy’s
effects. Journal of Consulting and Clinical Psychology, 75, 475–488. doi:10.1037/0022-
006X.75.3.475
Vittengl, J. R., Clark, L. A., & Jarrett, R. B. (2004). Improvement in social-interpersonal
functioning after cognitive therapy for recurrent depression. Psychological Medicine, 34,
643–658. doi:10.1017/S0033291703001478
Vittengl, J. R., Clark, L. A., & Jarrett, R. B. (2009a). Deterioration in psychosocial functioning
predicts relapse/recurrence after cognitive therapy for depression. Journal of Affective
Vittengl, J. R., Clark, L. A., & Jarrett, R. B. (2009b). Continuation-phase cognitive therapy’s
effects on remission and recovery from depression. Journal of Consulting and Clinical
Psychology, 77 , 367–371. doi:10.1037/a0015238
Vittengl, J. R., Clark, L. A., & Jarrett, R. B. (2010). Moderators of continuation phase cognitive
therapy’s effects on relapse, recurrence, remission, and recovery from depression. Behaviour
Vittengl, J. R., Clark, L. A., Kraft, D., & Jarrett, R. B. (2005). Multiple measures,
methods, and moments: A factor-analytic investigation of change in depressive symp-
toms during acute-phase cognitive therapy. Psychological Medicine, 35, 693–704.
doi:10.1017/S0033291704004143
Vittengl, J. R., Clark, L. A., Thase, M. E., & Jarrett, R. B. (2013, April 29). Nomothetic and
idiographic symptom change trajectories in acute-phase cognitive therapy for recurrent
depression. Journal of Consulting and Clinical Psychology. Advance online publication.
doi:10.1037/a0032879
Wang, P. S., Lane, M., Olfson, M., Pincus, H. A., Wells, K. B., & Kessler, R. C. (2005).
Twelve-month use of mental health services in the United States: Results from the

doi:10.1001/archpsyc.62.6.629
Ware, J., & Sherbourne, C. (1992). The MOS 36-item short-form health survey (SF-36). I.
Conceptual framework and item selection. Medical Care, 30, 473–483.
Weissman, M., & Bothwell, S. (1976). Assessment of social adjustment by patient self-report.
Wells, A. (2008). Metacognitive therapy: Cognition applied to regulating cog-
nition. Behavioural and Cognitive Psychotherapy, 36, 651–658. doi:10.1017/
S1352465808004803
Press.
Wells, K., Stewart, A., Hays, R., Burnam, M., Rogers, W., Daniels, M., … Ware, J. (1989). The
functioning and well-being of depressed patients. Results from the Medical Outcomes
Study. JAMA, 262, 914–919.
Wilson, K., Mottram, P., & Vassilas, C. (2008). Psychotherapeutic treatments for older
depressed people. Cochrane Database of Systematic Reviews (Online), 1, CD004853.
doi:10.1002/14651858.CD004853.pub2
Young, J., & Beck, A. T. (1980). Cognitive therapy scale: Rating manual. Philadelphia, PA:
Center for Cognitive Therapy.
49
Dysthymia and Chronic Major
Depression
Bruce A. Arnow and Kathleen M. Corcoran
Stanford University School of Medicine, United States
Michael E. Thase
Perelman School of Medicine of the University of Pennsylvania and Philadelphia
Veterans Affairs Medical Center, United States
Introduction
Chronic depression refers to those presentations in which depressive symptoms

persist for 2 years or longer. In the fourth edition (text revision) of the Diagnostic
and Statistical Manual of Mental Disorders (DSM-IV-TR; American Psychiatric
Association [APA], 1994), two principal types of chronic depression are described:
dysthymic disorder (DD) and major depressive episode (MDE), chronic type. Two
other diagnoses, namely recurrent major depressive disorder (MDD) without full
interepisode recovery and major depressive episode with residual symptoms, are
considered chronic when the full duration of illness lasts for 2 or more years.
The focus of this chapter will be on these forms of depression in adults, aged
18 and older. We first discuss diagnosis, epidemiology, and illness burden. We
then review the treatment literature on cognitive behavioral therapy (CBT) and
related approaches to psychotherapy for these conditions, how these compare to
psychopharmacologic intervention and combination treatment, and what is known
about moderators of outcome. Finally, we discuss some of the clinical challenges
in working with chronically depressed patients and how we have approached these
difficulties.

DOI: 10.1002/9781118528563.wbcbt49
DSM-IV Definitions of Dysthymic Disorder and Chronic

Major Depressive Disorder
Criteria for DD include depressed mood for a period of 2 years and at least two of
the following: (a) poor appetite or overeating, (b) insomnia or hypersomnia, (c) low
energy or fatigue, (d) low self-esteem, (e) poor concentration or difficulty making
decisions, and (f ) feelings of hopelessness.
An additional specifier for dysthymia in the DSM-IV is early (< 21 years) versus
late (> 21 years) onset. Compared with late onset DD, early onset is characterized
by more frequent family histories of mood disorders (Klein et al., 1999), higher rates
of anxiety and other Axis I disorders (Barzega, Maina, Venturello, & Bogetto, 2001;
Devanand et al., 2004; Klein, Taylor, Dickstein, & Harding, 1988) and personality
disorders (Garyfallos et al., 1999).
Although the symptomatic criteria for a diagnosis of DD are similar to those for
an MDE, the symptoms do not have to be as severe or pervasive. Moreover, in
order to meet criteria for an initial diagnosis of DD, the individual cannot meet
symptomatic criteria for an MDE (i.e., depressed mood or anhedonia plus at least
four other qualifying symptoms “most every day” throughout a 2-week period during
the qualifying 2-year time interval). Conversely, the diagnosis of DD cannot be made
when the chronic mild depressive syndrome has developed as a residuum of an MDE.
In the latter case, the episode is described as MDD with incomplete interepisode
recovery.
As the difference between DD and an MDE can involve only a modest shift in the
severity or frequency of only one or two symptoms, it is not surprising that the vast
majority of people with DD experience periods during which they meet criteria for
MDE (Keller et al., 1995; Klein, Shankman, & Rose, 2006). MDD superimposed on
dysthymia has been referred to as “double depression” (Keller & Shapiro, 1982). The
degree of overlap between DD and double depression has led to the suggestion that
the two presentations are better conceptualized as different phases of a single disorder
(Gureje, 2011; Klein, 2008).
Chronic MDD refers to those patients who meet full criteria for major depression
for a period of 2 or more years. Diagnosis of MDD includes either (a) depressed
mood or (b) loss of interest or pleasure in all or almost all activities, plus at least
four other symptoms (e.g., changes in appetite, insomnia or hypersomnia, agitation
or retardation, fatigue, feelings of worthlessness, diminished concentration, suicidal
ideation) totaling at least five. Chronic MDD is thus more severe than DD in that it
requires experiencing more symptoms. Moreover, in chronic MDD, depressed mood
is experienced “most of the day, nearly every day,” while in DD, depressed mood
is experienced “most of the day, for more days than not,” suggesting that chronic
MDD symptoms are more persistent than DD (Klein et al., 2006).
Dysthymia and Chronic Major Depression 1163
Epidemiology of Dysthymic Disorder and Chronic Major

Depressive Disorder
Community samples reveal that 12-month rates of DD are in the range of 0.5–2.5%.
Twelve-month prevalence was 2.5% in the National Comorbidity Survey (NCS; Kessler
et al., 1994), 1.5% in the NCS Replication Study (NCS-R; Kessler et al., 2005), and
0.5% in the National Epidemiologic Survey on Alcohol and Related Conditions
(NESARC; Blanco et al., 2010). Lifetime prevalence estimates in community samples
range from approximately 1 to 6%. Specifically, lifetime prevalence was 3.1% in the
Epidemiologic Catchment Survey (Weissman, Leaf, Bruce, & Florio, 1988), 6.4% in
the NCS (Kessler et al., 1994), 2.5% in the NCS-R (Kessler et al., 2005), 6.1% in
the National Health and Nutrition Examination Survey III (NHANES-III; Riolo,
Nguyen, Greden, & King, 2005), and 0.9% in the NESARC (Blanco et al., 2010).
Interestingly, compared to countries with lower incomes, rates of DD are elevated in
higher income countries (Gureje, 2011). As is the case with MDD, the prevalence of
DD in females is approximately twice as high as in males (Blanco et al., 2010; Kessler
et al., 1994; Weissman et al., 1988).
Based on data gathered from a community sample, Blanco et al. (2010) reported
12-month and lifetime prevalence of chronic MDD at 1.5% and 3.1%, respectively. In
a prospective population-based study that included 92 individuals with first lifetime
onset of MDD, Eaton et al. (2008) reported that while the median episode length was
12 weeks, in 15% of cases individuals did not experience one year free of symptoms
over a 23-year period. Data from two other studies suggest that about 20% of MDD
patients fail to recover within 2 years (Rhebergen et al., 2011; Spijker et al., 2002).
The Collaborative Depression Study (CDS), which included longitudinal follow-up
of more than 400 treatment-seeking individuals diagnosed with MDD, also found
that 20% of the sample did not recover within 2 years (Boland & Keller, 2002);
at 5 years and 10 years, 12% (Keller et al., 1992) and 7% (Mueller et al., 1996),
respectively, had not recovered.
Are There Differences among Individuals with Different

Forms of Chronic Depression?
Those studies comparing patients with chronic MDD and dysthymia on a variety of
indices have reported few differences (e.g., Yang & Dunner, 2001). No differences
were found between those with chronic MDD and double depression in either coping
style or social adjustment (McCullough et al., 1994). Studies comparing those with
dysthymia versus double depression have reported no differences in comorbidity
(Pepper et al., 1995), familial psychopathology (Klein et al., 1995), or levels of
adversity in childhood environments (Lizardi et al., 1995). A comparison of chronic

MDD patients with those meeting criteria for both DD and MDD in which the
latter was present for less than 2 years, and a third group comprised of patients
with chronic MDD superimposed on DD, found that the three groups were similar
in demographic and clinical characteristics as well as family history and response
to pharmacotherapy (McCullough et al., 2000). In a subsequent study comparing
patients with several forms of chronic depression (chronic MDD, double depression,
recurrent MDD without full interepisode recovery, and chronic MDD superimposed
on DD), few differences were found in demographic, clinical, familial, or psychosocial
characteristics, nor in treatment response across treatments including psychotherapy,
medication, and combined treatment (McCullough et al., 2003). Thus, we concur
with Klein (2008) who suggested that distinctions between the various presentations
of depression that are elaborated in the DSM-IV (APA, 1994) do not provide clinically
meaningful information.
Differences between Patients with Chronic and

Nonchronic Depression
While few differences have been found among subgroups of chronically depressed
patients, there appear to be substantial differences between individuals who suf-
fer chronic versus episodic forms of depression. Comparisons with nonchronically
depressed individuals reveal that those with chronic depression have higher levels
of anxiety disorders (Gilmer et al., 2005; Holm-Denoma, Berlim, Fleck, & Joiner,
2006; Mondimore et al., 2006), substance abuse (Angst, Gamma, Rossler, Ajdacic, &
Klein, 2009; Mondimore et al., 2006), and Axis II comorbidity (Garyfallos et al.,
1999; Pepper et al., 1995), as well as more intense suicidal ideation (Holm-Denoma
et al., 2006) and greater likelihood of having made a suicide attempt (Gilmer
et al., 2005; Holm-Denoma et al., 2006; Klein, Schwartz, Rose, & Leader, 2000;
Mondimore et al., 2006; Satyanarayana, Enns, Cox, & Sareen, 2009). Compared
with individuals with nonchronic MDD, those with chronic MDD report poorer
physical and social well-being (Gilmer et al., 2005; Holm-Denoma et al., 2006).
Those with chronic depression grow up in homes with greater levels of parental psy-
chopathology than do the episodically depressed (Lizardi & Klein, 2000) and report
significantly higher prevalence of childhood adversity (Lizardi & Klein, 2000; Wiersma
et al., 2009). Psychological factors that have been shown to differentiate chronically
from nonchronically depressed individuals include high levels of rumination, low
extraversion, and high external locus of control (Wiersma et al., 2011).
Burden of Chronic Major Depressive Disorder and Dysthymia
In addition to the subjective suffering borne by individuals who suffer depressive

disorders, societal burdens are substantial across multiple domains. These include the
impact on family members associated with decrements in role function, the effects
of absenteeism and reduced productivity in the work environment, costs to the

health care system, and costs associated with suicide or premature mortality related
to depression (Donohue & Pincus, 2007; Simon, 2003). According to the World
Health Organization Global Burden of Disease Study, in the year 2000 depression
was ranked as the fourth leading cause of disability (Ustun, Ayuso-Mateos, Chatterji,
Mathers, & Murray, 2004).
In the landmark Medical Outcomes Study, Wells et al. (1989) found that depres-
sion was associated with as much or more impairment in multiple domains than
most chronic medical illnesses. Moreover, in those with medical illness, depression-
associated impairment was found to be additive (Wells et al., 1989). A more recent
World Health Organization study reported similar results with depression associated
with significantly greater health decrements than a number of chronic medical ill-
nesses including angina, diabetes, and arthritis (Moussavi et al., 2007). In the NCS-R,
MDD was associated with 27 lost workdays per year, per ill individual (Kessler et al.,
2006). Stewart, Ricci, Chee, Hahn, and Morganstein (2003) reported that depressed
individuals lost 5.6 hours of productive work time weekly, compared to 1.5 hours
among nondepressed individuals. While suicide in the general population accounts
for 0.9% of all deaths, depression is the most important risk factor; two-thirds of
suicides occur in depressed patients (Sartorius, 2001). Depression is also associated
with a 50–75% increase in health care costs compared with nondepressed patients
even after accounting for medical illness (Simon, Ormel, VonKorff, & Barlow, 1995).
This effect is primarily due to greater medical costs; the actual costs of depression
treatment account for only 5–10% of the observed increase in costs (Simon, 2003).
Available evidence suggests that compared with episodic major depression, chronic
forms of depression are associated with greater economic and social burden. Decre-
ments in both daily function and social impairment are greater among chronically
depressed patients compared to those with episodic MDD (Hellerstein, Agosti,
Bosi, & Black, 2010; Leader & Klein, 1996; Satyanarayana et al., 2009). Compared
with the episodically depressed, those with chronic depression have lower educational
attainment, and are more likely to be unemployed (or less likely to work full time)
and to have lower family income (Angst et al., 2009; Blanco et al., 2010; Gilmer
et al., 2005; Hellerstein et al., 2010).
Comparisons of chronically and nonchronically depressed individuals reveal greater
medical morbidity, use of health care services, and mortality in the former group.
Compared with the episodically depressed, chronically depressed individuals are more
likely to suffer comorbid medical illness (Angst et al., 2009; Gilmer et al., 2005;
Rush et al., 2011; Satyanarayana et al., 2009). Chronic depression is also associated
with elevated health care utilization compared to nonchronic forms of depression
(Satyanarayana et al., 2009; Weissman et al., 1988). Chronically depressed individuals
demonstrated a 10-fold greater risk of psychiatric hospitalization compared to episodi-
cally depressed individuals (Klein et al., 2000). Compared to intermittent depression,
chronic depression predicted mortality among older individuals (aged 55–85)
after controlling for age, sex, chronic illness, and functional limitations (Geerlings,
Beekman, Deeg, Twisk, & Tilburg, 2002). Among patients aged 71 years or older,
those with chronic depression had an 88% excess risk of developing cancer compared
with nonchronically depressed individuals even after adjusting for age, sex, ethnicity,
cigarette smoking, alcohol intake, and physical disability (Penninx et al., 1998).
Effectiveness of Cognitive Behavioral Therapy for Dysthymia

and Chronic Depression
While there is a large literature devoted to the study of CBT for acute depression,
and the efficacy of CBT for depression is well established (Hollon & Ponniah, 2010),
fewer studies to date focus on the effectiveness of CBT for chronic presentations of
depression. In the section below, outcome studies for DD and chronic depression are
reviewed (see also Table 49.1).
Dysthymia
Only one study has directly compared the effectiveness of individual CBT to medica-
tion for the treatment of dysthymia. Thirty-one adults diagnosed with dysthymia were
assigned to 16 weeks of CBT or to fluoxetine (Dunner et al., 1996). Both treatments
were effective in reducing depressive symptoms, with no differences between groups,
providing preliminary evidence that CBT may be equally as helpful as medication in
reducing symptoms of dysthymia. However, response rates in both groups were lower
than those characteristic of treatment studies for MDD.
Hellerstein et al. (2001) compared fluoxetine alone to fluoxetine augmented by
16 sessions of group cognitive-interpersonal therapy in 40 patients who had partially
responded to medication treatment alone. Combination treatment was associated with
a somewhat higher percentage of responders (89%) at posttreatment than medication
alone (76%), although the observed difference was not significant. Patients were
followed for an additional 12 weeks after completing treatment, and combination
treatment maintained its advantage (61%) over medication alone (40%), though again
between-group differences were not significant.
In a sample of 97 adult dysthymic patients, Ravindran et al. (1999) investigated the
relative effectiveness of sertraline alone, sertraline augmented by brief group CBT (12
sessions), group CBT plus placebo, and placebo alone. There was some indication
that combined treatment resulted in a higher response rate (71%) than sertraline alone
(55%), though this difference did not reach statistical significance. The authors point
out that their sample size did not afford adequate statistical power to detect smaller
effect sizes. Moreover, given the 2 x 2 design, the study was underpowered in terms
of detecting interactions among the treatment arms. Nonetheless, the two treatments
that included medications resulted in significantly higher response rates compared to
those that did not, and response rates were similar for the CBT plus placebo and
placebo alone groups.
As reviewed above, there are few studies that examine the effectiveness of CBT for
dysthymia, and what research exists is mixed. The results of Dunner et al. (1996),
that individually administered CBT produces equivalent reductions in depression to
those produced by medication, are encouraging, although the absence of a control
group limits the conclusions that may be drawn. The findings of the two studies that
Table 49.1 Studies Examining the Effectiveness of Cognitive Behavioral Therapy and CBASP for Dysthymia and Chronic Depression
Study Treatment No. of Sample Age Diagnosis Setting Outcome Response
conditions sessions/ size and/or
duration remission
rates
Dysthymia
Dunner et al., 1. CBT 16 weeks 31 assi- 18–60 Dysthymia Outpatient Both treatments
1996 2. Fluoxe- gned (DSM- research showed
tine (20 25 com- III-R) clinic significant
mg fixed pleted improvement
dose) in depressive
symptoms; no
differences
between
treatments
Hellerstein 1. Fluoxe- Medication 40 assi- 21–65 DSM-III- Tertiary Combined Response rates:
et al., 2001 tine alone treat- gned R, early care treatment had Posttreatment:
ment for 35 com- onset teaching greater Combination = 89%
approx. pleted hospital reductions in Medication =76%
24 depressive
weeks symptoms at
posttreatment
2. Fluoxe- Medication
tine + 16 alone for Follow-up:
sessions 8 weeks Combination = 61%
group + 16 Medication = 40%
CBT weeks
medica-
tion +
group
CBT
(Continued Overleaf)
duration remission
rates
Ravindran 1. Sertraline Group 97 assi- 21–54 Primary Research Medication Response rates:
et al., 1999 alone CBT = 12 gned dys- outpa- significantly Sertraline = 54%
2. Sertraline weekly 94 com- thymia tient more effective Sertraline +
+ group 90- pleted (DSM- clinic than placebo; CBT = 71%
CBT minute III-R or combination Placebo alone = 33%
3. Placebo group DSM-IV treatment no Placebo +
alone sessions criteria) more effective CBT = 33%
4. Placebo + than
group medication
CBT
Chronic depression
CBT studies
Agosti & 1. Imipra- 16 weeks 65 adults 21–60 Early Research Active Response rates;
Ocepek- mine onset outpa- treatments Imipramine = 64%
Welikson, 2. CBT chronic tient were not CBT = 38%
1997 3. IPT depres- clinics significantly IPT = 35%
4. Placebo sion superior to Placebo = 27%
placebo;
approx. 50%
decrease in
depression
severity across
all treatments
Barker et al., 1. Pharma- 15 CBT 25 assi- <65 Chronic Inpatient Both treatments
1987 cotherapy sessions gned years MDD setting effective in
alone over 12 20 com- reducing
2. Pharma- weeks pleted symptoms of
cotherapy depression;
+ CBT combination
treatment no
more effective
than medi
-cation alone
de Jong et al., 1. Inpatient Individual 33 assi- Adults DSM-III Inpatient All treatment Response rates:
1986 CBT + + group gned criteria setting groups CBT + SC = 60%
social 30 com- for improved; CR = 30%
compe- pleted MDD trend for CBT WLC = 10%
tence + dys- + SC and CR
training thymia to be superior
(CBT + to WLC
SC)
2. Inpatient Individual
CR
3. Outpa-
tient
WLC
duration remission
rates
Harpin et al., 1. CBT + 1. Twice 12 assi- 21–60 Chronic Outpatient Significant

1982 social skills weekly gned depres- clinic pre-post
training sessions sion, improvement
2. WLC over 10 unre- in depressive
weeks sponsive symptoms in
2. 10-week to treat- treated group
WLC ment but not WLC;
no significant
difference in
outcome
measures
between
groups
Miller et al., 1. Pharma- Psychotherapy 26 assi- 18–65 Diagnostic Inpatient Combined Remission rates:
1999 cotherapy involved 5 gned Inter- setting treatment Combination = 43%
+ psy- sessions 21 com- view + 20 more effective Pharmacother-
chother- per week pleted Sched- weeks of than pharma- apy = 33%
apy (either while ule outpa- cotherapy
CBT or inpatient; diagno- tient alone in
social skills weekly sis of treat- reducing
training) sessions MDD ment depressive
2. Pharma- for 20 + dys- symptoms and
cotherapy weeks thymia improving
alone following social
treatment functioning
CBASP studies
Keller et al., 1. CBASP 1. CBASP 681 assi- 18–75 DSM-IV 12 aca- Efficacy of Response rates:
2000 2. Nefa- = 16–20 gned criteria demic CBASP and CBASP = 48%
zodone sessions 519 com- for centers nefazodone Nefazodone = 48%
(max. 600 over 12 pleted chronic similar; Combination = 73%
mg) weeks MDD combined Remission rates:
3. Combina- 2. Medica- treatment was CBASP = 33%
tion tion = 12 significantly Nefazodone = 29%
treatment weeks more effective Combination = 48%
treat- than both
ment monotherapies
with
nefa-
zodone
Kocsis et al., Phase 1: Phase 1: Phase 18–75 DSM-IV 8 academic No group Remission rates:
2009 Algorithm- 12 1 = 808 criteria centers differences on Medication: 39%
based weeks of for remission rates CBASP: 38%
medica- medica- current or changes in BSP: 31%
tion tion MDD depressive
treat- of at symptoms
ment least 4
weeks
and
depres-
sive
symp-
toms for
2 years
duration remission
rates
Phase 2: Phase 2: Phase

1. Medica- CBASP = 2 = 491
tion alone 16–20 nonre-
2. Medica- sessions sponders
tion + over 12 or
CBASP weeks partial
3. Medica- BSP = respon-
tion + 16–20 ders
BSP session
over 12
weeks
Schatzberg Crossover 1. CBASP 140 assi- 18–75 DSM-IV 12 aca- Both groups Overall response
et al, 2005 design; = 16–20 gned criteria demic improved over and/or remission,
After 12 sessions 110 com- for centers time. In ITT ITT sample:
weeks of over 12 pleted chronic sample, group CBASP = 57%
treatment, weeks MDD switched to Nefazodone = 42%
nonrespon 2. Medica- CBASP had Overall response
-ders to tion = 12 significantly and/or remission,
monother- weeks greater im- completers sample:
apy from treat- provement in CBASP = 64%
Keller ment depressive Nefazodone = 53%
et al., 2000, with symptoms than
were nefa- group switched
crossed zodone to nefazodone.
over to No differences
receive emerged in the
alternate completers
treatment sample.
Schramm 1. CBASP 22–24 30 adults 18–65 DSM-IV Outpatient CBASP led to Response rates:
et al., 2011 2. IPT sessions criteria medical greater CBASP = 64%
over 16 for setting reductions in IPT = 27%
weeks early- depressive Remission rates:
were onset symptoms CBASP = 57%
offered chronic IPT = 20%
depres-
sion of
at least
2 years
Notes. BSP = brief supportive psychotherapy, CBASP = cognitive behavioral analysis system of psychotherapy, CBT = cognitive behavior therapy, CR = cognitive
restructuring, IPT = interpersonal therapy, ITT = intent to treat, WLC = wait-list control. Response rates generally defined as a decrease of at least 50% on a
depression symptom measure.
evaluated group treatment are equivocal. We note that in the study by Ravindran et al.
(1999), in which results of group CBT were least impressive, the number of sessions
was limited to 12, which was less than those provided by Hellerstein et al. (2001).
Neither of these studies provided clear-cut evidence of benefit associated with CBT.
It is unclear whether group CBT is less helpful in dysthymia than in other forms of
depression, or whether the dose of group treatment was inadequate. Given the mixed
findings, small sample sizes, and sometimes short duration of treatment, there is a
clear need for further studies to investigate the effectiveness of CBT with and without
medication for dysthymic patients.
Chronic Major Depression

There is a small literature devoted to the examination of CBT, and its adaptations, for
the treatment of chronic depression. Several studies have explored the effectiveness of
psychotherapy compared to a wait-list control for chronic major depression. In one
such study, a comprehensive CBT program, which included cognitive restructuring,
behavioral activation, and social competence training, was compared to cognitive
restructuring alone or a wait-list control within a small sample of inpatients diagnosed
with double depression (de Jong, Treiber, & Henrich, 1986). The comprehensive
CBT treatment produced higher response rates and lower self-report scores than
either of the other conditions, and both CBT treatments were more effective than
the wait-list control in reducing depressive symptoms on clinician-rated measures.
Harpin et al. (1982) compared outpatient CBT to a wait-list control in a sample
of 10 patients with treatment-resistant chronic depression. While CBT produced
significant pre-post differences in depressive symptoms, there were no significant
differences between groups. The sample size of this study was very small, making it
difficult to test for between-group differences. In a comparison of the effectiveness
of 16 weeks of CBT for patients with chronic versus acute depression, chronically
depressed patients demonstrated lower remission rates and higher levels of depressive
symptoms throughout treatment compared with more acutely depressed individuals
(Thase et al., 1994).
CBT has also been compared to medication in the treatment of chronic depression.
Agosti and Ocepek-Welikson (1997) reported on the National Institute of Mental
Health Treatment of Depression Collaborative Research Program (Elkin et al., 1989)
findings for 65 of the original 250 participants who were diagnosed with early-
onset chronic depression. In this study, participants were randomized to one of four
treatments: imipramine, CBT, interpersonal therapy (IPT), or placebo plus clinical
management. In this subgroup analysis, the active treatments were no more effective
than pill placebo in patients with chronic depression, though there was a reduction of
approximately 50% in depressive symptoms across all groups.
Two studies have investigated whether CBT adds benefit to medication among
chronically depressed inpatients. Barker, Scott, and Eccleston (1987) randomly
assigned 25 inpatients to one of the two treatment groups, with psychotherapy
involving 15 CBT sessions over 12 weeks. The addition of CBT was not more
effective than medication alone in reducing depressive symptoms. In contrast, Miller,
Norman, and Keitner (1999) found that medication plus inpatient CBT that contin-
ued for 20 weeks postdischarge was more effective than medication alone in reducing
depressive symptoms and improving social functioning. The addition of psychother-
apy also resulted in higher remission rates at 12 months, though the group differences
were not significant.
Cognitive Behavioral Analysis System of Psychotherapy

for Chronic Depression
Two large-scale studies were conducted to investigate whether a variant of CBT,
cognitive behavioral analysis system of psychotherapy (CBASP; McCullough, 2000),
would prove effective for the treatment of chronic depression, either alone or in
combination with medication. CBASP, a treatment developed specifically for chronic
depression, targets thoughts, emotional responses, behaviors, and interpersonal pat-
terns that are prototypical of chronic presentations of depression. Keller et al. (2000)
compared the acute phase efficacy of CBASP, nefazodone, and their combination, in
681 patients at 12 sites. CBASP consisted of up to 20 sessions over the 12 weeks
of treatment. CBASP and medication were equally helpful in reducing depressive
symptoms, with intention-to-treat response rates of just below 50% in both groups.
The combination of the two treatments yielded response rates of over 70%, which
was significantly higher than the monotherapies. Similarly, remission rates were 29%,
33%, and 48% for nefazodone, CBASP, and combined treatment, respectively. The
combination of CBASP and nefazodone was thus significantly more effective than
either treatment alone and the magnitude of this advantage was clinically significant
(i.e., a number needed to treat of 5 for response and 7–8 for remission).
The Keller et al. (2000) trial also included a crossover study in which acute phase
nonresponders to CBASP or nefazodone were given the option to switch to the
alternate monotherapy (Schatzberg et al., 2005). Ninety-five percent and 84% of
CBASP and nefazodone nonresponders, respectively, agreed to cross over. Compared
to those participants who were switched to nefazodone, response rates of those who
crossed over to CBASP were significantly higher (57% vs. 42%, p = .03; Schatzberg
et al., 2005). There were no differences in the remission rates (36% receiving CBASP;
27% nefazodone).
A subsequent study by many of the same investigators examined whether adjunctive
CBASP would be effective for patients who did not respond to medication (Kocsis,
Gelenberg, et al., 2009). In this two-phase study, patients with chronic depression
were treated first with algorithm-guided medication. Those patients who showed
no response or a partial response after 8–12 weeks of medication treatment were
randomized to one of three groups: (a) a switch of antidepressant medications
(continued pharmacotherapy alone), (b) a switch of antidepressants plus CBASP, or
(c) a switch of antidepressants plus brief supportive therapy (BSP). The latter group
was included in this study to ascertain if the predicted additive effects of CBASP
were specific to the methods and techniques or, more simply, reflected the nonspecific
effects of seeing a psychotherapist. Of the approximately 800 patients who participated
in the first phase of the study, 491 were non- or partial responders to medication and
were included in phase 2, with 80% randomized to receive adjunctive psychotherapy
in addition to pharmacotherapy and 20% allocated to pharmacotherapy alone. No

differences emerged in remission rates or reductions in depressive symptoms across
the three groups in phase 2, with approximately 40% of the sample reaching remission
criteria. Thus, while Keller et al. (2000) concluded that the combination of CBASP
and medication was significantly superior to antidepressant medication alone (as well
as CBASP alone), Kocsis, Gelenberg, et al. (2009) concluded that neither CBASP nor
BSP added adjunctive benefit beyond that conferred by antidepressant medication.
There are several possible explanations for the discrepant findings in the two trials.
First, participants in the study by Kocsis, Gelenberg, et al. (2009) demonstrated a
degree of treatment resistance that was greater than that observed in the first CBASP
trial. Second, the pharmacotherapy algorithm employed by Kocsis, Gelenberg, et al.
(2009) was arguably more powerful than the single medication in the Keller et al.
(2000) trial. Third, participants in the two samples may have differed in their treatment
preferences, which in turn may have influenced outcome. Some evidence suggests that
patient preference affects treatment response in MDD (Kocsis, Leon, et al., 2009),
while other findings suggest that preference affects engagement in treatment in ways
that may include the number of sessions attended (Kwan, Dimidjian, & Rizvi, 2010).
Evidence that patient attitudes toward psychotherapy may have been less favorable in
the study by Kocsis, Gelenberg, et al. (2009) is that patients in this study used only
12.5 CBASP visits, versus 16 visits in the study by Keller et al. (2000), although the
number of sessions offered and the visit schedules for the two trials were identical.
A recent study comparing CBASP to IPT provides some further support for
CBASP’s efficacy. Schramm et al. (2011) randomly assigned 30 patients with
early-onset chronic depression to either CBASP or IPT. Both treatments involved
approximately 22 individual therapy sessions over 16 weeks. CBASP was associated
with greater reductions in depressive symptoms and significantly higher response and
remission rates than IPT (64% vs. 27% response rate and 57% vs. 20% remission rate
for CBASP and IPT, respectively), suggesting that CBASP may be more effective
than IPT in treating chronic depression. Additional research is needed to determine
if CBASP is a particularly effective treatment of chronic depression or if it is simply
one of several reasonable therapeutic strategies to consider.
Differential Predictors of Outcome

A few studies have examined whether specific patient characteristics might differentially
predict treatment response in chronic depression samples. In a post hoc analysis of the
Keller et al. (2000) data, Nemeroff et al. (2003) found that patients meeting criteria for
early child adversity were significantly more likely to achieve full remission with CBASP
compared to nefazodone; those without early adversity responded better—though
not significantly so—to pharmacotherapy. Klein et al. (2009) similarly found that
chronically depressed patients who met criteria for clinically significant abuse were
significantly less likely to achieve remission with algorithm-based pharmacotherapy
than those without such history. Thus, in patients with chronic depression where
a clinician is attempting to decide whether to begin with psychotherapy versus
pharmacotherapy, the presence of a history of child adversity may suggest starting
with the former.
Evidence suggests that when asked, depressed patients will express preference for
either medication or psychotherapy (Bedi et al., 2000). One study in chronically
depressed patients investigated whether being matched to one’s preferred treatment
might differentially predict outcome. Kocsis, Leon, et al. (2009) found an interactive
effect of preference and treatment group on outcome, such that patients who
were randomized to their preferred treatment—in this case CBASP, medication,
or combined therapy—were significantly more responsive to treatment than those
randomized to a treatment they did not prefer. This result was particularly apparent
among those who expressed a preference for one of the monotherapies. It is important
to note that Leykin et al. (2007), in a cohort of depressed patients not selected for
chronicity and randomized to either medication or CBT (there was no combined
treatment arm), did not find that being matched to one’s preferred treatment was
associated with outcome. It is possible that in a trial that involves combined treatment,
expressing a preference for monotherapy suggests a strong aversion to the alternate
monotherapy. That is, the patient who could receive medication plus psychotherapy,
and expresses a preference for medication only, may be more likely to be averse
to psychotherapy than the patient who simply chooses, between medication and
psychotherapy, one as the preferred treatment. Overall, however, the findings that
chronically depressed patients with histories of child adversity may predict response to
treatment and that treatment preference may also moderate treatment outcome are
promising and merit further investigation.
Conclusions: Efficacy of Cognitive Behavioral Therapy and Cognitive

Behavioral Analysis System of Psychotherapy for Chronic Depression
Few studies have investigated the efficacy of CBT for chronic depression, and what
research exists is spread among both inpatients and outpatients. It is clear that
more research effort is needed to provide guidance regarding the efficacy of CBT
for chronic MDD. As discussed above, the data on CBASP are mixed, but on the
whole we consider them encouraging and worthy of additional research attention.
The findings on patient preference and child adversity as moderators of outcome in
chronic depression may eventually assist mental health providers to make decisions
regarding how to begin treatment with the chronically depressed patient.
Clinical Issues in Working with the Dysthymic or Chronically

Depressed Patient
As the review above suggests, currently available treatments fall short of bringing
to remission a large percentage of patients with chronic presentations of depression.
Several adaptations to traditional CBT treatment are likely necessary to improve
outcomes and remission rates. We offer the following suggestions, which we describe
in further detail below:
1. a longer course of acute phase treatment, supplemented by maintenance booster

sessions;
2. ongoing symptom monitoring;

3. adapting treatment when patients are not responding to traditional CBT;
4. including an interpersonal focus; and
5. working with pessimism and hopelessness.
Length and Structure of Treatment

That a longer or more severe illness course might warrant a longer duration of
treatment is consistent with naturalistic studies on dose effect in psychotherapy
(Lambert & Ogles, 2004), and there is specific evidence from a recent meta-analysis
that suggests a relationship between duration of psychotherapy and treatment outcome
in chronic presentations of depression (Cuijpers et al., 2010). Moreover, results from
the first large CBASP study found that patients who received monthly maintenance
sessions of CBASP relapsed at a significantly lower rate (10%) than did those patients
randomized to an assessment-only condition (32%; Klein et al., 2004). Taking these
findings into consideration, we strongly advise that length of treatment be extended
when working with patients with chronic depression. Effective treatment of chronic
depression should also include maintenance sessions following acute phase treatment
in order to maintain treatment gains and help prevent relapse and recurrence.
In structuring treatment, we also suggest that combination treatment be considered
the treatment of choice. Although the findings of Kocsis, Gelenberg, et al. (2009)
do not support combined treatment versus medication alone with patients who have
already demonstrated some degree of treatment resistance, other findings, specifically
those of Keller et al. (2000), support the need for combined treatment. In a meta-
analysis of studies involving several models of psychotherapy in addition to CBT
and CBASP with chronically depressed patients, Cuijpers et al. (2010) found that
combination treatments appear to be more effective than monotherapy. Therefore,
a comprehensive treatment plan should, whenever possible, include both medication
and psychotherapy.
Routine Symptom Monitoring

Given the modest response and remission rates reported in trials examining treatment
of chronic depression, we recommend that regular symptom monitoring be a routine
part of clinical practice. Such monitoring allows for identification of patients who are
not responding to traditional CBT approaches and evidence suggests that monitoring
symptoms is associated with enhanced treatment response. For example, Lambert and
colleagues (Lambert, Whipple, Smart, Vermeersch, & Nielsen, 2001; Whipple et al.,
2003) conducted studies examining the effects of regular monitoring of symptoms
across a wide range of patient problems. In these studies, patients completed a
symptom measure at pretreatment and at regular intervals during treatment. Therapists
were provided with feedback on patients’ progress, including information on whether
patients were progressing or not progressing at the expected rate. Results from these
studies have been very encouraging; for those patients not progressing in treatment,
when therapists were given feedback on their patients’ progress, fewer patients
deteriorated and more achieved clinically significant change than when therapists
were not provided with feedback (Lambert, Harmon, Slade, Whipple, & Hawkins,
2005; Shimokawa, Lambert, & Smart, 2010). Based on these results, and the limited
effectiveness of current treatments for chronic depression, regular monitoring of
symptoms is strongly advised.
Adapting Treatment when Nonresponse Is Indicated

When nonresponse to treatment is identified, several adaptations to traditional CBT
should be considered. As a first step, we suggest that the case formulation be
revisited, with particular attention paid to the maladaptive core beliefs, assumptions,
and behavioral patterns that may be maintaining the depressive symptoms and the
extent to which there is agreement between therapist and patient on the formulation
itself. While case formulation has received relatively little empirical attention, there is
some evidence that a case formulation approach to treatment enhances outcome of
CBT (Persons, Roberts, Zalecki, & Brechwald, 2006). Additionally, when treatment
nonresponse is apparent, it is also important to pay increased attention to the
therapeutic alliance and to assess patients’ motivation for treatment. Attending to
these factors, among others, has been associated with increased treatment response
and reductions in the likelihood of treatment deterioration (Harmon et al., 2007).
Interpersonal Focus
There is considerable empirical research to suggest that chronic depression may
be associated with difficulties in interpersonal problem solving (Davila, Hammen,
Burge, Paley, & Daley, 1995), lack of assertiveness (Constantino et al., 2008;
Youngren & Lewinsohn, 1980), social role impairment (Evans et al., 1996), and
other interpersonal deficits (Leader & Klein, 1996). In addition, there is evidence
that interpersonal difficulties predict episode duration (Brown & Moran, 1994). Many
psychosocial treatments for chronic depression, including IPT and CBASP, include
an explicit focus on interpersonal difficulties, and it is recommended that CBT for
chronic depression include a focus on such deficits. Important targets of treatment
include improving communication and assertiveness, increasing effective interpersonal
problem solving, and improving the quality of relationships.
There are a number of ways to incorporate an interpersonal focus within CBT
treatment. During the assessment, details about the quality and quantity of inter-
personal relationships should be gathered. Patterns in interpersonal communication,
patients’ expectations of the responses of others, and patients’ comfort with assertive
communication should also be assessed. A useful strategy employed in CBASP, the
“Significant Other List” (McCullough, 2003), can be used to develop a better under-
standing of interpersonal patterns in the patient’s life. This strategy involves recording
the important relationships in the patient’s life, examining the ways in which the
relationships have been influential, and exploring the impact of these relationships on
the patient’s belief system.
As treatment progresses, the patient’s interpersonal concerns should be woven
into the case formulation. This includes examining core beliefs about the self and
others as well as focusing on assumptions about relationships (such as how patients
expect others to react to them). It is also important to explore behavioral patterns

regarding relationships, including communication patterns, assertiveness, the ability
to accurately express emotions, and the ability to effectively work through conflict.
Therapists are advised to maintain an interpersonal focus throughout CBT treatment
in order to help build confidence, optimism, and success experiences for their patients.
Pessimism, Hopelessness, and Dysfunctional Attitudes

Patients with chronic depression present unique challenges to the CBT practitioner.
One such challenge is that the chronicity of depressive symptoms can erode patients’
confidence and optimism, resulting in pervasive negative beliefs about the self, reduced
self-esteem, and a sense of hopelessness about the future. Moreover, patients with
chronic depression may have considerable evidence from life experience to suggest
that their negative beliefs and assumptions are valid. For example, years of being out
of work and socially isolated can contribute to negative beliefs about the self and
hopelessness about the future. As a result, chronically depressed patients may lack
evidence that would support adaptive beliefs and they may understandably express
skepticism about the effectiveness of a treatment designed to help them reappraise
their negative thoughts and beliefs.
In working with such patients, it can be helpful to focus on the patterns that have
developed as a result of the depression and to help patients treat their experience
of depression as separate from the self. For example, in borrowing a strategy from
interpersonal therapy, patients can be taught to differentiate the self from the
experience of depression. This can be helpful in allowing the patient to examine
how depressive illness has contributed to changes in behavior (e.g., withdrawing from
friends and family, participating in fewer rewarding activities), and then exploring how
these behavioral patterns are contributing to and maintaining depressive symptoms.
Patients are encouraged to stop attributing blame to the self (“I have no friends
and am unlikeable”) and to adopt healthier, more adaptive, beliefs (“As a result of
depression, I began withdrawing from relationships and reducing my engagement
with the world. I have fewer friends and supports than I would like, but if I
make changes in my behavior and begin reaching out to people, I may be able to
foster relationships”). In this way, the depression can be “blamed” for a number of
maladaptive patterns in the client’s life, and more adaptive behavioral patterns can
be explored and encouraged. Patients’ hopelessness can strongly impact the CBT
practitioner, and it is also important for therapists to develop ways of remaining
hopeful in the face of patients’ significant hopelessness.
Conclusions
Chronic forms of depression are a major public health problem. We reviewed findings
which suggested that while there are few differences among patients with different
forms of chronic depression when compared to those with episodic depression, those
with chronic depression show more extensive medical as well as psychiatric comorbid-
ity, with greater likelihood of suicide attempts and psychiatric hospitalizations, as well
as more pronounced economic and social burden as revealed by lower educational

attainment, higher likelihood of unemployment, and lower family income.
We offer the following observations on the treatment literature reviewed in this
chapter. First, the length of treatment in trials of chronic depression does not reflect the
long-term nature of the illness. More specifically, there is little empirical basis for the
dose of psychotherapy that was provided in the studies we reviewed. For instance, in
the Koscis, Gelenberg, et al. (2009) trial, it is quite possible that 12 weeks of treatment,
in a sample of chronically depressed patients with prospectively documented treatment
resistance, was simply not enough time to enable many of the participants to make
the necessary changes to alleviate their symptoms. We believe that dose–response
studies are necessary to adequately evaluate the efficacy of psychotherapy for chronic
depression. Second, the advent of the pharmacotherapy algorithm for depressed
patients will provide more difficult comparisons for psychotherapy in the future. Such
adaptive strategies, where changes in the treatment are made mid-stream in those cases
where there is poor or inadequate response, have not been made in psychotherapy. We
believe that in the future CBT, CBASP, and other forms of psychotherapy for chronic
and nonchronic forms of depression must provide alternate strategies for patients
who do not initially respond to therapy. Finally, ongoing (e.g., weekly) symptom
monitoring will be necessary to identify appropriate triage points where such changes
in psychotherapy strategy should be introduced.
References
Agosti, V., & Ocepek-Welikson, K. (1997). The efficacy of imipramine and psychotherapy in
early-onset chronic depression: A reanalysis of the National Institute of Mental Health
Treatment of Depression Collaborative Research Program. Journal of Affective Disorders,
43, 181–186. doi:10.1016/S0165-0327(97)01428-6
Angst, J., Gamma, A., Rossler, W., Ajdacic, V., & Klein, D. N. (2009). Long-term depres-
sion versus episodic major depression: Results from the prospective Zurich study of
a community sample. Journal of Affective Disorders, 115, 112–121. doi:10.1016/
j.jad.2008.09.023
Barker, W. A., Scott, J., & Eccleston, D. (1987). The Newcastle chronic depression study:
Results of a treatment regime. International Clinical Psychopharmacology, 2, 261–272.
Barzega, G., Maina, G., Venturello, S., & Bogetto, F. (2001). Dysthymic disorder: Clinical
characteristics in relation to age at onset. Journal of Affective Disorders, 66, 39–46.
doi:10.1016/S0165-0327(00)00293-7
Bedi, N., Chilvers, C., Churchill, R., Dewey, M., Duggan, C., Fielding, K., … Williams,
I. (2000). Assessing effectiveness of treatment of depression in primary care. Par-
tially randomised preference trial. British Journal of Psychiatry, 177 , 312–318.
doi:10.1192/bjp.177.4.312
Blanco, C., Okuda, M., Markowitz, J. C., Liu, S. M., Grant, B. F., & Hasin, D. S. (2010).
The epidemiology of chronic major depressive disorder and dysthymic disorder: Results
from the National Epidemiologic Survey on Alcohol and Related Conditions. Journal of
Boland, R. J., & Keller, M. B. (2002). Course and outcome of depression. In I. H. Gotlib &
C. L. Hammen (Eds.), Handbook of depression (pp. 43–60). New York, NY: Guilford
Press.
Brown, G. W., & Moran, P. (1994). Clinical and psychosocial origins of chronic depres-
sive episodes. I: A community survey. British Journal of Psychiatry, 165, 447–456.
doi:10.1192/bjp.165.4.447
Constantino, M. J., Manber, R., Degeorge, J., McBride, C., Ravitz, P., Zuroff, D. C., …
Arnow, B. A. (2008). Interpersonal styles of chronically depressed outpatients: Profiles
and therapeutic change. Psychotherapy: Theory, Research, Practice, Training, 45, 491–506.
doi:10.1037/a0014335
Cuijpers, P., van Straten, A., Schuurmans, J., van Oppen, P., Hollon, S. D., & Andersson, G.
(2010). Psychotherapy for chronic major depression and dysthymia: A meta-analysis.
Clinical Psychology Review, 30, 51–62. doi:10.1037/a0014335
Davila, J., Hammen, C., Burge, D., Paley, B., & Daley, S. E. (1995). Poor interpersonal problem
solving as a mechanism of stress generation in depression among adolescent women.
Journal of Abnormal Psychology, 104, 592–600. doi:10.1037/0021–843X.104.4.592
de Jong, R., Treiber, R., & Henrich, G. (1986). Effectiveness of two psychological treatments
for inpatients with severe and chronic depressions. Cognitive Therapy and Research, 10,
645–663. doi:10.1007/BF01173752
Devanand, D. P., Adorno, E., Cheng, J., Burt, T., Pelton, G. H., Roose, S. P., & Sackeim,
H. A. (2004). Late onset dysthymic disorder and major depression differ from early
onset dysthymic disorder and major depression in elderly outpatients. Journal of Affective
Disorders, 78, 259–267. doi:10.1016/S0165-0327(02)00307–5
Donohue, J. M., & Pincus, H. A. (2007). Reducing the societal burden of depression: A review
of economic costs, quality of care and effects of treatment. Pharmacoeconomics, 25, 7–24.
Dunner, D. L., Schmaling, K. B., Hendrickson, H., Becker, J., Lehman, A., & Bea, C. (1996).
Cognitive therapy versus fluoxetine in the treatment of dysthymic disorder. Depression, 4,
34–41. doi:10.1002/(SICI)1522-7162(1996)4:1<34::AID-DEPR4>3.0.CO;2-F
Eaton, W. W., Shao, H., Nestadt, G., Lee, H. B., Bienvenu, O. J., & Zandi, P. (2008).
Population-based study of first onset and chronicity in major depressive disorder. Archives
Elkin, I., Shea, M. T., Watkins, J. T., Imber, S. D., Sotsky, S. M., Collins, J. F., et al.
(1989). National Institute of Mental Health Treatment of Depression Collaborative
Research Program. General effectiveness of treatments. Archives of General Psychiatry,
46, 971–983.
Evans, S., Cloitre, M., Kocsis, J. H., Keitner, G. I., Holzer, C. P., & Gniwesch, L. (1996).
Social-vocational adjustment in unipolar mood disorders: Results of the DSM-IV field
trial. Journal of Affective Disorders, 38, 73–80. doi:10.1016/0165-0327(95)00045-3
Garyfallos, G., Adamopoulou, A., Karastergiou, A., Voikli, M., Sotiropoulou, A., Donias, S., …
Paraschos, A. (1999). Personality disorders in dysthymia and major depression. Acta
Psychiatrica Scandinavica, 99, 332–340. doi:10.1111/j.1600-0447.1999.tb07238.x
Geerlings, S. W., Beekman, A. T. F., Deeg, D. J. H., Twisk, J. W. R., & Tilburg, W. V. (2002).
Duration and severity of depression predict mortality in older adults in the community.
Psychological Medicine, 32. doi:10.1017/S0033291702005585
Gilmer, W. S., Trivedi, M. H., Rush, A. J., Wisniewski, S. R., Luther, J., Howland, R.
H., … Alpert, J. (2005). Factors associated with chronic depressive episodes: A prelim-
inary report from the STAR-D project. Acta Psychiatrica Scandinavica, 112, 425–433.
doi:10.1111/j.1600-0447.2005.00633.x
Gureje, O. (2011). Dysthymia in a cross-cultural perspective. Current Opinion in Psychiatry,
24, 67–71. doi:10.1097/YCO.0b013e32834136a5
Harmon, S. C., Lambert, M. J., Smart, D. M., Hawkins, E., Nielsen, S. L., Slade, K., &
Lutz, W. (2007). Enhancing outcome for potential treatment failures: Therapist–client
feedback and clinical support tools. Psychotherapy Research, 17 , 379–392.
Harpin, R. E., Liberman, R. P., Marks, I., Stern, R., & Bohannon, W. E. (1982). Cognitive-
behavior therapy for chronically depressed patients. A controlled pilot study. Journal of
Nervous & Mental Disease, 170, 295–301.
Hellerstein, D. J., Agosti, V., Bosi, M., & Black, S. R. (2010). Impairment in psychosocial
functioning associated with dysthymic disorder in the NESARC study. Journal of Affective
Disorders, 127 , 84–88. doi:10.1016/j.jad.2010.04.013
Hellerstein, D. J., Little, S. A., Samstag, L. W., Batchelder, S., Muran, J. C., Fedak, M., …
Winston, A. (2001). Adding group psychotherapy to medication treatment in dysthymia:
A randomized prospective pilot study. Journal of Psychotherapy Practice & Research, 10,
93–103.
Hollon, S. D., & Ponniah, K. (2010). A review of empirically supported psychological therapies
for mood disorders in adults. Depression & Anxiety, 27 , 891–932. doi:10.1002/da.20741
Holm-Denoma, J. M., Berlim, M. T., Fleck, M. P., & Joiner, T. E., Jr. (2006). Double
depression in adult psychiatric outpatients in Brazil: Distinct from major depression?
Psychiatry Research, 144, 191–196. doi:10.1016/j.psychres.2005.06.011
Keller, M. B., Klein, D. N., Hirschfeld, R. M., Kocsis, J. H., McCullough, J. P., Miller, I.,
et al. (1995). Results of the DSM-IV mood disorders field trial. American Journal of
Keller, M. B., Lavori, P. W., Mueller, T. I., Endicott, J., Coryell, W., Hirschfeld, R. M., &
Shea, T. (1992). Time to recovery, chronicity, and levels of psychopathology in major
depression. A 5-year prospective follow-up of 431 subjects. Archives of General Psychiatry,
49, 809–816.
Keller, M. B., McCullough, J. P., Klein, D. N., Arnow, B., Dunner, D. L., Gelenberg, A. J., …
Zajecka, J. (2000). A comparison of nefazodone, the cognitive behavioral-analysis system
of psychotherapy, and their combination for the treatment of chronic depression. New
England Journal of Medicine, 342, 1462–1470.
Keller, M. B., & Shapiro, R. W. (1982). “Double depression”: Superimposition of acute
depressive episodes on chronic depressive disorders. American Journal of Psychiatry, 139,
438–442.
Kessler, R. C., Akiskal, H. S., Ames, M., Birnbaum, H., Greenberg, P., Hirschfeld, R. M., …
Wang, P. S. (2006). Prevalence and effects of mood disorders on work performance in
a nationally representative sample of U.S. workers. American Journal of Psychiatry, 163,
1561–1568. doi:10.1176/appi.ajp.163.9.1561
Kessler, R. C., McGonagle, K. A., Nelson, C. B., Hughes, M., Swartz, M., & Blazer, D. G.
(1994). Sex and depression in the National Comorbidity Survey. II: Cohort effects.
Journal of Affective Disorders, 30, 15–26. doi:10.1016/0165-0327(94)90147–3
Klein, D. N. (2008). Classification of depressive disorders in the DSM-V: Proposal for a
two-dimension system. Journal of Abnormal Psychology, 117 , 552–560.
Klein, D. N., Arnow, B. A., Barkin, J. L., Dowling, F., Kocsis, J. H., Leon, A. C., … Wisniewski,
S. R. (2009). Early adversity in chronic depression: Clinical correlates and response to
pharmacotherapy. Depression & Anxiety, 26, 701–710. doi:10.1002/da.20577
Klein, D. N., Riso, L. P., Donaldson, S. K., Schwartz, J. E., Anderson, R. L., Ouimette, P. C., …
Aronson, T. A. (1995). Family study of early-onset dysthymia. Mood and personality
disorders in relatives of outpatients with dysthymia and episodic major depression and
normal controls. Archives of General Psychiatry, 52, 487–496.
Klein, D. N., Santiago, N. J., Vivian, D., Blalock, J. A., Kocsis, J. H., Markowitz, J.
C., … Keller, M. B. (2004). Cognitive-behavioral analysis system of psychotherapy
as a maintenance treatment for chronic depression. Journal of Consulting & Clinical
Psychology, 72, 681–688. doi:10.1037/0022-006X.72.4.681
Klein, D. N., Schatzberg, A. F., McCullough, J. P., Keller, M. B., Dowling, F., Goodman, D.,
… Harrison, W. M. (1999). Early- versus late-onset dythymic disorder: Comparison in
out-patients with superimposed major depressive episodes. Journal of Affective Disorders,
52, 187–196.
Klein, D. N., Schwartz, J. E., Rose, S., & Leader, J. B. (2000). Five-year course and outcome
of dysthymic disorder: A prospective, naturalistic follow-up study. American Journal of
Psychiatry, 157 , 931–939. doi:10.1176/appi.ajp.157.6.931
Klein, D. N., Shankman, S. A., & Rose, S. (2006). Ten-year prospective follow-up study of
the naturalistic course of dysthymic disorder and double depression. American Journal of
Klein, D. N., Taylor, E. B., Dickstein, S., & Harding, K. (1988). The early–late onset distinction
in DSM-III-R dysthymia. Journal of Affective Disorders, 14, 25–33. doi:10.1016/0165-
0327(88)90068–7
Kocsis, J. H., Gelenberg, A. J., Rothbaum, B. O., Klein, D. N., Trivedi, M. H., Manber, R., …
Thase, M. E. (2009). Cognitive behavioral analysis system of psychotherapy and brief
supportive psychotherapy for augmentation of antidepressant nonresponse in chronic
depression: The REVAMP Trial. Archives of General Psychiatry, 66, 1178–1188.
Kocsis, J. H., Leon, A. C., Markowitz, J. C., Manber, R., Arnow, B., Klein, D. N., &
Thase, M. E. (2009). Patient preference as a moderator of outcome for chronic forms of
major depressive disorder treated with nefazodone, cognitive behavioral analysis system
of psychotherapy, or their combination. Journal of Clinical Psychiatry, 70, 354–361.
doi:10.4088/JCP.08m04371
Kwan, B. M., Dimidjian, S., & Rizvi, S. L. (2010). Treatment preference, engagement, and
clinical improvement in pharmacotherapy versus psychotherapy for depression. Behavior
Research & Therapy, 48, 799–804.
Lambert, M. J., Harmon, C., Slade, K., Whipple, J. L., & Hawkins, E. J. (2005). Providing
feedback to psychotherapists on their patients’ progress: Clinical results and practice
suggestions. Journal of Clinical Psychology, 61, 165–174. doi:10.1002/jclp.20113
Lambert, M. J., & Ogles, B. M. (2004). The efficacy and effectiveness of psychotherapy. In
M. J. Lambert (Ed.), Bergin and Garfield’s handbook of psychotherapy and behavior change
(5th ed., pp. 139–193). New York, NY: John Wiley & Sons, Inc.
Lambert, M. J., Whipple, J., Smart, D., Vermeersch, D., & Nielsen, S. L. (2001). The effects
of providing therapists with feedback on patient progress during psychotherapy: Are
outcomes enhanced? Psychotherapy Research, 11, 49–68. doi:10.1080/713663852
Leader, J. B., & Klein, D. N. (1996). Social adjustment in dysthymia, double depres-
sion and episodic major depression. Journal of Affective Disorders, 37 , 91–101.
doi:10.1016/0165-0327(95)00076–3
Leykin, Y., DeRubeis, R. J., Gallop, R., Amsterdam, J. D., Shelton, R. C., & Hollon, S. D.
(2007). The relation of patients’ treatment preferences to outcome in a randomized
clinical trial. Behavior Therapy, 38, 209–217. doi:10.1016/j.beth.2006.08.002
Lizardi, H., & Klein, D. N. (2000). Parental psychopathology and reports of the childhood
home environment in adults with early-onset dysthymic disorder. Journal of Nervous &
Mental Disease, 188, 63–70.
Lizardi, H., Klein, D. N., Ouimette, P. C., Riso, L. P., Anderson, R. L., & Donaldson, S. K.
(1995). Reports of the childhood home environment in early-onset dysthymia and episodic
major depression. Journal of Abnormal Psychology, 104, 132–139. doi:10.1037/0021-
843X.104.1.132
McCullough, J. P. (2000). Treatment of chronic depression: Cognitive Behavioral Analysis System
of Psychotherapy (CBASP). New York, NY: Guilford Press.
McCullough, J. P., Jr. (2003). Treatment for chronic depression using Cognitive Behavioral
Analysis System of Psychotherapy (CBASP). Journal of Clinical Psychology, 59, 833–846.
McCullough, J. P., Jr., Klein, D. N., Borian, F. E., Howland, R. H., Riso, L. P., Keller,
M. B., & Banks, P. L. (2003). Group comparisons of DSM-IV subtypes of chronic
depression: Validity of the distinctions, part 2. Journal of Abnormal Psychology, 112,
614–622. doi:10.1037/0021-843X.112.4.614
McCullough, J. P., Jr., Klein, D. N., Keller, M. B., Holzer, C. E., 3rd, Davis, S. M.,
Kornstein, S. G., … Harrison, W. M. (2000). Comparison of DSM-III-R chronic major
depression and major depression superimposed on dysthymia (double depression): Validity
of the distinction. Journal of Abnormal Psychology, 109, 419–427. doi:10.1037/0021-
843X.109.3.419
McCullough, J. P., Roberts, W. C., McCune, K. J., Kaye, A. L., Hampton, C., Caldwell,
S. B., … Kornstein, S. G. (1994). Social adjustment, coping style, and clinical
course among DSM-III-R community unipolar depressives. Depression, 2, 36–42.
doi:10.1002/depr.3050020105
Miller, I. W., Norman, W. H., & Keitner, G. I. (1999). Combined treatment for patients
with double depression. Psychotherapy and Psychosomatics, 68, 180–185. doi:10.1159/
000012330
Mondimore, F. M., Zandi, P. P., Mackinnon, D. F., McInnis, M. G., Miller, E. B., Crowe, R.
P., … Potash, J. B. (2006). Familial aggregation of illness chronicity in recurrent, early-
onset major depression pedigrees. American Journal of Psychiatry, 163, 1554–1560.
doi:10.1176/appi.ajp.163.9.1554
Moussavi, S., Chatterji, S., Verdes, E., Tandon, A., Patel, V., & Ustun, B. (2007). Depression,
chronic diseases, and decrements in health: Results from the World Health Surveys.
Lancet, 370, 851–858. doi:10.1016/S0140-6736(07)61415-9
Mueller, T. I., Keller, M. B., Leon, A. C., Solomon, D. A., Shea, M. T., Coryell, W., &
Endicott, J. (1996). Recovery after 5 years of unremitting major depressive disorder.
Nemeroff, C. B., Heim, C. M., Thase, M. E., Klein, D. N., Rush, A. J., Schatzberg, A. F.,
… Keller, M. B. (2003). Differential responses to psychotherapy versus pharmacotherapy
in patients with chronic forms of major depression and childhood trauma. Proceedings of
the National Academy of Sciences of the United States of America, 100, 14293–14296.
doi:10.1073/pnas.2336126100
Penninx, B. W., Guralnik, J. M., Pahor, M., Ferrucci, L., Cerhan, J. R., Wallace, R. B., &
Havlik, R. J. (1998). Chronically depressed mood and cancer risk in older per-
sons. Journal of the National Cancer Institute, 90, 1888–1893. doi:10.1093/jnci/
90.24.1888
Pepper, C. M., Klein, D. N., Anderson, R. L., Riso, L. P., Ouimette, P. C., & Lizardi, H.
(1995). DSM-III-R axis II comorbidity in dysthymia and major depression. American
Persons, J. B., Roberts, N. A., Zalecki, C. A., & Brechwald, W. A. G. (2006). Naturalistic
outcome of case formulation-driven cognitive-behavior therapy for anxious depressed
outpatients. Behaviour Research and Therapy, 44, 1041–1051. doi:10.1016/j.brat.2005.
08.005
Ravindran, A. V., Anisman, H., Merali, Z., Charbonneau, Y., Telner, J., Bialik, R. J., …
Griffiths, J. (1999). Treatment of primary dysthymia with group cognitive therapy and
pharmacotherapy: Clinical symptoms and functional impairments. American Journal of
Psychiatry, 156, 1608–1617.
Rhebergen, D., Batelaan, N. M., de Graaf, R., Nolen, W. A., Spijker, J., Beekman, A.
T., & Penninx, B. W. (2011). The 7-year course of depression and anxiety in the
general population. Acta Psychiatrica Scandinavica, 123, 297–306. doi:10.1111/j.1600-
0447.2011.01677.x
Riolo, S. A., Nguyen, T. A., Greden, J. F., & King, C. A. (2005). Prevalence of depression by
race/ethnicity: Findings from the National Health and Nutrition Examination Survey III.
American Journal of Public Health, 95, 998–1000. doi:10.2105/AJPH.2004.047225
Rush, A. J., Wisniewski, S. R., Zisook, S., Fava, M., Sung, S. C., Haley, C. L., … Hollon, S. D.
(2011). Is prior course of illness relevant to acute or longer-term outcomes in depressed
out-patients? A STAR*D report. Psychological Medicine, 42, 1–19.
Sartorius, N. (2001). The economic and social burden of depression. Journal of Clinical
Psychiatry, 62(Suppl. 15), 8–11.
Satyanarayana, S., Enns, M. W., Cox, B. J., & Sareen, J. (2009). Prevalence and correlates
of chronic depression in the Canadian community health survey: Mental health and
well-being. Canadian Journal of Psychiatry, 54, 389–398.
Schatzberg, A. F., Rush, A. J., Arnow, B. A., Banks, P. L., Blalock, J. A., Borian, F. E., …
Keller, M. B. (2005). Chronic depression: Medication (nefazodone) or psychotherapy
(CBASP) is effective when the other is not. Archives of General Psychiatry, 62, 513–520.
Schramm, E., Zobel, I., Dykierek, P., Kech, S., Brakemeier, E. L., Kulz, A., & Berger, M.
(2011). Cognitive behavioral analysis system of psychotherapy versus interpersonal psy-
chotherapy for early-onset chronic depression: A randomized pilot study. Journal of
Affective Disorders, 129, 109–116. doi:10.1016/j.jad.2010.08.003
Shimokawa, K., Lambert, M. J., & Smart, D. W. (2010). Enhancing treatment outcome
of patients at risk of treatment failure: Meta-analytic and mega-analytic review of a
psychotherapy quality assurance system. Journal of Consulting and Clinical Psychology, 78,
298–311. doi:10.1037/a0019247
Simon, G. E. (2003). Social and economic burden of mood disorders. Biological Psychiatry,
54, 208–215. doi:10.1016/S0006–3223(03)00420–7
Simon, G. E, Ormel, J., VonKorff, M., & Barlow, W. (1995). Health care costs associated with
depressive and anxiety disorders in primary care. American Journal of Psychiatry, 152,
352–357.
Spijker, J., de Graaf, R., Bijl, R. V., Beekman, A. T., Ormel, J., & Nolen, W. A. (2002).
Duration of major depressive episodes in the general population: Results from The
Netherlands Mental Health Survey and Incidence Study (NEMESIS). British Journal of
Stewart, W. F., Ricci, J. A., Chee, E., Hahn, S. R., & Morganstein, D. (2003). Cost of
lost productive work time among US workers with depression. Journal of the American
Medical Association, 289, 3135–3144.
Thase, M. E., Reynolds, C. F., 3rd, Frank, E., Simons, A. D., McGeary, J., Fasiczka, A. L., …
Kupfer, D. J. (1994). Do depressed men and women respond similarly to cognitive
behavior therapy? American Journal of Psychiatry, 151, 500–505.
Ustun, T. B., Ayuso-Mateos, J. L., Chatterji, S., Mathers, C., & Murray, C. J. L. (2004).
Global burden of depressive disorders in the year 2000. British Journal of Psychiatry, 184,
386–392. doi:10.1192/bjp.184.5.386
Weissman, M. M., Leaf, P. J., Bruce, M. L., & Florio, L. (1988). The epidemiology of
dysthymia in five communities: Rates, risks, comorbidity, and treatment. American
Wells, K. B., Stewart, A., Hays, R. D., Burnam, M. A., Rogers, W., Daniels, M., … Ware, J.
(1989). The functioning and well-being of depressed patients. Results from the Medical
Outcomes Study. Journal of the American Medical Association, 262, 914–919.
Whipple, J. L., Lambert, M. J., Vermeersch, D. A., Smart, D. W., Nielsen, S. L., & Hawkins,
E. J. (2003). Improving the effects of psychotherapy: The use of early identification
of treatment and problem-solving strategies in routine practice. Journal of Counseling
Psychology, 50, 59–68. doi:10.1037/0022-0167.50.1.59
Wiersma, J. E., Hovens, J. G., van Oppen, P., Giltay, E. J., van Schaik, D. J., Beekman, A.
T., & Penninx, B. W. (2009). The importance of childhood trauma and childhood life
events for chronicity of depression in adults. Journal of Clinical Psychiatry, 70, 983–989.
Wiersma, J. E., van Oppen, P., van Schaik, D. J., van der Does, A. J., Beekman, A. T., &
Penninx, B. W. (2011). Psychological characteristics of chronic depression: A longitudinal
cohort study. Journal of Clinical Psychiatry, 72, 288–294.
Yang, T., & Dunner, D. L. (2001). Differential subtyping of depression. Depression & Anxiety,
13, 11–17. doi:10.1002/1520-6394(2001)13:1<11::AID-DA2>3.0.CO;2-W
Youngren, M. A., & Lewinsohn, P. M. (1980). The functional relation between depression
and problematic interpersonal behavior. Journal of Abnormal Psychology, 89, 333–341.
doi:10.1037/0021-843X.89.3.333
50
Bipolar Disorder
Samantha J. Moshier and Michael W. Otto
Characterized by recurrent periods of mood instability, bipolar disorder (BD) is a

chronic illness associated with significant social and functional impairment (Judd
et al., 2008), high rates of suicidality (Brown, Beck, Steer, & Grisham, 2000), and
tremendous global burden (World Health Organization, 2001). Pharmacotherapy
(with mood stabilizers in particular) has been and remains the gold standard for
treatment of BD. However, in the past two decades it has become clear that
psychosocial interventions, including cognitive behavioral therapy (CBT), can be
powerful adjunctive treatment strategies for BD. In this chapter we discuss the
empirical status of CBT for BD across a range of treatment targets, the elements
of treatment, and common clinical issues unique to this patient group. In order
to provide readers with a solid foundation, we begin with an overview of the
phenomenology of BD and current standards for pharmacotherapy.
Clinical Phenomenology
The defining symptoms of BD include the occurrence of a manic, hypomanic, or

mixed mood episode. According to DSM-IV-TR criteria, a full manic episode consists
of a period of at least one week (unless interrupted by treatment or hospitalization)
of abnormally elevated, expansive, or irritable mood. In addition, at least three other
symptoms must be present, including inflated self-esteem, decreased need for sleep,
increased talkativeness, flight of ideas, distractibility, increased goal-directed activities,
and excessive involvement in risky activities (American Psychiatric Association, 2000).
A hypomanic episode is defined by the same symptoms as a manic episode, with the
qualification that these are present for at least 4 days but less than one week. A mixed
episode is characterized by mood which rapidly shifts between sadness, irritability, and

DOI: 10.1002/9781118528563.wbcbt50
euphoria. The bipolar disorder I subtype refers to individuals who have experienced
a full manic episode, whereas the bipolar II subtype refers to those who have met
criteria for a hypomanic episode and one or more major depressive episodes (but not
a full manic episode). Individuals with cyclothymic disorder experience alternating
periods of high and low moods that are not severe enough to meet criteria for a full
mood episode, but last for over 2 years.
Estimates of the lifetime prevalence of BD fall in the range of 1–3% (Kessler, Chiu,
Demler, & Walters, 2005; Regier et al., 1990). The average age of onset is in the
mid-teenage years, with earlier age of onset predicting a more severe course (Perlis
et al., 2004; Yatham, Kauer-Sant’anna, Bond, Lam, & Torres, 2009). Although the
disorder presents equally among men and women (Kessler et al., 1994), studies have
found that women typically have an earlier age of onset (Suominen et al., 2007),
a higher rate of recurrence, and a lower rate of comorbid substance use disorder
(Suominen et al., 2009).
The course of BD is chronic, with more than 90% of individuals with BD expe-
riencing recurrence during their lifetime (Solomon, Keitner, Miller, & Shea, 1995).
Despite the use of mood-stabilizing medications, data suggest that 40% of patients
relapse within one year, and the majority (73%) relapse within 5 years (Gitlin,
Swendsen, Heller, & Hammen, 1995; Tohen, Waternaux, & Tsuang, 1990). Impor-
tantly, higher levels of residual symptoms at recovery predict recurrence (Perlis et al.,
2006).
BD is dimensional in nature, with many patients experiencing all levels of affective
symptom severity (Judd et al., 2002; Judd et al., 2003). It is estimated that patients
with BD experience affective symptoms approximately 50% of the time (Joffe, Mac-
Queen, Marriott, & Young, 2004; Judd et al., 2002), and that subsyndromal or
minor depressive symptoms are the most frequently experienced affective symptoms
within both BD subtypes. For example, across subtypes, patients are three-and-a-half
times more likely to experience depressive symptoms than manic symptoms (Judd
et al., 2002; Kupka et al., 2007).
Despite the high prevalence of depressive episodes in BD, it should also be noted
that nearly one-third of individuals with BD do not experience a major depressive
episode during their lifetime (see Cuellar, Johnson, & Winters, 2005, for a review).
However, these individuals may be less likely to be seen clinically, given that depressive
symptoms are often a key motivating factor for seeking treatment.
BD has profoundly negative effects on educational and occupational attainment,
social relationships, and even physical health quality. Importantly, these impairments
continue into periods of relative wellness (Fagiolini et al., 2005). One 15-year
longitudinal study found that patients with BD I and II were completely unable to
carry out work role functions for 30% and 20% of the time assessed, respectively
(Judd et al., 2008). Others have repeatedly shown that only a minority of patients
(30–40%) return to premorbid levels of occupational, social, or residential functioning
following the first affective episode (MacQueen, Young, & Joffe, 2001). Functional
recovery is further complicated by the consequences of risky or harmful behavior,
and hospitalization, during acute bipolar episodes. A number of factors are associated
with poorer functional outcomes, including cognitive dysfunction (Green, 2006;
Martinez-Aran et al., 2007), number of past mood episodes (MacQueen et al.,
Bipolar Disorder 1191
2001), and premorbid functional status (O’Connell, Mayo, Flatlow, Cuthbertson, &
O’Brien, 1991; Tohen et al., 1990).
In addition to functional impairment, BD is associated with significant medical
and psychiatric comorbidity. Rates of medical conditions including heart disease,
diabetes, and migraines occur at higher rates greater than chance in patients with
BD (Kupfer, 2005), and greater chronicity and severity of BD is associated with
further increases in medical comorbidity (Magalhães et al., 2011). Anxiety disorder
comorbidity is also common, with lifetime prevalence rates of 51% (Simon et al.,
2004b). Rates of substance use comorbidity are estimated to be 21–45% (Brady,
Castro, Lydiard, Malcolm, & Arana, 1991; Goldberg, Garno, Leon, Kocsis, &
Portera, 1999; Kessler et al., 1997; Regier et al., 1990). These common psychiatric
comorbidities further complicate treatment of BD and are associated with decreased
proportion of days well, increased suicide attempts, poorer functioning, and lower
response to medication (Henry et al., 2003; Otto et al., 2006; Simon et al., 2004b).
More specifically, comorbid substance use disorders are associated with decreased
medication adherence (Goldberg et al., 1999; Keck et al., 1996) and more instances
of hospitalization (Brady et al., 1991; Reich, Davies, & Himmelhoch, 1974).
Environmental and psychosocial factors also influence the course, severity, and
response to treatment in BD. Life events can play a powerful role and appear to
differentially influence depressive as compared to manic symptoms. For instance,
negative life events predict greater occurrence of bipolar depression over time (S. L.
Johnson, 2005) as well as delayed recovery (Ellicott, Hammen, Gitlin, Brown, &
Jameson, 1990; S. L. Johnson & Miller, 1997). On the other hand, goal-attainment
life events, particularly those which disrupt sleep or social rhythms, often precede
hypomanic or manic episodes (Johnson et al., 2000; Malkoff-Schwartz et al., 2000).
Much of this research has assumed that the effect of life events and stressors on BD
is consistent throughout the course of the disorder. However, proponents of Post’s
(1992) kindling hypothesis suggest that psychosocial stressors have greater influence
early in the disorder and that mood episodes may become more autonomous over
time. Studies of the validity of the kindling hypothesis in application to BD have
been lacking in methodological rigor and have so far yielded mixed results (Bender
& Alloy, 2011).
Family attitudes and environment are also strongly associated with BD outcomes.
Miklowitz, Goldstein, Nuechterlein, Snyder, and Mintz (1988) found a five-fold
increase in the likelihood of relapse in patients with families with high levels of
expressed emotion (critical attitudes, hostility, overprotection). Patients’ cognitive
styles may also be important; dysfunctional attitudes and negative interpretive biases
have been found to interact with negative life events to predict increased depressive
symptoms in individuals with BD (Reilly-Harrington, Alloy, Fresco, & Whitehouse,
1999).
Suicide is strongly associated with BD. One 20-year longitudinal study of 7,000
psychiatric patients found that those with BD had the highest rates of completed
suicide (Brown et al., 2000). A separate study found that among a group of 406
patients previously hospitalized for BD, 11% committed suicide over a 40-year period
(Angst, Angst, Gerber-Werder, & Gamma, 2005).
Pharmacological Treatment
Mood stabilizers are the standard first-line pharmacotherapy for BD and are rec-
ommended for stabilization following an acute episode as well as for prevention of
episode recurrence. Lithium (Eskalith, Lithobid) has been used to treat BD for over
30 years. Anticonvulsants such as such as divalproex (brand name Depakote) and
lamotrigine (brand name Lamictal), as well as some novel antipsychotics (olanzapine,
risperidone), also demonstrate mood-stabilizing effects.
Complementing mood-stabilizing agents with antidepressants or anxiolytics has
been common clinical practice in the treatment of BD. However, there is growing
evidence that these agents add little clinical benefit. Benzodiazepines are used to
calm acute hypomanic or manic symptoms, or to treat comorbid anxiety, but they
are not likely to speed time to recovery or prevent recurrence (American Psychiatric
Association, 2002; Moller & Nasrallah, 2003; Simon et al., 2004a). Similar lack of
support is present for adjunctive antidepressant treatment (Nemeroff et al., 2001;
Sachs et al., 2007). For example, in STEP-BD, one of the largest randomized
controlled trials (RCTs) of BD to date, adjunctive selective serotonin reuptake
inhibitor treatment failed to outperform placebo when added to a mood-stabilizing
regimen (Sachs et al., 2007). Notably, and described in greater detail later in this
chapter, adjunctive CBT did add benefit to treatment with mood stabilizers (Miklowitz
et al., 2007a). Additionally, a recent meta-analysis of six RCTs (N = 1,034) found
that antidepressant treatment did not differ significantly from placebo (relative risk
= 1.18; p = .06) or standard treatment (relative risk = 1.12; p = .10; Sidor &
MacQueen, 2011).
There has also been concern that antidepressant treatment may increase the risk
of mood switches or recurrence. Although one meta-analysis found no evidence
for increased risk of mood switches (Sidor & MacQueen, 2011), it appears that
antidepressant use following an acute manic or mixed episode may be associated with
risk of recurrence. A study of over 2,000 patients found that one-third continued
antidepressant use in the 12 months following an index episode, and that this group
of patients had 1.43–1.51 times increased odds of being rehospitalized within the
next 12 months (Sussman et al., 2012).
Cognitive Behavioral Therapy for Bipolar Disorder: Rationale

and Core Elements
Although it was once thought that psychosocial interventions such as CBT had little
place in the treatment of BD, significant support for their use has developed in the
past two decades. This has occurred for several reasons. Despite significant advances
made in the development of mood-stabilizing medications for BD, clear limitations
exist in their efficacy, as evidenced by high rates of relapse and residual symptoms and
low rates of functional recovery (Judd et al., 2002; Judd et al., 2008; Perlis et al.,
2006). Additionally, a large body of research has documented a host of modifiable
psychosocial variables, such as cognitive style, family communication patterns, and life
events, that influence illness course and outcome. This knowledge has led to increased
demand for interventions that directly target these variables.
The range of interventions available in CBT for BD can be grouped into three
broad elements: informational, cognitive restructuring, and activity assignments.
Informational Intervention
Informational components are at the foundation of CBT for BD. These include
psychoeducation about the nature of BD, common symptoms, and relapse prevention;
as well as didactic instruction around the CBT model. Enhancing understanding of
the disorder and its symptoms from a biological and stress-vulnerability model can
aid motivation for medication adherence and reduction of other risk factors for
recurrence. In addition, building patients’ knowledge about the self-perpetuating
cycle of thoughts, feelings, and behaviors that contribute to depressive symptoms
lays the groundwork for subsequent efforts at cognitive restructuring and behavior
change.
According to the cognitive behavioral model, symptoms are maintained by inaccurate
or unhelpful thoughts which influence emotions and behaviors (A. T. Beck, 1979).
Cognitive restructuring strategies are used throughout treatment to address depres-
sogenic automatic thoughts and core beliefs, as well as comorbid conditions such as
anxiety disorders. Additionally, cognitive restructuring can be used to identify and
challenge thoughts that may reduce medication adherence (e.g., “I’m not fun when
I’m taking my medication”).
The aim of cognitive restructuring is to help patients identify maladaptive thoughts
and consider more accurate or useful perspectives. This is encouraged using a number
of strategies such as Socratic questioning, guided discussions, and behavioral exper-
iments in which patients test out a belief. It is essential that cognitive restructuring
is not viewed as a simple exercise in replacing negative thoughts with positive ones.
Instead, it is a process of thorough and collaborative evaluation of existing thoughts
and the guided development of more adaptive, accurate thoughts. This process may
involve framing the automatic thought as a hypothesis and examining the evidence
for its accuracy, or treating a thought as a behavior and evaluating its usefulness.
Activity Assignments
Activity assignments are used to encourage depressed patients to incorporate pleasant
and rewarding activities into their schedule. A first step toward this goal is collaborative
assessment of the patient’s current activities, which can provide a platform for cognitive
restructuring around the relevant beliefs, such as expected level of performance. The
inclusion of regularly scheduled rewarding activities attenuates mood symptoms and
can also be used as a stabilizing tool once recovery is achieved. In addition, activity
monitoring serves an early intervention tool; patients can learn to recognize difficulties
in completing activities as a sign of a forthcoming mood episode.
Cognitive Behavioral Therapy: Targets for Treatment

and Practical Issues
Given the complex nature of BD, the aims of CBT for BD are several, including (a)
increasing medication adherence, (b) early recognition and intervention, (c) alleviating
acute bipolar depression, (d) stress and lifestyle management, and (e) treatment of
comorbid conditions (Otto, Reilly-Harrington, & Sachs, 2003). We will discuss the
empirical support for CBT in relation to each of these targets and describe specific
interventions within each target area in greater detail. We begin with a brief description
of common clinical issues that are important to consider when initiating CBT for BD.
Structure of Treatment
Otto et al. (2009a, 2009b) recently manualized a comprehensive CBT package
which attends to each of the targets described above. Treatment is organized around
the delivery of 30 sessions and is structured to distinguish between four formal
treatment phases: a depression-focused phase, a treatment contract phase, a problem
list phase, and a well-being phase. In most cases, patients initiate treatment during
an acute depressive episode, and, hence, alleviation of these symptoms should be the
primary goal. Therefore, this phase shares many of the components of traditional
cognitive therapy for unipolar depression, including cognitive restructuring and
related behavioral experiments (A. T. Beck, 1979; J. S. Beck, 1995). An additional
emphasis is placed on activity management, explaining the diathesis–stress model and
the importance of medication, as well as on monitoring and recognition of prodromal
symptoms. After amelioration of depressive symptoms, a treatment contract may be
introduced to create a plan for prevention, early recognition, and efficient treatment
of future mood episodes. In the third phase, treatment elements may be applied
flexibly based on a problem list developed in association with the patient. Elements of
treatment may range from problem solving to social skills training to management of
extreme emotions. Finally, the well-being phase encourages patients to incorporate
well-being promotion and relapse prevention strategies into daily life.
Structure of Therapy Sessions

In keeping with the goal-oriented approach of CBT, the format of each session is
clear, structured, and problem-focused. We suggest that the session begin with a
review of the patient’s mood chart (described later in this chapter) and a review of
homework. With this information, the therapist and patient may then collaboratively
set an agenda. After the material on the agenda has been addressed, the therapist may
wish to ask the patient to summarize what was discussed. Review and summary of
the session is especially important for patients with BD, given the known attentional,
memory, and executive function impairment that commonly exists with BD and
depression (Sole et al., 2011; Xu et al., 2012). Each session should conclude with
assignment of homework (or “home practice”) that fits with the material covered in
that session. It is especially important that the therapist reserve time to identify and
problem solve potential barriers to homework completion.
Treatment Engagement and Motivation

Attendance and homework compliance are primary concerns relating to treatment
engagement; both can present challenges for clinicians working with patients with
BD. For instance, individuals receiving CBT in the STEP-BD study attended an
average of 13 of the 30 sessions in the treatment protocol (Miklowitz et al., 2007a).
More research is needed to explore factors that might lead to nonattendance and
intervention strategies that might promote treatment engagement.
Cognitive Behavioral Therapy for Medication Adherence

in Bipolar Disorder
Medication adherence is a major clinical problem in the treatment of BD. Rates of
nonadherence have been estimated to range from 18 to 52% (Scott et al., 2001). In a
sample of over 1,000 patients prescribed lithium, the median duration of continuous
adherence was only 76 days (R. E. Johnson & McFarland, 1996). There are several
likely factors that contribute to this issue. As is the case with most long-term
medication regimens, patients do not receive any immediate symptom reduction or
“reward” for regular adherence, and often experience frustrating and uncomfortable
side effects. Thus, patients must be motivated to maintain adherence by memory of
previous mood episodes and by understanding that BD is a relapsing condition for
which preventative care is needed. This is particularly challenging for patients with
BD, who may remember periods of mania as being pleasant or productive. This is
further complicated by the fact that BD is characterized by sustained attention deficits
and high levels of trait impulsivity (Clark, Iversen, & Goodwin, 2002; Swann, Lijffijt,
Lane, Steinberg, & Moeller, 2009).
Medication adherence was the main target of the earliest study of CBT for
BD (Cochran, 1984). In a brief, six-session protocol, therapists introduced Beck’s
cognitive model and identified and modified thoughts and behaviors that were
interfering with medication adherence. Compared to a treatment-as-usual group,
participants in the intervention condition demonstrated significantly higher lithium
adherence at endpoint and 6-month follow-up assessments. More specifically, eight
of the 14 patients in the CBT condition were rated as compliant on a three-point
Compliant Index, while only two of the 14 patients in the standard treatment group
were rated as compliant (U = 34, p < .05). Others have since confirmed the effects
of CBT on medication adherence in BD (e.g., Lam et al., 2003). While many
have used strategies involving cognitive restructuring, Colom et al. (2003) found
that adherence increased after participation in a group psychoeducation protocol.
Following 21 sessions discussing the nature and symptoms of BD and early signs and
symptoms of mood episodes, patients demonstrated higher and more stable levels of
serum lithium than patients who received standard care.
Given the high cost of nonadherence, management of the patient’s medication
regimen is essential. Time should be devoted to reviewing adherence at the beginning
of each session; this can easily be incorporated into mood charting, described in
more detail later in this chapter. If this assessment reveals difficulties with adherence,
the therapist should assess barriers to adherence, which commonly include side
effects, beliefs about being “dependent” on medications, low social support, absence
of symptoms that indicate the necessity of medication, and conflicts between the
medication-taking schedule and other demands on the patient’s time.
Interventions that educate the patient about the nature of BD and reasons for
regular medication-taking can have positive effects on adherence (e.g., Colom et al.,
2003). These interventions can also help correct erroneous beliefs that contribute
to nonadherence, which commonly include, “I don’t need medication when I feel
well” or, “It’s pointless, the other medications didn’t work.” Cognitive restructuring
and related behavioral experiments can also be used to evaluate the accuracy of these
beliefs.
As with any psychoeducation, care needs to be taken to avoid presenting patients
with a laundry list or lecture of the reasons to continue medication treatment.
Strategies adapted from motivational enhancement therapy (MET) may be useful
here, where treatment recommendations are firmly grounded within the patient’s
stated goals. As such, the therapist should use guided questioning to elicit from the
patient the reasons that continued treatment may be helpful for him or her. What
symptoms does the patient wish to avoid in the future? How has treatment helped
him or her in the past? Therapists should ask patients to describe previous mood
episodes, the life circumstances surrounding them, and the type and effectiveness of
treatment during those times.
Lastly, patients who continually forget or have other time demands interfering with
medication adherence may benefit from behavioral strategies (see Safren et al., 2001).
Linking medication taking with daily events such as teeth-brushing or lunch can make
medication taking as automatic as these other regular habits. Those who travel or
spend most of the day away from home can be encouraged to carry a second supply
of pills in their bag or car. Regular monitoring of medication adherence may identify
barriers and alert the therapist when adherence begins to lapse.
Cognitive Behavioral Therapy for Early Recognition and Intervention

in Bipolar Disorder
Recognizing that most full mood episodes are preceded by prodromal symptoms
in the weeks prior to onset, Perry, Tarrier, Morriss, McCarthy, and Limb (1999)
developed and evaluated a protocol focused on (a) recognizing early signs of a manic
or depressive episode and (b) developing and rehearsing an action plan. The authors
compared this brief (7–12 sessions) intervention in a group of individuals with BD
who had experienced a relapse within the previous year. Those who received CBT
saw a significantly reduced likelihood of manic relapse over the next 18 months (27%
relapse rate in the CBT condition compared with 57% relapse rate in the control
condition, p =.013) as well as improvements in social functioning and employment.

A number of other more comprehensive treatment protocols have included similar
interventions and have demonstrated similar positive effects on time until recurrence
(Lam et al., 2003, Scott et al., 2001).
Two key elements for intervention in this area are the development of a treatment
contract (see Box 50.1) and regular self-monitoring. Establishing a treatment contract
is useful at any stage of illness, but may be especially relevant as the patient begins to
recover from an acute mood episode. The treatment contract should be explained to
the patient as an important step in managing the disorder. It provides a plan for the
early detection of and more effective coping with bipolar episodes, which, in turn,
may decrease the intensity and length of episodes as well as decrease the subsequent
psychosocial disruption. Importantly, the patient now has a say in what he or she
wants to happen when he or she is ill. Planning ahead allows the patient to retain
power and utilize the treatment providers and support systems of his or her choice
when a mood episode occurs.
Box 50.1 Treatment contract

The purpose of this contract is to organize my care for bipolar disorder, with
attention to both the prevention of mood episodes and the efficient treatment
of these episodes should they occur. My first step in guiding my care is the
selection of my support team. The team members should include people with
whom I have regular contact, who can help me identify episodes should they
occur and help me put into practice some of the tools I use to manage my
bipolar disorder.
(Select members of your treatment team to be part of your support team;
for example, you may select your psychiatrist, psychologist, social worker, or
primary care physician.)
Treatment Contract: Support Team

Role/relationship Name Contact information
My psychiatrist Phone:
My therapist Phone:
My PCP Phone:
Phone:
Phone:
Phone:
My second step in developing this contract is to identify tools I will use to
help control my bipolar disorder so that I can best pursue my life goals. Many of
these tools have been identified in previous chapters. My goal now is to identify
some of the tools that I want to plan to use.
For every tool or strategy listed, please place a checkmark next to the ones
you plan to incorporate as a part of your treatment contract.
(Continued)
Monitor My Mood for Early Intervention
I know from my own patterns that I should watch out for the following signs:
Depressed thoughts
Depressed symptoms
Depressed behavior
Hypomanic thoughts
Hypomanic symptoms
Hypomanic behaviors
Take Early Action if I Notice Signs of Depression or Mania

Contact my psychiatrist at phone no. .
Contact my therapist at phone no. .
Contact my support person at phone no. .
Maintain a regular schedule of sleep and activities.
Maintain a regular schedule of pleasant events.
Evaluate my thoughts for negative or hyperpositive thinking.
Talk with my family about ways to cope.
Limit my alcohol use and avoid all nonmedication drugs.
Other __________________________________________.
Other __________________________________________.
Other __________________________________________.
Other __________________________________________.
Take Active Steps to Keep My Mood in the Desired Range

Take all medications as prescribed by my doctor.
Maintain regular appointments with my psychiatrist at ______/month.
Maintain regular appointments with my therapist at ______/month.
Keep a regular sleep schedule.
Maintain a schedule including at least three valued activities each day as a
buffer against stress.
Avoid excessive use of alcohol.
Avoid all use of illicit drugs.
Use no alcohol for the next 30 days.
Use no recreational drugs for the next 30 days.
Keep a perspective on my thoughts and evaluate my thoughts for accuracy.
Share with my family information on communication styles that may reduce

stress.
Other __________________________________________.
Other __________________________________________.
Other __________________________________________.
Other __________________________________________.
Contact the Following People Should I Ever Have Strong Suicidal Thoughts
Contact my psychiatrist at phone no. ___________________.
Contact my therapist at phone no. _____________________.
Contact my support person at phone no. ________________.
Other action ______________________________________.
Keep Myself Safe Until I Can Be Seen or Go to a Local Emergency Room if I Ever
Fear I May Act on Suicidal Thoughts
If I start to become depressed, I would like my support team to:
Talk to me about my symptoms (who ___________________)
Make plans for a pleasant event (who ___________________)
If I Start to Become Manic, I Would Like My Support Team to:

Talk to me about my symptoms (who ____________________)
Talk to me about reducing activities (who _________________)
Allow me to be alone if I am irritable (who ________________)
Take care of the kids/pets/other (who _____________________)
Take away my credit cards (who _________________________)
Take away my car keys (who ____________________________)
Take me to the hospital (preferred hospital _________________)
Other _______________________________________________
Other _______________________________________________
Other _______________________________________________
I understand that this contract is designed by me so that I can take an active
role in my treatment. My goal is to maximize my control by arranging for my
support team to take care of me. So that any future decisions are well considered,
I agree to change this contract only after giving two weeks written notice to all
parties to this contract.
Signatures for Contracting Individuals

_________________________ Signature Date _________________________
_________________________ Signature Date _________________________
_________________________ Signature Date _________________________
_________________________ Signature Date _________________________
Note. Extracts from pp. 117–123 of Living with Bipolar Disorder: A Guide for
Individuals and Families by M. W. Otto et al. (2011) by permission of Oxford
University Press, USA.
Once the rationale is explained, several sessions should be taken to thoroughly

draft and rehearse the treatment contract. As demonstrated in the sample contract
provided in Box 50.1, important components include a statement of the purpose of
the treatment contract, the names and contact information of each treatment team
member, and a list of characteristic symptoms and intervention strategies that the
team will put into motion when such symptoms arise (Otto et al., 2003). Patients are
encouraged to draw support from people they know well and have contact with on
a regular basis, including psychiatrists, therapists, family members, significant others,
friends, and coworkers. Inviting members of the support team to join these sessions
can help them to better understand their role on the treatment team and provide
additional information to the therapist and patient.
Mood charting provides the therapist and patient with a snapshot of daily changes
in mood, sleep patterns, medication adherence, and stressful life events. As such, it
is a useful tool for informing each session’s agenda, using session time efficiently,
and identifying warning signs for mood changes. These benefits should be clearly
described upon introducing patients to the mood chart. Sample mood charts are
available from a number of sources (e.g., Otto et al., 2009b; Otto et al., 2011). Mood
charts may appear complex upon first introduction, so ample time should be reserved
for reviewing and completing examples within session. Patients should be encouraged
that with practice, daily charting can routinely take under a minute.
As part of early recognition of hypomania, therapists may also introduce patients
to the idea that biased hyperpositive thinking styles accompany and exacerbate hypo-
mania. Therapists should begin with discussion of how the patient’s thoughts have
changed during previous manic or hypomanic episodes, and introduce a list of hypo-
manic cognitive errors. These commonly include errors such as positive fortune telling
(being overly optimistic about unknown outcomes), overreliance on luck (i.e., assum-
ing you can “get away with it”), disqualifying the negative, and overvaluing of immedi-
ate gratification. For patients with experience in recognizing and challenging depres-
sive thoughts, the steps of challenging hypomanic cognitive errors will be familiar.
For patients with a history of hypomania or mania, prevention of risky, destructive
behaviors should also be discussed. Behavioral strategies may include refraining from
substance use or having the patient agree to turn over his or her credit card to a
family member during a hypomanic episode. Rules to guide adaptive decision making
during manic episodes include a “2-person feedback rule” (checking in with two
trusted individuals before making a major decision) and a “48-hour decision rule”
(waiting 48 hours before acting on a new plan or idea; Newman, Leahy, Beck,
Reilly-Harrington, & Gyulai, 2001).
Cognitive Behavioral Therapy for

Bipolar Depression: Elements
CBT strategies for acute depressive symptoms in BD were developed following the
success of cognitive therapy for unipolar depression. In keeping with Beck’s cognitive
model, treatment protocols for depressive episodes in BD focus on the identification
and challenging of distorted or unhelpful thoughts.
A number of studies now provide evidence that these strategies reduce depression
symptoms and prolong time until relapse. Scott et al. (2001) found that compared with
a wait-list condition, those who received CBT reported fewer depressive symptoms
at 6-month follow-up. Additionally, those who received CBT demonstrated a 60%
reduction in relapse rates in the following 18 months (compared with the 18 months
prior to treatment). Lam et al. found similar results in both a pilot study (Lam et al.,
2000) and a later randomized trial (Lam et al., 2003) comparing 12–18 individual
sessions of CBT to treatment as usual. Patients who received CBT experienced
significantly lower depression symptoms 4 and 6 months later, compared to controls.
Additionally, rates of relapse in the following 12 months were significantly lower in
the CBT group (44% of CBT patients as compared to 75% of control group patients).
A longitudinal follow-up to this study showed that patients who received CBT
had a lower proportion of days spent in a mood episode in the following 18
months (Lam, Hayward, Watkins, Wright, & Sham, 2005). However, relapse rates
were not significantly different between groups at this time point, suggesting that
booster sessions may be an important element of treatment when focusing on
relapse prevention. Consistent with this, a separate study found that compared with
treatment as usual, 6 months of CT for BD led to reduced depressive symptoms and
dysfunctional attitudes, and a trend toward increased time until relapse, and that these
effects continued but diminished over a 12-month follow-up period (Ball et al., 2006).
Introduction and Psychoeducation

In the earliest stage of depression-focused treatment, the primary aims are to orient
the patient to CBT and to help the patient begin to notice and shift self-deprecating
thoughts (“depression about depression”). Thus, the first session should begin with
a discussion of the nature of depression and a review of the range of symptoms that
occur.
To further orient the patient to the assumptions and methods of CBT, the therapist
should also lead the patient in discussion of the role of cognitions in depression.
A personal story can be used to illustrate the effect that a depressed mood can have
on attitudes about the self, the world, and the future as per A. T. Beck (1979). The
therapist should also talk more broadly about how cognitions (defined as thoughts,
attitudes, and images that occur on a moment-by-moment basis) can have a strong
effect on what we do and how we feel. It should be emphasized that cognitions
are influential even at times when they are not true. This sets up the therapist to
provide patients with the rationale for self-monitoring mood and cognitions. Lastly,
the therapist should talk about how depression can lead to a decrease in activity levels,
which as a consequence leads to more negative thoughts and fewer opportunities for
positive experiences.
Activity Scheduling
Before initiating activity scheduling, patients should first monitor their baseline activity
levels and discuss the effect of their current activities on their mood. Therapists can
then introduce the concept of “buffering activities” as pleasurable activities that serve
to break up stressful activities throughout the day. Patients are informed that buffering
activities are even more important during times of low mood because of depression’s
tendency to reduce motivation and pleasure. During a depressive episode, they may
have great difficulty generating any activity that they may find enjoyable or soothing.
Thus, early in treatment, patients are not asked to generate ideas for themselves, but
are asked to select activities they might enjoy from a list.
Therapists should be aware of the motivational difficulties accompanying depres-
sion and should therefore spend time scheduling these activities with patients and
troubleshooting barriers to completion. After incorporation of pleasant activities, the
therapist should also work with the patient to establish regular activities related to
mastery. As the patient proceeds through treatment and increasingly takes responsi-
bility for illness management, he or she is encouraged to schedule and carry out these
activities independently.
Now that patients have been introduced to the concept of biased thoughts in
depression, more formal identification of cognitive errors can begin. The thought
record is an important component in organizing the process of cognitive restructuring.
It serves as a reminder of the steps of cognitive restructuring and is the basis of rehearsal
of more adaptive thoughts. Therapists should emphasize that writing out cognitive
errors holds value in that it allows for more objective evaluation of the thought
when compared to simply holding it in one’s mind. As with the introduction of any
new skill, thought records should be practiced in session using an example salient to
the patient. After the patient has gained experience in noticing his or her cognitive
errors, focus turns to evaluating such thoughts and generating alternatives. Patients
are taught a range of strategies for doing so, including considering the evidence that
the thought is true or untrue, and evaluating the usefulness of the thought. If this
process suggests that the negative thought is likely to be accurate, the conversation
should be directed toward coping with the situation effectively.
Although the teaching of cognitive errors and methods by which to challenge
them can be didactic, therapists should take care to make the process of evaluation of
thoughts a collaborative process rather than a lecture or a debate. Socratic questioning
is fundamental to this idea, and J. S. Beck (1995) provides a good discussion of basic
procedures of a Socratic approach to cognitive restructuring. Behavioral experiments
are another powerful strategy for learning because they allow the patient to directly
compare his or her thought with observed outcomes from the specified experiment.
This is often useful for beliefs tied to activity assignments; for example, a common
belief held by depressed patients is, “I can’t accomplish anything while depressed.”
Cognitive Behavioral Therapy for Lifestyle and Stress

Management in Bipolar Disorder
As described earlier, BD is influenced by a range of psychosocial variables and life

stressors. Thus, another important aim of CBT is the building of stress management
skills and health-promoting lifestyle habits. A number of treatment elements are

available to work toward this goal. As described in Otto et al. (2009a), the collaborative
development of a prioritized “problem list” may help to organize this phase of
treatment, with the benefit that these interventions may be flexibly applied to fit the
unique needs of each patient.
Problem Solving
Patients with BD may be limited in their ability to solve problems effectively due to
the frequent presence of depressive symptoms. Training in problem solving can help
patients to consider a wider array of solutions and to evaluate these systematically
before giving up. Ultimately, enhancement of problem-solving skills may serve to
reduce interpersonal conflict and negative life events. Although problem-solving
training has not been evaluated in isolation as an intervention for patients with BD, it
has been a component of efficacious treatment packages (Deckersbach et al., 2010).
Additionally, this intervention forms the basis of problem-solving therapy, which has
demonstrated efficacy for unipolar depression (Nezu, 1986).
The steps of traditional problem solving are as follows:
1. Identify and clearly define the problem.

2. Brainstorm all possible solutions.
3. Evaluate the advantages and disadvantages of each solution.
4. Select a solution (or a combination) taking into account the evaluation.
5. Implement the solution.
6. Evaluate the effectiveness of the solution.
Problem solving may be introduced informally and modeled in session using an

issue that has the patient feeling overwhelmed or frustrated. It may also be more
formally described and practiced through the use of problem-solving worksheets and
weekly structured home practice.
Social Skills and Communication

Given that high levels of expressed emotion and interpersonal conflict may exacerbate
the course of BD, patients may be able to buffer themselves against these effects
with strong social and communication skills. However, patients with BD may have
difficulty in this area for several reasons. Irritable mood, a symptom frequently present
in both depressive and manic episodes, may lead to frequent conflict with others.
For some, comorbid social anxiety or high levels of isolation may require a need
for conflict management or assertiveness training. Functional analysis of a patient’s
thoughts, feelings, and behaviors when in social situations may provide information
about the nature of the patient’s difficulties. This information should then be used
to set realistic behavioral goals that are focused on behaviors rather than emotions
(for example, “I will speak up at least once in the meeting” instead of “I will go to
the meeting and not feel nervous”). After establishing goals, social skills training can
proceed using several strategies:
1. Modeling of social behaviors

2. Coaching or instructional training
3. Behavioral rehearsal
4. Corrective feedback
5. Reinforcement of social skills.
Therapists should also attend to cognitive distortions that may be influencing the
patient’s actions. Common beliefs such as, “I won’t have anything to say” can be
examined in behavioral experiments.
Regardless of the strength of patients’ social skills and communication abilities,
many are likely to experience situations or time periods in which they have difficulty
engaging in effective strategies for communication. Therapists can identify these
situations and help patients plan how they will handle them. For example, some
patients may wish to avoid discussions about stressful topics while experiencing mood
symptoms. Others may benefit from identifying the signs that a conversation is
becoming too intense; in these situations, a signal to family members for a “time-out”
may be useful.
Activity Scheduling and Schedule Management

Although activity scheduling was described in greater detail as a tool for reducing
depressive symptoms, it should also be kept in mind as a way for patients to maintain a
stable routine. Patients should be educated about the importance of keeping a regular
schedule; much like a pianist uses a metronome, a patient can use routine patterns in
eating, sleeping, working, and so on, as a way to maintain a consistent rhythm. Activity
charting is encouraged throughout periods of recovery, with emphasis on maintaining
a balance of pleasant, stress-buffering activities and activities related to mastery.
Patients should be informed of the importance of maintaining a regular sleep sched-
ule, especially during times of stress. CBT strategies for insomnia are used for those
having difficulties sleeping. These include a range of interventions such as cognitive
restructuring of sleep-specific beliefs, relaxation training, basic sleep hygiene (i.e.,
avoid bright light at night, practice a relaxing bedtime routine), and stimulus control
guidelines (i.e., go to bed only when tired, wake up at the same time each morning).
Cognitive Behavioral Therapy for Comorbid Conditions in

Bipolar Disorder
Comorbid conditions may not only worsen the course of BD, they may also hinder
treatment. For instance, a patient with comorbid panic disorder with agoraphobia may
have greater difficulty engaging in components of CBT such as behavioral experiments
or activity assignments. Those with comorbid substance use disorders may respond
poorly to treatment due to medication nonadherence (Keck et al., 1996).
There is some evidence to suggest that treatment of a comorbid condition leads to
better outcomes in BD. For instance, STEP-BD patients who experienced sustained
remission from a substance use disorder fared more positively than those with a current
substance use disorder, especially with regard to role functioning (Weiss et al., 2005).
Additionally, integrated group cognitive behavioral treatment for substance use and
BD has been shown to reduce substance use and decrease risk of mood episode
recurrence in a community setting (Weiss et al., 2009). However, more research on
the impact of treatment of comorbid anxiety is sorely needed. The CBT strategies
described in other chapters within this volume may be of benefit when working with
BD patients with comorbid conditions such as anxiety disorders.
Additional Psychosocial Intervention Strategies
Other psychosocial treatments have also been shown to be efficacious for the
treatment of BD. Family-focused therapy (FFT) includes patients’ spouses or parents
in treatment and focuses on improving communication, support, and understanding
within the family (Miklowitz & Goldstein, 1997). Interpersonal and social rhythm
therapy (IPSRT) emphasizes three goals: stabilizing patients’ routines and sleep–wake
patterns, improving patients’ insight into the bidirectional nature of mood and
interpersonal events, and reducing interpersonal conflicts (Frank, 2007). There is
significant support for both of these interventions (see Miklowitz, 2006, for a review),
and, to date, the research suggests that these treatments are of comparable efficacy.
A large RCT conducted as part of STEP-BD found that adjunctive CBT, IPSRT, and
FFT were each more effective than a three-session psychoeducational intervention.
Patients who received any of the three intensive treatment modalities were 1.58 times
more likely to be well at any month during the study compared to those receiving
the brief psychoeducational treatment. However, no differences were found between
CBT, IPSRT, and FFT in percent recovered or time to recovery (Miklowitz et al.,
2007b).
Although these empirically supported treatments arose from different theoretical
orientations, they share a surprising number of common elements. Each includes (a)
psychoeducation around the nature and course of BD and the lifestyle factors that
influence it (e.g., sleep patterns, life events, medication use), (b) problem-solving
and communication enhancement techniques designed to reduce stress and family
conflict, and (c) emphasis on early detection and intervention for mood episodes
(Otto & Applebaum, 2010). Beyond these core elements, treatment strategies such
as cognitive restructuring interventions, treatment contracting, family sessions, and
sleep management strategies are added.
Conclusion and Future Directions
The empirical literature strongly suggests that CBT is a powerful adjunctive inter-
vention for BD across a variety of treatment outcomes. As the evidence for the
efficacy of CBT for BD has grown, some attention has turned to portability and
cost-effectiveness. Results indicate that the costs of outpatient CBT are offset by
a reduction in inpatient psychiatric care. For instance, in a trial in which patients
receiving CBT did significantly better than those receiving standard treatment, Lam
et al. (2005) found that the extra cost of providing CBT was offset by reduced service
utilization elsewhere (most frequently by reduced need for inpatient care). Over the
course of the 30-month study, those receiving cognitive therapy incurred £1,300 less
in service costs than those receiving standard treatment (a nonsignificant difference;
Lam et al., 2005). Bauer et al. (2006) found that direct all-treatment costs for CBT
did not differ significantly from standard care, yet reduced time spent in affective
episodes by over 6 weeks.
There are several promising new directions in cognitive behavioral treatment strate-
gies for BD. Research demonstrating that most patients, even when recovered, do
not return to premorbid levels of psychosocial function has led to an increased
emphasis on intervention strategies that might directly target functioning as a primary
outcome. Deckersbach et al. (2010) completed an open trial of a new cognitive
remediation treatment for employed patients with BD who suffered from residual
mood symptoms. This 14-session intervention focused on techniques to improve
three problem areas: mood monitoring and residual mood symptoms, organization
and time management, and attention and memory. Over the course of treatment,
patients demonstrated significantly reduced Hamilton Rating Scale for Depression
scores (pretreatment mean = 8.65, posttreatment mean = 5.41, p = .001). Addition-
ally, patients demonstrated reductions in total lost work performance (pretreatment
mean days lost = 9.37, posttreatment mean days lost = 7.03, p = .004) and
improvements in psychosocial functioning as measured by the LIFE-RIFT Range of
Impaired Functioning Tool (pretreatment mean = 11.29, posttreatment mean = 9.76,
p = .03) (Deckersbach et al., 2010).
Given that residual symptoms have been shown to be a strong predictor of future
recurrence, others have begun to develop and test interventions geared toward
reduction of residual depressive symptoms. In rumination-focused CBT, behavioral
activation principles are applied specifically to address rumination as an unhelpful
avoidance behavior. Treatment emphasizes functional analysis and coaches patients to
recognize rumination as unhelpful and shift to a more effective strategy or response.
In the first RCT of rumination-focused CBT, Watkins et al. (2011) found that 12
individual treatment sessions reduced residual symptoms (effect size d = 0.94) and
improved remission rates as compared with treatment as usual (62% remitted in the
CBT condition compared with 25% remitted in the treatment as usual condition,
p < .05). Moreover, this treatment was shown to reduce Axis II comorbidity and
trend toward reducing Axis I comorbid symptoms, suggesting that these strategies
may have benefit across diagnostic boundaries.
Mindfulness-based techniques are also being incorporated into treatment of BD.
Two small trials have found that mindfulness-based cognitive therapy (MBCT)
reduces residual depressive symptoms and improves well-being, emotion regulation,
and psychosocial functioning (Deckersbach et al., 2011; Miklowitz et al., 2009).
Additionally, MBCT has been found to increase attentional readiness and frontal con-
trol in BD patients in a pilot electroencephalography study (Howells, Ives-Deliperi,
Horn, & Stein, 2012). Notably, traditional mindfulness techniques may need to
be adjusted in consideration of difficulties patients may have with organization and
sustained attention. For instance, Deckersbach et al. (2011) modified the MBCT
protocol for this group by increasing the number of mindfulness exercises involv-
ing movement (such as yoga) and reducing the duration of sitting or body scan
exercises.
Despite the clear advances in CBT treatment for BD, future work is needed in several
areas. Larger RCTs with active comparison conditions are needed to carry out more
rigorous tests of the efficacy of new innovations in treatment such as mindfulness-
and rumination-focused CBT protocols. There is also a need to clarify the active
ingredients of CBT and other psychosocial treatments for BD to create more efficient,
focused treatments. Studies of this are already underway; for example, one research
group in the United Kingdom is comparing the efficacy of curriculum-based group
psychoeducation and unstructured peer group support in public treatment settings
(Morriss et al., 2011). Zaretsky, Lancee, Miller, Harris, and Parikh (2008) found
that psychoeducation plus an individual course of CBT was associated with fewer
days depressed compared to those who received psychoeducation alone. Additionally,
there is a great need for studies of the effect of treatment of comorbid disorders on the
course and outcome of BD. Also absent from many CBT approaches are interventions
for the anger and irritability that can accompany both phases (manic and depressive)
of the disorder (for example, see Otto et al., 2011). Also, given that comorbid anxiety
is strongly associated with poor outcomes in BD and the well-established efficacy of
CBT for anxiety disorders (Hofmann & Smits, 2008), there is promise that CBT may
be of particular use in this area.
References
Angst, J., Angst, F., Gerber-Werder, R., & Gamma, A. (2005). Suicide in 406 mood-disordered
patients with and without long-term medication: A 40 to 44 years follow-up. Archives of
Suicide Research, 9, 279–300. doi:10.1080/13811110590929488
Ball, J. R., Mitchell, P. B., Corry, J. C., Skillecorn, A., Smith, M., & Malhi, G. S. (2006). A
randomized controlled trial of cognitive therapy for bipolar disorder: Focus on long-term
change. Journal of Clinical Psychiatry, 67 , 277–286.
Bauer, M. S., McBride, L., Williford, W. O., Glick, H., Kinosian, B., Altshuler, L., … Coauthors
for the Cooperative Studies Program 430 Study Team. (2006). Collaborative care for
bipolar disorder. Part II: Impact on clinical outcome, function, and costs. Psychiatric
Services, 57 , 937–945.
Beck, A. T. (1979). Cognitive therapy of depression. New York, NY: Guilford Press.
Beck, J. S. (1995). Cognitive therapy: Basics and beyond. New York, NY: Guilford Press.
Bender, R. E., & Alloy, L. B. (2011). Life stress and kindling in bipolar disorder: Review of the
evidence integration with emerging biopsychosocial theories. Clinical Psychology Review,
31, 383–398.
Brady, K., Castro, S., Lydiard, R., Malcolm, R., & Arana, G. (1991). Substance abuse in an
inpatient psychiatric sample. American Journal of Drug and Alcohol Abuse, 17 , 389–397.
doi:10.3109/00952999109001598
Brown, G. K., Beck, A. T., Steer, R. A., & Grisham, J. R. (2000). Risk factors for suicide in
psychiatric outpatients: A 20-year prospective study. Journal of Consulting and Clinical
Psychology, 68, 371–377. doi:10.1037//0022-006X.68.3.371
Clark, L., Iversen, S. D., & Goodwin, G. M. (2002). Sustained attention deficit in bipolar
disorder. British Journal of Psychiatry, 180, 313–319. doi:10.1192/bjp.180.4.313
Cochran, S. D. (1984). Preventing medical noncompliance in the outpatient treatment of
bipolar affective disorders. Journal of Consulting and Clinical Psychology, 52, 873–878.
doi:10.1037//0022-006X.52.5.873
Colom, F., Vieta, E., Martinez-Aran, A., Reinares, M., Goikolea, J. M., Benabarre, A., …
Corominas, J. (2003). A randomized trial on the efficacy of group psychoeducation in
the prophylaxis of recurrences in bipolar patients whose disease is in remission. Archives of
General Psychiatry, 60, 402–407. doi:10.1001/archpsyc.60.4.402
Cuellar, A., Johnson, S. L., & Winters, R. (2005). Distinctions between bipolar and unipolar
depression. Clinical Psychology Review, 25, 307–339. doi:10.1016/j.cpr.2004.12.002
Deckersbach, T., Hölzel, B. K., Eisner, L. R., Stange, J. P., Peckham, A. D., Dougherty,
D. D., … & Nierenberg, A. A. (2011), Mindfulness-based cognitive therapy for non-
remitted patients with bipolar disorder. CNS Neuroscience & Therapeutics, 18, 133–141.
doi:10.1111/j.1755–5949.2011.00236
Deckersbach, T., Nierenberg, A. A., Kessler, R., Lund, H. G., Ametrano, R. M., Sachs, G., …
Dougherty, D. (2010). RESEARCH: Cognitive rehabilitation for bipolar disorder: An
open trial for employed patients with residual depressive symptoms. CNS Neuroscience &
Therapeutics, 16, 298–307. doi:10.1111/j.1755–5949.2009.00110.x
Ellicott, A., Hammen, C., Gitlin, M., Brown, G., & Jameson, K. (1990). Life events and the
course of bipolar disorder. American Journal of Psychiatry, 147 , 1194–1198.
Fagiolini, A., Kupfer, D. J., Masalehdan, A., Scott, J. A., Houck, P. R., & Frank, E. (2005).
Functional impairment in the remission phase of bipolar disorder. Bipolar Disorders, 7 ,
281–285. doi:10.1111/j.1399–5618.2005.00207.x
Frank, E. (2007). Interpersonal and social rhythm therapy: A means of improving depression
and preventing relapse in bipolar disorder. Journal of Clinical Psychology, 63, 463–473.
doi:10.1002/jclp.20371
Gitlin, M. J., Swendsen, J., Heller, T. L., & Hammen, C. (1995). Relapse and impairment in
bipolar disorder. American Journal of Psychiatry, 152, 1635–1640.
Goldberg, J., Garno, J., Leon, A., Kocsis, J., & Portera, L. (1999). A history of substance abuse
complicates remission from acute mania in bipolar disorder. Journal of Clinical Psychiatry,
60, 733–740. doi:10.4088/JCP.v60n1103
Green, M. F. (2006). Cognitive impairment and functional outcome in schizophrenia and
bipolar disorder. Journal of Clinical Psychiatry, 67 (Suppl. 9), 3–8.
Henry, C., Van den Bulke, D., Bellivier, F., Etan, B. K., Rouillon, F., & Leboyer, M. (2003).
Anxiety disorders in 318 bipolar patients: Prevalence and impact on illness severity and
response to mood stabilizer. Journal of Clinical Psychiatry, 64, 331–335. doi:10.4088/
JCP.v64n0316
Hofmann, S. G., & Smits, J. A. (2008). Cognitive-behavioral therapy for adult anxiety disorders:
A meta-analysis of randomized placebo-controlled trials. Journal of Clinical Psychiatry,
69, 621–632.
Howells, F. M., Ives-Deliperi, V. L., Horn, N. R., & Stein, D. J. (2012). Mindfulness based
cognitive therapy improves frontal control in bipolar disorder: A pilot EEG study. BMC
Psychiatry, 12, 15. doi:10.1186/1471-244X-12-15
Joffe, R. T., MacQueen, G. M., Marriott, M., & Young, L. (2004). A prospective, longitudinal
study of percentage of time spent ill in patients with bipolar I or bipolar II disorders. Bipolar
Disorders, 6, 62–66. doi:10.1046/j.1399–5618.2003.00091.x
Johnson, R. E., & McFarland, B. H. (1996). Lithium use and discontinuation in a health
maintenance organization. American Journal of Psychiatry, 153, 993–1000.
Johnson, S. L. (2005). Life events in bipolar disorder: Towards more specific models. Clinical
Johnson, S. L., & Miller, I. (1997). Negative life events and time to recovery from episodes of
bipolar disorder. Journal of Abnormal Psychology, 106, 449–457. doi:10.1037//0021-
843X.106.3.449
Johnson, S. L., Sandrow, D., Meyer, B., Winters, R., Miller, I., Keitner, G., & Solomon, D.
(2000). Increases in manic symptoms after life events involving goal-attainment. Journal
of Abnormal Psychology, 109, 721–727. doi:10.1037//0021-843X.109.4.721
Judd, L. L., Akiskal, H. S., Schettler, P. J., Endicott, J., Maser, J., Solomon, D. A., … Keller,
M. B. (2002). The long-term natural history of the weekly symptomatic status of bipolar
I disorder. Archives of General Psychiatry, 59, 530–537.
Judd, L. L., Akiskal, H. S., Schettler, P. J., Coryell, W., Endicott, J., Maser, J. D., … Keller,
M. B. (2003). Prospective investigation of the natural history of the long-term weekly
symptomatic status of bipolar II disorder. Archives of General Psychiatry, 60, 261–269.
doi:10.1001/archpsyc.60.3.261
Judd, L. L., Schettler, P., Solomon, D. A., Maser, J. D., Coryell, W., Endicott, J., & Akiskal, H.
S. (2008). Psychosocial disability and work role function compared across the long-term
course of bipolar I, bipolar II and unipolar major depressive disorders. Journal of Affective
Keck, P., McElroy, S., Strakowski, S., Stanton, S., Kizer, D., Balistreri, T., … West, S. A.
(1996). Factors associated with pharmacologic noncompliance in patients with mania.
Journal of Clinical Psychiatry, 57 , 292–297.
Kessler, R., Chiu, W., Demler, O., & Walters, E. (2005). Prevalence, severity, and comorbidity
of twelve-month DSM-IV disorders in the National Comorbidity Survey Replication
(NCS-R). Archives of General Psychiatry, 62, 617–627. doi:10.1001/archpsyc.62.6.617
Kessler, R., Crum, R., Warner, L., Nelson, C., Schulenberg, J., & Anthony, J. (1997). Lifetime
co-occurrence of DSM-III-R alcohol abuse and dependence with other psychiatric disor-
ders in the National Comorbidity Survey. Archives of General Psychiatry, 54, 313–321.
doi:10.1001/archpsyc.1997.01830160031005
Kessler, R., McGonagle, K., Zhao, S., Nelson, C., Hughes, M., Eshleman, S., … Kendler,
K. S. (1994). Lifetime and 12-month prevalence of DSM-III-R psychiatric disorders in
the United States: Results from the National Comorbidity Survey. Archives of General
Kupfer, D. J. (2005). The increasing medical burden in bipolar disorder. Journal of the
American Medical Association, 293, 2528–2530. doi:10.1001/jama.293.20.2528
Kupka, R. W., Altshuler, L. L., Nolen, W. A., Suppes, T., Luckenbaugh, D. A., Leverich,
G. S., … Post, R. M. (2007). Three times more days depressed than manic or
hypomanic in both bipolar I and bipolar II disorder. Bipolar Disorders, 9, 531–535.
doi:10.1111/j.1399-5618.2007.00467.x
Lam, D., Bright, J., Jones, S., Hayward, P., Schuck, D., Chisholm, D., & Sham, P. (2000).
Cognitive therapy for bipolar illness: A pilot study of relapse prevention. Cognitive Therapy
and Research, 24, 503–520. doi:10.1023/A:1005557911051
Lam, D. H., Hayward, P., Watkins, E. R., Wright, K., & Sham, P. (2005). Relapse prevention
in patients with bipolar disorder: Cognitive therapy outcome after 2 years. American
Lam, D. H., McCrone, P., Wright, K., & Kerr, N. (2005) Cost-effectiveness of relapse-
prevention cognitive therapy for bipolar disorder: 30-month study. British Journal of
Lam, D. H., Watkins, E. R., Hayward, P., Bright, J., Wright, K., Kerr, N., … Sham, P. (2003).
A randomized controlled study of cognitive therapy of relapse prevention for bipolar
affective disorder: Outcome of the first year. Archives of General Psychiatry, 60, 145–152.
doi:10.1001/archpsyc.60.2.145
MacQueen, G. M., Young, L., & Joffe, R. T. (2001). A review of psychosocial out-
come in patients with bipolar disorder. Acta Psychiatrica Scandinavica, 103, 163.
doi:10.1034/j.1600-0447.2001.00059.x
Magalhães, P. V., Kapczinski, F., Nierenberg, A. A., Deckersbach, T., Weisinger, D., Dodd, S.,
& Berk, M. (2011). Illness burden and medical comorbidity in the Systematic Treatment
Enhancement Program for Bipolar Disorder. Acta Psychiatrica Scandinavica, 125, 1–6.
doi:10.1111/j.1600-0447.2011.01794.x
Malkoff-Schwartz, S., Frank, E., Anderson, B. P., Hlastala, S. A., Luther, J. F., … Kupfer, D. J.
(2000). Social rhythm disruption and stressful life events in the onset of bipolar and unipo-
lar episodes. Psychological Medicine, 30, 1005–1016. doi:10.1017/S0033291799002706
Martinez-Aran, A., Vieta, E., Torrent, C., Sanchez-Moreno, J., Goikolea, J. M., Salamero,
M., … Ayuso-Mateos, J. L. (2007). Functional outcome in bipolar disorder: The role
of clinical and cognitive factors. Bipolar Disorders, 9, 103–113. doi:10.1111/j.1399-
5618.2007.00327.x
Miklowitz, D. J. (2006). A review of evidence-based psychosocial interventions for bipolar
disorder. Journal of Clinical Psychiatry, 67 , 28–33.
Miklowitz, D. J., Alatiq, Y., Goodwin, G. M., Geddes, J. R., Fennell, M. J. V., Dimid-
jian, S., … Williams, M. G. (2009). A pilot study of mindfulness-based cognitive
therapy for bipolar disorder. International Journal of Cognitive Therapy, 2, 373–382.
doi:10.1521/ijct.2009.2.4.373
Miklowitz, D. J., & Goldstein, M. J. (1997). Bipolar disorder: A family-focused treatment
Miklowitz, D. J., Goldstein, M., Nuechterlein, K., Snyder, K., & Mintz, J. (1988). Family
factors and the course of bipolar affective disorder. Archives of General Psychiatry, 45,
225–231.
Miklowitz, D. J., Otto, M. W., Frank, E., Reilly-Harrington, N. A., Wisniewski, S. R., Kogan,
J. N., … Sachs, G. S. (2007a). Psychosocial treatments for bipolar depression: A 1-year
randomized trial from the Systematic Treatment Enhancement Program. Archives of
Miklowitz, D. J., Otto, M. W., Frank, E., Reilly-Harrington, N. A., Kogan, J. N., Sachs, G. S.,
… Wisniewski, S. R. (2007b). Intensive psychosocial intervention enhances functioning
in patients with bipolar depression: Results from a 9-month randomized controlled trial.
Moller, H. J., & Nasrallah, H. A. (2003). Treatment of bipolar disorder. Journal of Clinical
Morriss, R., Lobban, F., Jones, S., Riste, L., Peters, S., Roberts, C., … Mayes, D. (2011).
Pragmatic randomised controlled trial of group psychoeducation versus group support in
the maintenance of bipolar disorder. BMC Psychiatry, 11, 114–123. doi:10.1186/1471-
244X-11-114
Nemeroff, C. B., Evans, D. L., Gyulai, L., Sachs, G. S., Bowden, C. L., Gergel, I. P., …
Pitts, C. D. (2001). Double-blind, placebo-controlled comparison of imipramine and
paroxetine in the treatment of bipolar depression. American Journal of Psychiatry, 158,
906–912. doi:10.1176/appi.ajp.158.6.906
Newman, C. F., Leahy, R. L., Beck, A. T., Reilly-Harrington, N. A., & Gyulai, L. (2001).
Bipolar disorder: a cognitive therapy approach. Washington, DC: American Psychological
Association.
Nezu, A. M. (1986). Efficacy of a social problem-solving therapy approach for unipolar

depression. Journal of Consulting and Clinical Psychology, 54, 196–202. doi:10.1037//
0022-006X.54.2.196
O’Connell, R., Mayo, J., Flatlow, L., Cuthbertson, B., & O’Brien, B. (1991). Outcome of
bipolar disorder on long-term treatment with lithium. British Journal of Psychiatry, 159,
123–129. doi:10.1192/bjp.159.1.123
Otto, M. W., & Applebaum, A. J. (2010). The nature and treatment of bipolar disorder and
the bipolar spectrum. In D. H. Barlow (Ed.), Oxford handbook of clinical psychology (pp.
294–310). New York, NY: Oxford University Press.
Otto, M. W., Reilly-Harrington, N., Knauz, R. O., Henin, A., Kogan, J. N., & Sachs, G.
S. (2011). Living with bipolar disorder: A guide for individuals and families, (updated
edition). New York, NY: Oxford University Press.
Otto, M. W., Reilly-Harrington, N. A., Kogan, J. N., Henin, A., Knauz, R. O., & Sachs, G.
S. (2009a). Managing bipolar disorder: A cognitive-behavioral approach (therapist guide).
Otto, M. W., Reilly-Harrington, N. A., Kogan, J. N., Henin, A., Knauz, R. O., & Sachs,
G. S. (2009b). Managing bipolar disorder: A cognitive-behavioral approach. (workbook).
Otto, M. W., Reilly-Harrington, N., & Sachs, G. S. (2003). Psychoeducational and cognitive-
behavioral strategies in the management of bipolar disorder. Journal of Affective Disorders,
73, 171–181.
Otto, M., Simon, N., Wisniewski, S. R., Miklowitz, D., Kogan, J., Reilly-Harrington, N.,
… Step-BD Investigators. (2006). Prospective 12-month course of bipolar disorder in
outpatients with and without comorbid anxiety disorders. British Journal of Psychiatry,
189, 20–25. doi:10.1192/bjp.bp.104.007773
Perlis, R., Miyahara, S., Marangell, L., Wisniewski, S. R., Ostacher, M., DelBello, M.,
… Nierenberg, A. A. (2004). Long-term implications of early onset in bipolar
disorder: Data from the first 1000 participants in the systematic treatment enhance-
ment program for bipolar disorder (STEP-BD). Biological Psychiatry, 55, 875–881.
doi:10.1016/j.biopsych.2004.01.022
Perlis, R. H., Ostacher, M. J., Patel, J. K., Marangell, L. B., Zhang, H., Wisniewski, S. R.,
… Thase, M. E. (2006). Predictors of recurrence in bipolar disorder: Primary outcomes
from the systematic treatment enhancement program for bipolar disorder (STEP-BD).
American Journal of Psychiatry, 163, 217–224. doi:10.1176/appi.ajp.163.2.217
Perry, A., Tarrier, N., Morriss, R., McCarthy, E., & Limb, K. (1999). Randomised con-
trolled trial of efficacy of teaching patients with bipolar disorder to identify early
symptoms of relapse and obtain treatment. British Medical Journal, 16, 149–153.
doi:10.1136/bmj.318.7177.149
Post, R. M. (1992). Transduction of psychosocial stress into the neurobiology of recurrent
affective disorder. American Journal of Psychiatry, 149, 999–1010.
Regier, D., Farmer, M., Rae, D., Locke, B., Keith, S., Judd., L., … Goodwin, F.K. (1990).
Comorbidity of mental disorders with alcohol and other drug abuse: Results from the
Epidemiologic Catchment Area (ECA) study. Journal of the American Medical Association,
264, 2511–2518. doi:10.1001/jama.1990.03450190043026
Reich, L., Davies, R., & Himmelhoch, J. (1974). Excessive alcohol use in manic-
depressive illness. American Journal of Psychiatry, 131, 83–86. doi:10.1001/jama.1990.
03450190043026
Reilly-Harrington, N. A., Alloy, L. B., Fresco, D. M., & Whitehouse, W. G. (1999). Cognitive
styles and life events interact to predict bipolar and unipolar symptomatology. Journal of
Abnormal Psychology, 108, 567–578. doi:10.1037//0021-843X.108.4.567
Sachs, G. S., Nierenberg, A. A., Calabrese, J. R., Marangell, L. B., Wisniewski, S. R.,
Gyulai, L., … Thase, M. E. (2007). Effectiveness of adjunctive antidepressant treat-
ment for bipolar depression. New England Journal of Medicine, 356, 1711–1722.
doi:10.1056/NEJMoa064135
Safren, S. A., Otto, M. W., Worth, J. L., Salomon, E., Johnson, W., Mayer, K., & Boswell, S.
(2001). Two strategies to increase adherence to HIV antiretroviral medication: Life-steps
and medication monitoring. Behavior Research and Therapy, 39, 1151–1162.
Scott, J., Garland, A., & Moorhead, S. (2001). A pilot study of cognitive therapy in bipolar
disorders. Psychological Medicine, 31, 459–467. doi:10.1017/S0033291701003373
Sidor, M. M., & MacQueen, G. M. (2011). Antidepressants for the acute treatment of bipolar
depression: A systematic review and meta-analysis. Journal of Clinical Psychiatry, 72,
156–167. doi:10.4088/JCP.09r05385gre
Simon, N. M., Otto, M. W., Weiss, R., Bauer, M. S., Miyahara, S., Wisniewski, S. R., … &
Pollack, M. H. (2004b). Pharmacotherapy for bipolar disorder and comorbid conditions:
Baseline data from STEP-BD. Journal of Clinical Psychopharmacology, 24, 512–520.
doi:10.1097/01.jcp.0000138772.40515.70
Simon, N. M., Otto, M. W., Wisniewski, S. R., Fossey, M., Sagduyu, K., Frank,
E., … Pollack, M. H. (2004a). Anxiety disorder comorbidity in bipolar disorder
patients: Data from the first 500 participants in the Systematic Treatment Enhance-
ment Program for Bipolar Disorder (STEP-BD). American Journal of Psychiatry, 161,
2222–2229. doi:10.1176/appi.ajp.161.12.2222
Sole, B., Bonnin, C. M., Torrent, C., Martinez-Aran, A., Popovic, D., Tabarés-Seisdedos,
R., & Vieta, E. (2011). Neurocognitive impairment across the bipolar spectrum. CNS
Neuroscience and Therapeutics, 18, 194–200.
Solomon, D. A., Keitner, G. I., Miller, I. W., & Shea, T. M. (1995). Course of illness and
maintenance treatments for patients with bipolar disorder. Journal of Clinical Psychiatry,
56, 5–13.
Suominen, K., Mantere, O., Valtonen, H., Arvilommi, P., Leppämäki, S., & Isometsä, E.
(2009). Gender differences in bipolar disorder type I and II. Acta Psychiatrica Scandinav-
ica, 120, 464–473. doi:10.1111/j.1600-0447.2009.01407.x
Suominen, K., Mantere, O., Valtonen, H., Arvilommi, P., Leppämäki, S., Paunio, T., &
Isometsä, E. (2007). Early age at onset of bipolar disorder is associated with more
severe clinical features but delayed treatment seeking. Bipolar Disorders, 9, 698–705.
doi:10.1111/j.1399-5618.2007.00388.x
Sussman, M., Friedman, M., Korn, J. R., Hassan, M., Kim, J., & Menzin, J. (2012). The
relationship between use of antidepressants and resource utilization among patients with
manic or mixed bipolar disorder episodes: Findings from a managed care setting. Journal
of Affective Disorders, 138, 425–432. doi:10.1016/j.jad.2011.12.048
Swann, A. C., Lijffijt, M., Lane, S. D., Steinberg, J. L., & Moeller, F. (2009). Increased trait-
like impulsivity and course of illness in bipolar disorder. Bipolar Disorders, 11, 280–288.
doi:10.1111/j.1399-5618.2009.00678.x
Tohen, M., Waternaux, C. M., & Tsuang, M. T. (1990). Outcome in mania: A 4-year prospec-
tive follow-up of 75 patients utilizing survival analysis. Archives of General Psychiatry, 47 ,
1106–1111. doi:10.1001/archpsyc.1990.01810240026005
Watkins, E. R., Mullan, E., Wingrove, J., Rimes, K., Steiner, H., Bathurst, N., … Scott, J.
(2011). Rumination-focused cognitive-behavioural therapy for residual depression: Phase
II randomised controlled trial. British Journal of Psychiatry. doi:10.1192/bjp.bp.110.
090282
Weiss, R. D., Griffin, M. L., Jaffee, W. B., Bender, R. E., Graff, F. S., Gallop, R. J., &
Fitzmaurice, G. M. (2009). A “community-friendly” version of integrated group therapy
for patients with bipolar disorder and substance dependence: A randomized controlled
trial. Drug and Alcohol Dependence, 104, 212–219. doi:10.1016/j.drugalcdep.2009.
04.018
Weiss, R. D., Ostacher, M. J., Otto, M. W., Calabrese, J. R., Fossey, M., Wisniewski, S. R., …
Sachs, G. S. for STEP-BD Investigators. (2005). Does recovery from substance use matter
in patients with bipolar disorder? Journal of Clinical Psychiatry, 66, 730–735.
World Health Organization. (2001). The World Health Report 2001. Mental health: New
understanding, new hope. Geneva, Switzerland: Author.
Xu, G., Lin, K., Rao, D., Dang, Y., Ouyang, H., Guo, Y., … Chen J. (2012). Neuropsycholog-
ical performance in bipolar I, bipolar II and unipolar depression patients: A longitudinal,
naturalistic study. Journal of Affective Disorders, 136, 328–339.
Yatham, L. N., Kauer-Sant’anna, M., Bond, D. J., Lam, R. W., & Torres, I. (2009). Course
and outcome after the first manic episode in patients with bipolar disorder: Prospective
12-month data from the systematic treatment optimization program for early mania
project. Canadian Journal of Psychiatry, 54, 105–112.
Zaretsky, A. E., Lancee, W., Miller, C., Harris, A., & Parikh, S. V. (2008). Is CBT more
effective than psychoeducation in the treatment of bipolar disorder? Canadian Journal of
51
Borderline Personality Disorder
Alec L. Miller and Miguelina Germán
Montefiore Medical Center/Albert Einstein College of Medicine, United States
Andrea Fortunato
New School for Social Research, United States
We begin this chapter with a description of borderline personality disorder (BPD)

using Figure 51.1 as a starting point. At first glance, it is explicitly clear that the
young woman in the picture appears to be in intense emotional pain. We know a bit
about the content of her thoughts from what she has written on the wall of her room:
fear, abandonment, anger, despair, suicidal tendencies, and finally no reason. Taken
together, this information fits the clinical picture of BPD which often involves a deep
fear of abandonment, intense feelings of anger, self-injurious and suicidal behaviors,
and chronic feelings of emptiness—a type of “not knowing” who you are and a
lack of understanding about why painful, interpersonal experiences recur (American
Psychiatric Association [APA], 2000; Walter et al., 2009). Affective instability is a
core feature of this disorder, and patients with borderline personality disorder are
often described as being extremely emotionally intense and labile. It is not surprising
that the person in this image is female, as women are more frequently diagnosed with
BPD than men (APA, 2000).
Nature of the Disorder
The Diagnostic and Statistical Manual of Mental Disorders (4th ed., text rev.; DSM-
IV-TR; APA, 2000) defines personality disorders as “an enduring pattern of inner
experience and behavior that differs markedly from the expectations of the individual’s
culture, is pervasive and inflexible, has an onset in adolescence or early adulthood, is
stable over time, and leads to distress or impairment” (p. 685). Unlike the discrete
conditions listed on Axis I, the personality disorders of Axis II have long been
considered intractable, untreatable personality deficits (Widiger & Frances, 1985).
BPD, in particular, is feared by mental health professionals because of the sometimes

DOI: 10.1002/9781118528563.wbcbt51
Figure 51.1 Intense emotional pain experienced in borderline personality disorder. Printed
with permission from Michael Roth.
emotionally demanding presentation of individuals with BDP and because of the high
rates of self-harm and suicidal behaviors in this population. Nonsuicidal self-injury
(NSSI) and suicide attempts are common (Lieb, Zanarini, Schmahl, Linehan, &
Bohus, 2004) and a full 8–10% of individuals with BPD complete suicide (Lieb
et al., 2004). In mental health settings, prevalence rates have been measured at
10% in outpatient mental health clinics and 15–20% among psychiatric inpatients
(APA, 2000). Fabrega, Ulrich, Pilkonis, and Mezzich (1992) found 68% of BPD
patients met criteria for some Axis I disorder. Symptoms of BPD can include
substance abuse, disordered eating, affective lability, and psychotic experiences. These
symptoms predispose BPD patients toward the co-occurrence at clinical levels of the
corresponding Axis I disorders, especially MDD, dysthymia, and the bipolar disorders
(APA, 2000; Zanarini, Gunderson, & Frankenburg, 1989).
BPD in adolescents presents similarly symptomatically as it does in adults (Miller,
Muehlenkamp, & Jacobson, 2008). There are general factors in childhood and
adolescence that serve as risk factors for mental health problems, and even for
personality disorders more generally, but none that uniquely predicts BPD (Rogosch
& Cicchetti, 2005; Winograd, Cohen, & Chen, 2008). The current and fourth
edition of the DSM lists nine diagnostic criteria, of which five must be present for an
individual to meet the diagnostic threshold. Since no individual criterion is specified
as either necessary or sufficient (i.e., BPD has a polythetic criterion set), there are
151 possible diagnostic combinations. Thus, any two individuals diagnosed with
BPD could potentially overlap on only one criterion, resulting in high levels of
heterogeneity within the diagnostic group. As a result of this heterogeneity, as well
Borderline Personality Disorder 1217
as other problems with the overall categorical nature of the Axis II system (Widiger
& Frances, 1985), there have been many challenges to the validity of the DSM-IV
definition. The challenges will likely result in significant revisions for the DSM-5.
Overview of Borderline Personality Disorder

Treatment Literature
The purpose of this chapter is to describe a cognitive behavioral treatment for

borderline personality disorder called dialectical behavior therapy (DBT). We will give
brief mention to several other treatments developed for BPD and review the empirical
evidence for each treatment before describing DBT in greater depth.
Psychoanalytic and psychodynamic psychotherapies have generally conceptualized
BPD as a disturbance of character fluctuating between neurosis and psychosis,
and the treatment purports to address the individual’s defense mechanisms such as
“splitting” in an effort to better integrate the positive and negative aspects of self and
others. Kernberg (1985) described individuals with BPD as having weak egos and
an inability to endure analyses of regression to childhood conflicts in psychotherapy.
Transference-focused psychotherapy (Clarkin, Levy, Lenzenweger, & Kernberg,
2007) is an evidence-based structured dynamic treatment shown to be effective in
one randomized trial when compared with DBT and supportive psychotherapy.
Mentalization-based therapy (MBT; Bateman & Fonagy, 2008) is an approach that
is rooted in object relations theory and has been manualized to treat BPD. Mental-
ization involves attending to the mental state, and the corresponding behaviors, of
self and others; this focus on self-awareness and self-regulation in mentalization-
based treatment makes it particularly applicable for the treatment of BPD. In
their randomized controlled trial (RCT), Bateman and Fonagy (2008) found that
mentalization-based treatment for BPD showed greater improvements in suicidality,
diagnostic status, service use, medication adherence, and global functioning than
treatment as usual at 5 years posttreatment.
From a cognitive therapy perspective, Jeffrey Young and Aaron Beck theorize that
patients with BPD tend to have dysfunctional “schemas,” or cognitive structures.
These individuals are considered to have aspects of self, or modes, that interact in
a harmful and irrational manner. These schemas include: the abandoned or abused
child; the angry and impulsive child; the detached protector; the punitive parent; and
the healthy adult (Young, Klosko, & Weishaar, 2003). Schema-focused therapy uses
four healing mechanisms to address the special consideration of each mode for BPD
patients: reparenting, emotion-focused work, cognitive restructuring, and behavioral
pattern-breaking (Kellogg & Young, 2006). In an RCT, schema-focused therapy
was found to be superior to psychodynamically informed treatment in reducing
psychopathological dysfunction and improving quality of life for patients with BPD
(Giesen-Bloo et al., 2006).
Systems training for emotional predictability and problem solving (STEPPS; Blum
et al., 2008) is a 20-week adjunctive group therapy that has been used to treat
outpatients with BPD. STEPPS treatment for BPD emphasizes family systems,
such that family members and other significant figures in the patient’s life receive
psychoeducation on how best to respond to behaviors and emotional dysregulation

associated with BPD. This psychoeducation is one of three main components of
STEPPS, along with emotion management and behavior management skills training.
In an RCT, subjects participating in STEPPS combined with treatment as usual
showed greater improvements in impulsivity, negative affectivity, mood, and global
functioning than treatment as usual alone at one year posttreatment (Blum et al.,
2008).
Development of Dialectical Behavior Therapy and

Empirical Evidence
DBT was the first empirically supported treatment designed to treat severe and chronic,
suicidal and self-injurious patients who met diagnostic criteria for BPD. The treatment
combines elements of behavioral science, Zen practice, and a dialectical philosophy.
Since the early efficacy trials (Linehan, Kanter, & Comtois, 1999; see Lieb et al., 2004)
were published, DBT has been found to be an effective treatment for BPD and asso-
ciated problems in multiple RCTs conducted by at least three other research groups
around the world (Bedics, Atkins, Comtois, & Linehan, 2012; McMain et al., 2009;
Verheul et al., 2003). In multiple RCTs (Linehan et al., 2006; Soler et al., 2009), DBT
has been found to be superior to comparison treatments at reducing suicide attempts,
self-injurious behavior, anger, impulsivity, and other behaviors that interfered with
outpatient treatment such as premature dropout and inpatient/emergency room
admissions and days, while simultaneously improving global and social adjustment.
Moreover, DBT has been found to effectively target problems associated with Axis I
disorders such as drug abuse and depression (Lieb et al., 2004). Posttreatment, the
patients who received DBT reported fewer instances of severe behavioral dyscontrol
(the highest priority behavioral target in DBT), were less likely to drop out of treat-
ment, and had improvements in mood and functionality. Given the preponderance
of evidence, DBT has thus earned a designation as a “well established” empirically
supported treatment for BPD by the American Psychological Association, according
to the criteria outlined by Chambless and Hollon (1998), and is recommended as an
efficacious treatment for BPD by the American Psychiatric Association (APA, 2000).
The Dialectical Behavior Therapy Approach to

Marsha Linehan (1993a), the treatment developer of DBT, posits a reorganization of

the nine diagnostic criteria that comprise BPD to reflect “dysregulation” in five func-
tional domains that can be targeted by clinicians. The five domains are emotion dys-
regulation, interpersonal dysregulation, self dysregulation, behavioral dysregulation,
and cognitive dysregulation (see Table 51.1). The theoretical underpinnings of DBT
have been described in detail elsewhere (Koerner and Linehan, 1992; Linehan, 1993a;
Table 51.1 Linehan’s Reorganization of the Nine DSM-IV Diagnostic Criteria into Five
Areas
Emotion dysregulation: Affective lability

Problems with anger
Interpersonal dysregulation: Chaotic relationships
Fears of abandonment
Self dysregulation: Identity disturbance/confused sense of self
Sense of emptiness
Behavioral dysregulation: Parasuicidal behavior
Impulsive behavior
Cognitive dysregulation: Dissociative responses and/or paranoid ideation
Note. Adapted from Linehan (1993a).
Miller, Rathus, and Linehan, 2007) and are only briefly reviewed here. Dialectics,
Zen, behaviorism, and the biosocial theory are the theoretical underpinnings of DBT.
Dialectics
A dialectical philosophy emphasizes an understanding of reality or truth from
multiple perspectives. A dialectical view on the nature of reality posits that: (a)
apparent contradictions can both bear truth; (b) reality is in constant change; and (c)
this change is brought about by finding a synthesis that integrates elements of the
opposing positions into a new “truth.” In this way, dialectics is a way to embrace
conflict rather than try to refute competing ideas with logic. The overarching
dialectic in DBT is acceptance of oneself in the moment and trying to change oneself.
A dialectical philosophy provides a rationale for a treatment structure that integrates
acceptance and validation strategies with procedures to change behavior and suicidal
crises. The fundamental dialectic in DBT is that patients need to change their behavior
while simultaneously accepting themselves as they are now. The therapist facilitates
change by helping the client to embrace the contradictions in multiple viewpoints
rather than attempting to refute them with pure logic. These contradictions arise
both within a session and in everyday life, and to the extent that the therapist can
help the client reconcile opposing contradictions and find a synthesis, the client will
be moving toward greater balance in his or her thoughts, actions, and emotional
reactions. We characterize this as “walking the middle path” between extreme
positions. The dialectical position guides the application of all other DBT strategies.
Zen
A central tenet of Zen is radical acceptance of the moment without change.
To experience the world as it is, patients are asked to develop greater awareness of the
present moment, without filters. The primary tools for this in DBT are mindfulness
skills in which clients are taught to observe and describe the world without judgment,
and to notice their experience without getting caught up in it. Zen also describes the
consequences of not seeing reality, or maintaining an attachment to reality being a cer-
tain way. In DBT, an attempt is made to help clients radically accept painful experiences
rather than fighting reality as it is and in turn perpetuating their own suffering.
Behaviorism
DBT is, above all else, a “behavioral” treatment in the classical (or radical) sense
of the term—that is, DBT is based upon the principles of learning theory. With
roots in the basic work of Pavlov (classical conditioning) and Skinner (operant
conditioning), and extensions by modern-day behaviorists such as Bandura (social
learning), practicing DBT requires a consistent focus on basic stimulus–response
patterns, as well as the context in which these behaviors occur, that have garnered
clinical and empirical evidence for more than 100 years. Cognitive interventions
are employed at times as intervention strategies in DBT; however, contingency
management and exposure-based interventions are more typical. The use of learning
theory to conceptualize clients’ problems leads to a focus on defining behaviors and
implementing interventions that can be described precisely, measured, and tracked.
Identification and analysis of controlling variables in DBT gives essential information
about how a therapist can best intervene to help a client to change. This iterative
process of understanding the unfolding links between thoughts, emotions, and
behaviors forms the backbone of DBT.
In the present, dysfunctional behaviors related to strong emotional responses are
often maintained through negative reinforcement. For example, engaging in self-harm
behavior such as cutting may serve to distract from dysphoria or refocus the emotions
of an individual with BPD on a newer, less emotionally evocative stimulus (i.e., pain in
one’s arm due to superficial self-injury). While the behavior may have some negative
results for the individual (bleeding, shame), the emotionally reinforcing properties of
dysfunctional behaviors such as NSSI cannot be minimized.
Biosocial Theory
Linehan’s (1993a) biosocial theory suggests that BPD criterion behaviors stem from
a combination of biological and environmental factors. Specifically, these factors
are emotion dysregulation, which is biological in origin, and invalidating environ-
ments, where inadequate emotion regulation coaching and dysfunctional learning
take place—hence the term biosocial theory (Miller et al., 2007).
Emotion dysregulation. The biosocial theory argues that there is a pervasive dysfunc-
tion in the emotion regulation system that of course is neurobiologically based. There
may be genetic, prenatal, and traumatic childhood events that affect the development
of the brain and nervous system. Borderline behavioral patterns are functionally related
to or are unavoidable consequences of this fundamental dysregulation across emo-
tions, including both positive and negative emotions. Systematic dysregulation is due
to high “emotional vulnerability” coupled with difficulties in modulating emotional
reactions. High emotional vulnerability is conceptualized as high sensitivity to emo-

tional stimuli, intense emotional responses, and a slow return to emotional baseline.
Deficits in emotion modulation include difficulties in (a) inhibiting mood-dependent
dysfunctional behaviors, (b) organizing behavior in the service of goals, independent
of current mood, (c) increasing or decreasing physiological arousal as needed, (d)
distracting attention from emotionally evocative stimuli, and/or (e) experiencing
emotion without either immediately withdrawing or producing an extreme secondary
negative emotion (Linehan, 1993a).
Invalidating environment. Since most individuals with an initial temperamental

vulnerability to intense emotionality do not develop BPD, the theory suggests that
particular developmental environments are necessary. Linehan (1993a) characterizes
an “invalidating environment” as one that is defined by persistently responding to an
individual’s thoughts, feelings, or behaviors, as if they are wrong, inappropriate, or
invalid. Invalidating environments tend to punish, trivialize, dismiss, or attribute to
socially unacceptable characteristics (e.g., the person is being lazy, a manipulator, or
being overreactive). Some invalidating environments emphasize controlling emotional
expressiveness, oversimplify the ease of problem solving, and are intolerant of displays
of negative affect. Sometimes, it is merely a “poorness of fit” between a caretaker and
a child that may result in chronic invalidation that is bidirectional and thus worsens
over time (Crowell, Beauchaine, & Linehan, 2009). For example, take one family in
which one of the four children is significantly more emotionally expressive than the
other three and than the preferred level of emotionality in the household.
While some of these environments derive from pervasively invalidating family
interactions, others derive from the benign intentions of family members, teachers,
peers, coaches, therapists, medical doctors, and so on. In other words, saying to a
teenager who is crying after just failing her test, “Don’t worry honey, you’ll do fine
next time—it’s just one test,” may be experienced by the teen as invalidating even
though it is a reasonable assumption that the caregiver did not intend it to be.
Regardless of its source, the overall consequences of the transactional pattern
between emotion dysregulation and the invalidating environment are the emotional
and behavioral patterns exhibited by an individual with BPD. Such a person has
never effectively learned how to label and regulate her own emotional arousal, how
to tolerate emotional distress, or even when to trust his or her own feelings as valid.
Over time, an individual who fails to trust his or her own experience ultimately relies
on the environment for cues about how to act, think, or feel. This reliance on others
affects the development and maintenance of interpersonal relationships, one’s stable
sense of self, and a capacity to self-regulate emotions (Miller et al., 2007).
The invalidating environment’s tendency to trivialize or ignore the expression of
negative affect tends to shape an expressive style later seen in individuals with BPD.
This style vacillates between inhibition and suppression of emotional experience
and extreme emotional displays. Self-injury, drug use, and disordered eating, to
name a few, may have affective regulating properties as well as being effective at
eliciting helping behaviors from an environment that otherwise ignores efforts to
ameliorate intense emotional pain. When conceptualized from this vantage point,
the dysfunctional behaviors of BPD can be viewed as maladaptive solutions to

overwhelming and painful negative affect.
Due to the aforementioned problems, Linehan (1993a) and Miller et al. (2007)
have identified behavioral patterns that often interfere with effective therapy and fall
on six bipolar dimensions.
Dialectical Dilemmas: Dysfunctional Behavior Patterns in

These six dysfunctional behavior patterns are defined as dialectical dilemmas, because
individuals with BPD often attempt to regulate their emotional responses in an
over- or under-regulated manner and tend to swing between the two poles. These
vacillations tend to perpetuate themselves over time and create new problems. Indeed,
they can destroy treatment progress if not addressed skillfully. DBT seeks to move
clients away from these behavioral extremes and toward more balanced, synthesized
behavior. Finding more moderated emotional and behavioral responses to these
dialectical dilemmas are called secondary targets in DBT.
Linehan’s (1993a) standard dialectical dilemmas and corresponding secondary
targets that were developed originally for adults and are also applicable to teens with
BPD are listed in Table 51.2. Rathus and Miller (2000) developed three additional
Table 51.2 Linehan’s Standard Dialectical Dilemmas
Dialectical dilemma Treatment targets
1. Emotional vulnerability vs. (a) increasing emotion modulation and

self-invalidation decreasing emotional reactivity
(b) increasing self-validation; decreasing

self-invalidation
2) Active passivity vs. apparent (a) increasing active problem solving;

competence decreasing active passivity
(b) increasing accurate communication of

emotions and competence; decreasing
mood-dependent behavior
3) Unrelenting crises vs. (a) increasing realistic decision making and

inhibited experiencing judgment; decreasing crisis generating
behaviors
(b) increasing emotional experiencing;

decreasing inhibited experiencing
Note. Adapted from Linehan (1993a).

Table 51.3 Dialectical Dilemmas for Adolescents and Families
Dialectical dilemma Targets
1. Excessive leniency vs. (a) increasing authoritative discipline;

authoritarian control decreasing excessive leniency
(b) increasing adolescent self-determination;

decreasing authoritarian control
2. Normalizing pathological (a) increasing recognition of normative

behavior vs. pathologizing behaviors; decreasing pathologizing of
normative behavior normative behaviors
(b) increasing identification of pathological

behaviors; decreasing normalizing of
pathological behaviors
3. Forcing autonomy vs. (a) increasing individuation; decreasing

fostering dependence excessive dependence
(b) increasing effective reliance on others;

decreasing excessive autonomy
Note. Adapted from Miller, Rathus, & Linehan (2007).
dialectical dilemmas that are common among adolescents with their families and
treatment providers which are listed in Table 51.3. It is important to note that
each patient is unique and typically engages in a subset of the dialectical dilemmas.
Clinicians should identify which dialectical dilemmas apply to their specific patient
and aim to decrease the patient’s engagement in these dysfunctional behavior patterns
by tailoring the patient’s treatment to the specific targets which correspond to the
patient’s particular dysfunctional pattern. Treatment targets are also listed in Tables
51.2 and 51.3.
Structure of Treatment: Comprehensive and Multimodal
An assumption of DBT is that effective treatment for multiproblem patients must

be sufficiently broad-ranging to meet the needs of a complex patient and the sys-
tem working to treat them. Thus, as opposed to most forms of CBT which are
delivered in a single modality, DBT includes multiple components to address five
specific functions relevant to any intervention intended to be comprehensive. Stan-
dard outpatient DBT meets these functions in the following ways: (a) it improves
motivation to change and reduces behaviors antithetical to a life worth living through
weekly individual psychotherapy that involves a blend of behavioral, cognitive, and
acceptance-oriented interventions; (b) it enhances capabilities via weekly, group-based

behavioral skills training focused on development of skills to regulate emotions, to
tolerate emotional distress when change is slow or unlikely, to increase interpersonal
skills, and to influence or control attention in order to participate skillfully in the
present moment; (c) it ensures that newly acquired capabilities are generalized to
daily life through the modality of as-needed phone coaching as well as through a
variety of other means such as homework assignments; (d) active work is undertaken
to maintain and enhance therapist motivation and skill to treat clients effectively
through a weekly therapist consultation team in which therapists apply DBT prin-
ciples and strategies to each other; and (e) the environment is structured, when
needed, to support therapist capabilities and reinforce client skilled behaviors (Linehan,
1993a).
Structure of Dialectical Behavior Therapy by Treatment Mode

Structure of individual therapy. Individual therapy typically occurs once weekly for
approximately one hour. The individual therapist functions as the primary therapist
(i.e., the point person) for the treatment of a patient. That is, the individual therapist is
responsible for overall treatment planning, monitoring and ensuring progress toward
all DBT targets, integration of all modes of therapy, consulting with the patient
about how to have effective interactions with other treatment providers, and the
management of all life-threatening behaviors and crises. In Stage 1, treatment time is
allotted to address the behavioral targets described earlier.
Each Stage 1 DBT session begins with a collaborative review of the week via the
use of a self-monitoring form—called a diary card—that provides a way for clients to
track emotions, primary targets (e.g., suicidal ideation), use of DBT skills, and other
relevant behaviors for a particular client (e.g., disordered eating behaviors). Clients
are asked to complete this self-monitoring form daily between sessions. The therapist
reviews the diary card collaboratively with the client at the start of each session, and
structures their time in session according to the problem behaviors that were present
in the preceding week. There are very few rigid rules in DBT, but one of them is that
if there was a target 1 behavior (i.e., suicidal or nonsuicidal self-injurious behavior) in
the previous week, the therapist must conduct a behavioral assessment. This means
that all NSSIs, suicide crisis behavior, intrusive or intense suicidal ideation, images,
or communications, as well as significant changes in suicidal ideation or urges to self-
harm, are addressed as soon as possible after their occurrence. Self-harm, regardless
of lethality or intent, is never ignored; these behaviors are among the best predictors
of future lethal acts (Bergen et al., 2012), can cause substantial harm, and must be
brought under control before treatment can progress.
The primary tool for implementing individual therapy is a behavioral “chain” anal-
ysis, which is an exhaustive detailing of the antecedents, behaviors, and consequences
preceding, during, and following a target 1 behavior. This tool allows the therapist to
analyze problem behaviors and also provides the framework for generating solutions
to such behavior. Chains are conducted each week based on behaviors that present
on the diary card, and the behavior of focus is determined based upon the target
hierarchy.
Telephone consultation. A unique and integral part of DBT is the provision of

telephone consultation to (a) help the patient transfer or generalize new behaviors to
his or her natural environment, (b) provide crisis intervention and coaching on skillful
behavior before the patient engages in dysfunctional behavior (i.e., cutting), and
(c) to address any conflicts or misunderstandings that arise during therapy sessions,
instead of waiting until the next session to deal with the emotions (see Koons, 2011,
for a discussion). For patients who are reluctant to call even after being oriented and
encouraged to call, the therapist should conduct a practice call in session and/or
progress to scheduled phone calls in order to shape the client’s behavior. An important
point regarding phone coaching is that DBT patients are encouraged to call before
crises or NSSI incidents occur; an adult client who has self-injured is told she is not
to contact her therapist for 24 hours afterward. In DBT with adolescents, we do not
enforce the 24-hour rule for medical-legal reasons; however, we are mindful not to
reinforce problem behavior and, if called after a self-injurious act, the therapist only
conducts a brief assessment as to whether medical attention is necessary and then
quickly brings the phone call to an end.
Skills training group. DBT assumes that many of the problems experienced by patients
who are chronically suicidal or who engage in NSSI result from a combination of
motivational problems and skills deficits. That is, we assume that these clients have
simply never learned the necessary skills to cope with their painful emotions and
behavior, and our goal is to enhance their motivation to learn new ways to cope with
their emotional pain. For this reason, DBT emphasizes skills-building to facilitate
behavior change and acceptance. In standard DBT, the four skills modules are taught
weekly in 2- or 2.5-hour psychoeducation skills training groups. Each module is
taught for 8 weeks. These skills, for adult BPD patients, are outlined and described
in detail in Linehan’s (1993b) skills training manual. For adolescent BPD patients,
the adolescent and family members attend skills group. A skills training manual
for this population is in press (Rathus & Miller, in press). Groups use a standard
behavior therapy skills-building format and procedures: didactic instructions, modeled
examples, coached rehearsal of new skills, feedback, and homework assignments.
A typical format for a group is to dedicate the first half of the session to a review of
the previous week’s homework and the second half to teaching new skills.
The four DBT skills training modules target the behavioral, emotional, and
cognitive dysregulation of BPD: mindfulness, interpersonal effectiveness, emotion
regulation, and distress tolerance. The first 2 weeks of each new module are spent
on mindfulness and the remaining 6 weeks are spent on the particular module. The
target hierarchy for group therapy differs from that of individual therapy in that the
primary focus is on acquisition of the DBT skills according to the curriculum outlined
in the manual. The only target higher than skills acquisition is therapy-destroying
behavior, which is relatively rare as such behaviors must be egregious (e.g., violence
toward another group member; self-injuring during group therapy).
Therapist consultation team. DBT was developed to treat emotionally distressed clients
at high risk for suicide. With such clients, ruptures in the therapeutic relationship are
common. Thus, peer consultation was included as a key component of the original
treatment model to avoid therapist burnout, a common occurrence with this patient
population. Consultation to the therapist has several purposes. Most importantly,
the team must ensure that the clinician remains in the therapeutic relationship and
remains effective throughout the course of a treatment that may well be tumultuous.
Without ongoing supervision and consultation, clinicians working with this client
population can become “stuck” in extreme positions, and increasingly less open to
feedback from others. Therapists may blame themselves or their patients, and may
become emotionally exhausted over time, and thus ineffective.
In an adherent DBT program, the consultation team functions as therapy for the
therapist, in which the members apply DBT principles directly to each other in order
to provide support, maintain morale, and ensure fidelity to the model. The team is
comprised of individual therapists, skills trainers, and pharmacotherapists who meet
once weekly (typically for 1–2 hours). Each therapist who joins the team makes
a commitment to adhere to six agreements that maintain the treatment frame and
promote more effective and productive interactions among team members. These
agreements include: (a) to avoid polarization by taking a dialectical stance; (b) to
maintain a nonjudgmental, phenomenological empathic stance toward oneself, team
members, and clients; (c) to acknowledge fallibility; (d) to observe their own personal
limits and be aware that limits may vary across team members; (e) to agree to consult
to the patient about how to interact with other team members rather than speaking
on another person’s behalf (either the client or another provider); and (f) to agree
that team members do not have to have exactly the same limits, or reactions to clients,
and therefore do not have to be “consistent” with one another at all times.
When therapists violate these agreements (e.g., by adopting a defensive and
judgmental stance toward patients and family members) or otherwise engage in team-
interfering behaviors (e.g., repeatedly missing the team meeting), these actions are
addressed during the team meeting—in much the same way that problematic client
behaviors are targeted in individual sessions. For example, if a therapist attends a con-
sultation team meeting and describes a client as “hateful” or “manipulative,” members
of an adherent DBT team will highlight the problem behavior (i.e., taking a judgmen-
tal, pejorative stance); validate the therapist’s sense of feeling overwhelmed, angry, and
ineffective; help the therapist generate nonjudgmental behavioral descriptors about
the client’s behaviors; and assist the therapist to develop empathic interpretations
of client behavior, perhaps by referring back to the biosocial model and the client’s
idiographic case conceptualization history to highlight the client’s emotional suffering.
The precise structure of the team meeting is not dictated in the treatment manual.
However, the team must have a leader (i.e., a program leader), and each meeting must
be led by a meeting chairperson (which need not be the team leader), who takes the
role of keeping time and collaboratively setting the agenda with other team members.
Meetings typically begin with a participant-led mindfulness exercise which facilitates
therapists’ personal mindfulness practice and enhances focus on the meeting. Unlike
a traditional case review meeting, it is the emotions, cognitions, and behaviors of the
therapist (instead of the patient) that are the primary focus, and members are asked
to describe where they need help in the treatment of the patient. Although patient
updates may occur, they are kept to a minimum.
Therapeutic Relationship
The DBT clinician fosters a therapy relationship that is genuine and in which the
therapist and client have equal status. The relationship is “real” as opposed to role-
bound, and the therapist will make efforts to reduce the power difference between
client and therapist. This stance is reflected most pointedly by the therapist behaving
in a radically genuine manner. It is also explicit at a broad level in the assumptions
about clients and therapists, and it clearly permeates all the DBT strategies. This style
is advocated for all DBT clinicians who interact with the client (e.g., skills trainers,
individual therapists, pharmacotherapists, etc.).
These therapeutic relationships are used to shape adaptive behavior on the part of
the client. This means that clinicians must be acutely aware of how their response
can influence client behavior. This is particularly true in the individual therapy
context, where the relationship can serve as a powerful reinforcer to keep the client
motivated to remain in treatment, to practice skills in daily life, and to work hard
during and between sessions. Indeed, the DBT clinician’s reaction to a client’s in-
session behaviors can be a critical contingency management strategy to shape adaptive
behaviors. The therapist can respond differentially depending on whether an in-
session behavior is adaptive or problematic. For example, the therapist may explicitly
communicate what he or she likes about the patient and be responsive to his or her
requests—especially when requests are skillfully made. Common reinforcing therapist
responses for adaptive client behaviors (e.g., collaborating, spontaneously generating
solutions, or fully participating in a role play) include increasing validation, expressing
more concern or interest, decreasing attempts to control the client, and offering to
extend or shorten the session according to the client’s requests. Conversely, the DBT
clinician may use principles of extinction to withhold a reinforcer for maladaptive
behaviors. For example, Christina would at times repeat, “I don’t know”, or “I can’t
remember” in response to questions. This is not uncommon among clients who have
learned in other contexts that such questions may block additional questions and
stop the assessment. Christina’s therapist successfully extinguished the behavior by
persisting with the questions with responses such as, “Let’s keep trying to figure
it out. What is the last moment you remember that day?” At other times, a DBT
clinician may apply a mild aversive by withdrawing attention or warmth (assuming
that the client finds this desirable) in response to problematic behavior.
Another corollary is that DBT identifies therapist self-disclosure as a strategy that
reflects one aspect of the radically genuine nature of the therapeutic relationship.
The DBT clinician shows a willingness to reveal more information about him- or
herself in the context of the therapy relationship to enable clients to use the relation-
ship as a means to learn about themselves and about relationships more generally.
Therapists follow two general guidelines to ensure that their self-disclosures resem-
ble a nontherapy relationship while also remaining within professional limits. First,
therapists observe their own limits in relation to the amount of self-disclosures.
Second, therapists must disclose information that is in the best interest of the client.
Hence, therapists must remain vigilant of the effect on clients, and modify as needed.
Finally, the individual therapist fosters a strong alliance with the client, marked
by a style that is responsive, genuine, and communicates liking. While this is typical
of many therapy approaches, it is unusual when applied to clients or patients with a
diagnosis of BPD, which is often viewed in an extremely negative light.
Major Strategies and Techniques
In individual DBT, the therapist combines strategies in a flexible manner to treat the
primary target behavior that has occurred since the last session and any problematic
behaviors that occur in session. The core strategies in DBT can be broadly classified
as either primarily change-oriented or primarily acceptance-oriented, although both
are woven together in the treatment of any given behavior regardless of the treatment
modality. Described below are the three major classes of strategies used in DBT.
Problem-Solving Strategies
Linehan (1993a, 1993b) includes in her treatment a wide array of standard behavioral
assessment strategies and behavior therapy techniques that are broadly classified
as problem-solving strategies or change-oriented strategies. Identification of the
problem is often difficult. Clients are usually taught early in treatment to view
dysfunctional behaviors, such as self-injury, as signals of a problem that needs to be
solved. The therapist and the client then conduct a thorough behavior analysis of what
led up to these behaviors. The therapist attempts to identify the variables controlling
the behavior by obtaining an exhaustive, detailed, moment-by-moment account of
the antecedents, the behavior, and the consequences through a chain analysis. The
therapist then generates hypotheses based on the biosocial model and behavioral
theories about causal relationships among the links. When in doubt as to which links
are the most important, the biosocial theory suggests attending to the emotions.
Next, alternative response chains (i.e., adaptive solutions) are identified via a solution
analysis. Through this process, the therapist is able to identify what was interfering
with more adaptive behavior, and then suggests change procedures on this basis.
Validation Strategies
The essence of the validation strategies is for the therapist to actively accept the
patient’s experience and communicate this acceptance to the patient. Validation
strategies lead the therapist to search for the inherent validity and functionality of
the patient’s responses. This is in contrast to most cognitive and behavior therapies,
in which a primary focus of treatment is to search for and replace dysfunctional
behaviors. The therapist serves as a contrast to the invalidating environments often
experienced by the patient.
Linehan (1997) has described how validation can be conceptualized in six levels.
The first three levels generally reflect basic therapeutic strategies for building and
maintaining rapport. The second three focus on communicating accurately the
valid and invalid nature of the patient’s behavior and emotional responses. Level 1
validation refers to demonstrating via active listening and nonverbal expression

that one is “awake” and responsive to the subtle behaviors of the patient as they
occur. That is, the therapist is responsive to the patient and listening without being
controlled by bias and preconceived notions. Level 2 is accurately reflecting the
content of the patient’s statements to provide reassurance that the patient is being
heard correctly. Level 3 can be termed “mind-reading” and consists of stating
the content of the patient’s communications and experience that are not explicitly
verbalized. Unlike the making of interpretations, mind-reading requires clear and
explicit verification of its accuracy from the patient. Level 4 is communicating to
the patient that his or her behavior is completely understandable (i.e., valid) given
the patient’s learning history and/or biological make-up. Level 5 validation, by
contrast, conveys to the patient that his or her behavior is actually valid or normative
in terms of the present context (e.g., “Most people would feel that way in this
type of situation”). Finally, Level 6 validation is called radical genuineness, and is a
broader, more general style that reflects the DBT position that the therapy relationship
should be as similar as possible to a nontherapy relationship (while also remaining
professional). It also refers to a stance in which the therapist responds to the client
as a person, rather than as a category such as “patient.” Radical genuineness is
believing in the client’s inherent capacity and wisdom, and holding the bar high,
rather than assuming he or she is highly fragile and different from the rest of
humanity.
Dialectical Strategies
The specific dialectical strategies all share an inherent blend of acceptance and change
strategies that promote progression in therapy sessions. Dialectical strategies include
the use of metaphors and storytelling, entering the paradox, playing devil’s advocate,
extending, and “making lemonade out of lemons.” Below, we provide a fuller
description and examples of some of these techniques.
When telling a story or using a metaphor, for example, the therapist tries to
communicate both an acceptance of the client’s position, and yet present an alternative
that will allow the client to make a move forward.
The strategy of extending is much like a technique employed in the martial art
aikido, when the practitioner accepts and moves with the energy of the opponent’s
attack rather than against it—hence allowing the opponent to be propelled forward
to the point of being knocked off balance. As a therapy technique, the clinician alters
the direction of the session by unexpectedly accepting and extending an attack by
the client. Doing so disarms the client and enables the therapist to change course
without damaging the session or the therapy relationship. The therapist joins with
the client and allows the behavior, and then carries it beyond the point intended by
the client.
Entering the paradox requires the therapist to highlight contradictions as they arise
to help clients tolerate them until they can find a synthesis in the two positions. For
example, when Christina became self-judgmental and viewed herself as “lame” and
“stupid” because she had cried in front of her ex-boyfriend and told him she loved
him, her therapist highlighted that being able to express emotion and be vulnerable
was a sign of strength.
Relapse Prevention
In DBT, relapse is conceptualized as a natural part of the change process; hence,
if problem behaviors recur, the therapist would apply the same DBT principles
discussed previously. The stage theory described earlier can incorporate the possibility
that individuals may fall back in to old behaviors. A client who enters treatment in
Stage 2 who has not self-injured for several years may engage in the behavior again in
the face of acute stress. A DBT clinician would rely on the existing case formulation
to develop hypotheses about the function of this behavior. A chain analysis should
always be conducted as a means to assess hypotheses, and also because previous
behaviors may recur in response to entirely new prompting events and be linked with
new controlling variables.
Clinical Case
To illustrate key concepts in DBT, we will refer to our composite client, Christina,
a 16-year-old white female who attends a local high school. Christina was referred
to outpatient treatment following a 2-day visit in the emergency room after she
threatened to jump off a bridge when her boyfriend broke up with her via text
messaging. Her mother, who was with her at the time, reported that she had
to physically restrain her daughter from jumping. She took her daughter to the
psychiatric emergency room, where she was kept for 2 nights before being released
with a referral for outpatient treatment.
Christina has a long history in the mental health system. She had experienced two
psychiatric hospitalizations following suicide attempts that required medical attention
(i.e., overdosing on her mother’s prescription medication) and also a history of panic
attacks, learning disability, and oppositional behavior that complicate her clinical
picture. Christina reports having engaged in NSSI in the form of cutting herself,
chewing on her cheeks until they bled, and occasionally burning herself since the age
of 12 years. She reported having had three outpatient therapists but both she and
her mother reported that outpatient therapy helped “a little” but overall did not help
to make Christina better. At the time of intake, Christina met diagnostic criteria for
a number of DSM-IV diagnoses including bipolar disorder, social anxiety disorder,
panic disorder without agoraphobia, and intermittent explosive disorder, as measured
by the semistructured interview called the Kiddie-Schedule for Affective Disorders
and Schizophrenia (K-SADS), and borderline personality disorder as measured by a
structured clinical interview called the Structured Interview for DSM-IV Personality
(SIDP-IV).
In terms of her family and social history, it appeared that she experienced significant
invalidation from her environments. When she was 9 years old, her parents went
through an acrimonious divorce, and Christina reported that her mother often
confided in her, crying to her about her father’s extramarital affairs, while her father
alternated between showering her with affection and attention or disappearing with
no contact for months at a time. Her father had remarried, had a new daughter, and
had not contacted Christina for 6 months. Her learning disabilities were untreated
and unsolved in school. She apparently had never been able to articulate her emotions
well, and coped either by withdrawing to her room for days at a time, or through
physical aggression. She felt different from her family members. Her mother stated
that she did not understand her daughter, explaining that “all family members had
been through tough times but that Christina was extremely sensitive and needed to
toughen up to get through life.”
Overview of Treatment Protocol
Addressing the multiple problems of a client like Christina requires the therapist to
respond flexibly to circumstances that may vary greatly from week to week. Indeed,
in the initial sessions that were focused more on behavioral assessment, Christina
presented quite variably. In one session, she sobbed constantly as she reported
avoidance of social activities, several recent panic attacks, and having cut herself
superficially with a razor on her arms. In the next session, Christina expressed intense
anger at her school counselor and reported she had threatened to kill herself if her
mother made her go to school. Christina, who had already missed 10 straight days of
school and was failing most of her classes, was refusing to go because of her avoidance
of seeing her ex-boyfriend. When the therapist had a collateral session with Christina’s
mother, her mother reported that she thought it was better to keep Christina at
home and calm rather than get into an argument about her school attendance and
admitted she was completing Christina’s homework assignments to help her pass some
classes. Christina also had a number of therapy-interfering behaviors that complicated
treatment delivery, including showing up late, missing some appointments, and not
completing homework assignments. The level of complexity and comorbidity detailed
here, which are typical of this client group, would clearly make it impossible to adhere
to a single, highly structured treatment protocol. Which problem would a therapist
target first? What changes would they need to make when other problem behaviors
function to derail any given singular focus?
In developing DBT, Linehan (1993a) focused on deriving and codifying principles
for treatment rather than one specific protocol. A protocol-based treatment is highly
specified, and may outline specific steps and strategies for each treatment task or
even each session. By comparison, DBT is a treatment frame guided by the biosocial
theory that employs multiple (at times competing) strategies. Reliance on theory and
an unwavering focus on case conceptualization helps the clinician’s efforts toward
“knowing what to do” in a given moment as well as any given session. Treatment
is conducted by prioritizing the problems to be addressed according to the level of
threat that they pose to a reasonable quality of life. That is, the more threatening,
debilitating, and complex problems must be addressed first. This principle helps the
DBT clinician to address the client’s truly urgent needs while not being distracted by
other, less threatening situations that inevitably arise from week to week.
Structure of Treatment: Stages and Targets

Linehan (1993a) describes five stages of treatment, each of which is oriented around
an overarching problem area that impedes client progress toward a “life worth living”
as the client defines it. The two stages upon which Linehan and others have conducted
most of the research and which we will summarize below are the Pretreatment Stage
and Stage 1.
Pretreatment Stage. All clients who begin DBT are in Pretreatment, in which the
primary target is building and strengthening commitment to the treatment. In this
stage, the therapist orients the client to the philosophy, structure, length, and assump-
tions about treatment. Clients are asked to give clear verbal consent to participate
in all necessary treatment modes, and to work on the goals of treatment—including
DBT’s hierarchy of behavioral targets—which places eliminating suicidal behavior
and NSSI as the top priority. The therapist must work strategically to gain the client’s
commitment to engage in the treatment by constantly linking the client’s individual
life goals (e.g., developing a romantic relationship; keeping a job) to the reduction
in suicidal behavior (or, more broadly, to the DBT target hierarchy). Because DBT
requires voluntary rather than coerced consent, both the therapist and the client
should have the option of committing to DBT as opposed to another (non-DBT)
treatment or to defer treatment until a later time.
Importantly, the onus is on the therapist to strategically “sell” the treatment and not
only elicit but strengthen commitment. This is also the opportunity for the therapist
to assess and problem solve potential obstacles to therapy that are likely to arise for a
given client. For example, Christina reported a significant history of social anxiety and
described herself as “hyper-sensitive to people not liking me and dumping me.” As
an example, she noted that her anxious feelings and fears of being cheated on while
dating her ex-boyfriend had led her to constantly demand to check his cell phone and
e-mail messages, which, in turn, he found intrusive and overwhelming. He decided
to break up with her and reportedly told several of their mutual friends that she
was “crazy.” Christina experienced such intense embarrassment and shame about her
behavior toward her ex-boyfriend (whom she generally liked and respected) that she
refused to return to school.
A DBT clinician, anticipating the potential for similar problems to arise in therapy,
would bring up this possibility directly: “This treatment is for a year and in that time,
there is the potential for a lot of things to happen, some of which might result in you
feeling ashamed. We need to make sure that shame doesn’t get you dropped from
treatment for missing four individual or group sessions in a row. So let’s think now
about how you might handle this later.” The therapist sets the stage for problem
solving but also works to build commitment by highlighting a chance to break out of
what might be a dysfunctional pattern, and by linking attendance to a goal beyond
skills acquisition and also to the client’s overall goal of reduction of social anxiety. It is
important to note that standard DBT treatment programs have an attendance policy
for each modality of treatment (see Linehan, 1993a, and Miller et al., 2007, for more
details).
Under ideal circumstances, Pretreatment is completed during the first four sessions
(postintake evaluation) for a one-year standard DBT program. Although it can be done
in fewer sessions, particularly in a briefer program, it is a crucial stage of treatment
that can have a major impact on treatment success. In our experience, novice DBT
clinicians may rush through Pretreatment too quickly, missing a unique window of
opportunity to strengthen a superficial commitment or troubleshoot potential therapy-
interfering behaviors. Attentiveness to this stage is especially important for BPD clients
who tend to lack problem-solving skills and may also be a sign of mood-dependent
behavior. The main idea, however, is to remain in Pretreatment targeting commitment
until the client has agreed to the treatment as it has been adapted to their particular
problem behaviors and circumstances.
Christina was clearly most appropriate for Stage 1, in which the overall goal is to
improve behavioral control and develop basic capacities in order to stay connected to,
and ultimately benefit from, treatment. In order of priority, specific behavioral targets
included: (a) suicidal or homicidal or other imminently life-threatening behavior;
(b) therapy-interfering behavior of the therapist or client; (c) behavior that severely
compromises the client’s quality of life; and (d) deficits in behavioral skills needed to
make life changes.
Behavioral analyses of Christina’s suicidal behaviors just prior to the start of
treatment, and those early in treatment, indicated some consistent behavioral patterns.
First, Christina tended to have highly conflictual relationships and to engage in out-
of-control behaviors (e.g., cutting, pushing others, school refusal) emblematic of
Stage 1 within hours of an aversive interpersonal interaction. She reported becoming
flooded with emotions during these conflicts, such that she felt “overwhelmed, empty,
and ashamed.” These interactions occurred with a variety of people including her
boyfriend, family members, friends, and even strangers. In these situations, Christina
often had urges to cut herself, and, when she did so, the self-injurious behavior
decreased her emotional arousal (thus, negatively reinforcing cutting as a mood
regulation strategy).
For example, the therapist may place an emphasis on assessment of emotion and
ask: “So it sounds like cutting your arm reduces your anxiety … at least in the short
term. If we could find other ways to help you manage your emotions since you don’t
like the look of your scars on your arms, would you be interested?”
In Christina’s case, they developed a list of problem behaviors based on the Stage 1
target hierarchy: (a) cutting her arms when distressed; (b) showing up late to therapy
appointments; (c) refusing to attend school due to anticipatory anxiety; and (d) lack
of usage of alternative distress tolerance and emotion regulation strategies to deal
with painful emotions that have fewer negative consequences. The therapist should
consistently link these problem behaviors as obstacles to Christina’s stated goals
for her life (i.e., improving her physical appearance, becoming a model, graduating
high school) to help keep Christina motivated to change. Signs that Christina may
have reached the end of Stage 1 are the cessation of suicidal behaviors, NSSI, and
other major therapy-interfering behaviors in conjunction with an increase in skillful
behavior. At this point, the client and therapist should assess the client’s remaining
problems and consider the next steps given available treatment resources.
Difficulties Encountered During Treatment
The case that has been described is quite typical and was chosen to illustrate the
potential for focused, intensively delivered DBT. There are also common difficulties
that DBT clinicians encounter which we highlight in this section.
Lack of Specificity in the Chain Analysis

Chain analysis and solution analysis are the backbone of DBT and lay the foundation
for problem solving and any behavior change. However, this is also one of the most
common areas of difficulty for novice DBT clinicians, who have the task of assessing
the circumstances surrounding a target behavior in sufficient detail to be able to
also generate solutions that the client will use in similar future circumstances. For
maximum effectiveness, the analysis must be done quickly enough to ensure enough
time for solution generation, and yet must also be done collaboratively to ensure
cooperation.
Lack of a Clear Definition of the Target

Thus, identifying the right target quickly is important. At times it is quite clear that
the target is cutting oneself. At other times, however, the problem behavior is not
well defined. Feeling “depressed”, for example, needs to be further assessed so that
it is framed in terms of a behavioral excess or deficit on the part of the client. For
instance, Christina would state in session that she felt depressed, which the therapist
helped her to frame as “not going to school today because you feel depressed.”
Where to Begin (Too Much Breadth, Not Enough Depth)

Because a chain analysis is essentially a slice of time, it may not have a clear beginning.
Theoretically speaking, the beginning point is the prompting event; however, this is
not easily identifiable. In our experience, therapists frequently spend too much time
focused on events that occurred far back in time—a general rule of thumb is to focus
on links that occurred in the hours (or minutes) just prior to the target behavior, and
then to work outward as needed. It is often quite useful to pinpoint the moment in
which the client felt an urge to engage in the target behavior that eventually happened
(e.g., the urge to steal), or when the client made a choice to engage in the problem
behavior (“At what point did you make the decision that you were going to ignore
the alarm and stay in bed?”).
Inadequate Specificity
Similarly, therapists often allow the client to tell a long narrative with a great deal of
extraneous information. This often happens in response to the clinician asking, “What
happened?” Telling a story is a perfectly understandable behavior for a client, since
this is often how we relay information to significant others in our lives. However, a
chain analysis is not simply a story of what happened in an incident. It is up to the
therapist to orient the client to why and how this is a problem, and to guide the
structuring of the chain so that there is enough time to pinpoint key links.
Difficulties in the Solution Analysis

It is a problem when generated solutions in session are not matched to specific links
in the chain. Also, clients need to be asked to state explicitly whether they will use the
particular skill in that particular context to deal with that link. An important context
for these clients is their mood, and a common shortcoming of the solution analysis
is that the generated solution is not feasible when they are highly distressed. For
example, cognitive strategies may not be useful if the client is highly anxious and at
that point simple skills that can directly lower the physiological arousal are needed
as a first step. Therapists should also be mindful to generate multiple solutions for
critical links in the chain in order to enhance flexibility in the client.
Inadvertent Reinforcement of Avoidance Behaviors in the Session

Another common problem is that therapists are not mindful of their responses to
clients, and inadvertently reinforce in-session escape behaviors. What is often blocking
the client from problem solving are thoughts such as, “I can’t,” “This is too hard,” and
another similar hopeless thoughts and associated emotions. If a therapist subsequently
drops the topic, that can prove to be negatively reinforcing the client’s behavior and
ultimately maintaining the client’s passive problem-solving style. To not do this
requires almost hyperalertness on the part of the therapist—who must be mindful of
the client’s behavior, the likely function of the behavior (i.e., avoidance), and how his
or her own response could be reinforcing (most commonly by moving off the topic
at hand, frequently by problem solving). Hence, DBT emphasizes therapists using
their own mindfulness skills during sessions. In addition, a therapist may tape his
or her sessions and play them for a colleague to obtain feedback about the possible
reinforcing aspects of certain responses.
Therapist’s Emotions Interfering with Treatment

One of the most common problems among therapists working with BPD patients
is when the therapist becomes dysregulated. Common patterns we have noticed are
therapists becoming highly anxious and hence becoming rigid and attempting to
control the patient; therapists “falling in the pool” of hopelessness with the client—in
effect agreeing to give up; and therapists becoming angry toward their clients and
judgmental of their behavior. A common reason for this last pattern is when the
therapist assumes intent on the part of the client based on the consequences of the
behavior. For example, a therapist may feel overwhelmed and preoccupied by a highly
distressed client who often calls for coaching on weekends or in the evenings. The
therapist, worried about the client’s behavior and unsure if he or she will call, has
difficulty enjoying downtime with family and friends. The therapist may begin to
think, “This client is so needy and deliberately trying to punish me by sabotaging

my personal life so that I will only be focused on her needs.” While the therapist’s
personal life may indeed be suffering in those instances, it is important to separate
those painful consequences from the intent of the client. Important means to address
this therapist behavior include getting help from the consultation team to practice
skills such as mindfulness, dialectical thinking, and emotion regulation; therapists
being honest with their clients about their personal limits; and therapists reviewing
their assumptions about patients in DBT.
Clinical Decision Making: Integrating Science and Practice
Decisions about which strategy to use in DBT is guided by research in behavioral

science. Self-injury and suicidal behavior are targeted first in part because research has
shown them to be among the strongest predictors of eventual suicide. The approach
to emotion dysregulation is based on basic emotion research. For example, data
suggest that certain emotion regulation approaches are best deployed based on the
level of arousal (Gottman & Katz, 2002). Clients must first be coached to reduce
physiological arousal, then reorient attention, and only then can they think about
strategies that involve higher-level processes that can help organize their behavior
toward longer-term (non-mood-dependent) goals. Further, much of DBT, which
assists clients to engage their problems directly rather than to avoid them, can also
be seen as exposure and response prevention, for which there are substantial research
data (Foa, Yadin, & Lichner, 2012).
Most of the behavioral strategies in DBT have an empirical basis—even if only
indirectly by indication of their efficacy as part of other treatments. Behavioral theory
and evidence for the efficacy of behavioral rehearsal is one of the reasons that there is
a preference for targeting in-session behaviors whenever possible.
Conclusion
DBT is the leading evidence-based treatment for clients diagnosed with BPD, and for
those with suicidal, nonsuicidal self-injurious, and other severe behavioral difficulties.
The treatment is principle-driven in order to be maximally flexible while still following
a coherent theory and structure; it is comprehensive and multimodal, and integrative.
It places an emphasis on treating emotions. A great deal of attention is paid to helping
the therapist to remain engaged and motivated and to prevent therapist burnout.
DBT has the most empirical support for the treatment of BPD, yet additional research
is needed to determine which specific modes and strategies of DBT are associated
with improved outcomes.
References
Bateman, A., & Fonagy, P. (2008). 8-year follow-up of patients treated for borderline
personality disorder: Mentalization-based treatment versus treatment as usual. American
Journal of Psychiatry, 165(5), 631–638. doi:10.1176/appi.ajp.2007.07040636
Bedics, J. D., Atkins, D. C., Comtois, K. A., & Linehan, M. M. (2012). Treatment differ-
ences in the therapeutic relationship and introject during a 2-year randomized controlled
trial of dialectical behavior therapy versus nonbehavioral psychotherapy experts for bor-
derline personality disorder. Journal of Consulting and Clinical Psychology, 80, 66–77.
doi:10.1037/a0026113
Bergen, H., Hawton, K., Waters, K., Ness, J., Cooper, J., Steeg, S., & Kapur, N. (2012).
How do methods of non-fatal self-harm relate to eventual suicide? Journal of Affective
Disorders, 136(3), 526–533. doi:10.1016/j.jad.2011.10.036
Blum, N., St. John, D., Pfohl, B., Stuart, S., McCormick, B., Allen, J., … Black, D. W.
(2008). Systems training for emotional predictability and problem solving (STEPPS)
for outpatients with borderline personality disorder: A randomized controlled trial and
1-year follow-up. American Journal of Psychiatry, 165(4), 468–478. doi:10.1176/appi.
ajp.2007.07071079
Chambless, D. L., & Hollon, S. D. (1998). Defining empirically supported therapies. Journal
of Consulting and Clinical Psychology, 66(1), 7–18. doi:10.1037/0022-006X.66.1.7
Clarkin, J. F., Levy, K. N., Lenzenweger, M. F., & Kernberg, O. F. (2007). Evaluating three
treatments for borderline personality disorder: A multiwave study. American Journal of
Psychiatry, 164(6), 922–928. doi:10.1176/appi.ajp.164.6.922
Crowell, S. E., Beauchaine, T. P., & Linehan, M. M. (2009). A biosocial developmental
model of borderline personality: Elaborating and extending Linehan’s theory. Psychological
Bulletin, 135(3), 495–510. doi:10.1037/a0015616
Fabrega, H., Ulrich, R., Pilkonis, P., & Mezzich, J. E. (1992). Pure personality disorders in an
intake psychiatric setting. Journal of Personality Disorders, 6(2), 153–161. doi:10.1521/
pedi.1992.6.2.153
Foa, E. B., Yadin, E., & Lichner, T. K. (2012). Exposure and response (ritual) prevention for
obsessive-compulsive disorder: Therapist guide (2nd ed.). New York, NY: Oxford University
Press.
Giesen-Bloo, J., van Dyck, R., Spinhoven, P., van Tilburg, W., Dirksen, C., van Asselt, T., …
Arntz, A. (2006). Outpatient psychotherapy for borderline personality disorder: Random-
ized trial of schema-focused therapy vs transference-focused psychotherapy. Archives of
General Psychiatry, 63(6), 649–658.
Gottman, J. M., & Katz, L. F. (2002). Children’s emotional reactions to stressful parent–child
interactions: The link between emotion regulation and vagal tone. Marriage & Family
Review, 34(3–4), 265–283. doi:10.1300/J002v34n03_04
Kellogg, S. H., & Young, J. E. (2006). Schema therapy for borderline personality disor-
der. Journal of Clinical Psychology, 62(4), 445–458. doi:10.1002/jclp.20240
Kernberg, O. F. (1985). Borderline conditions and pathological narcissism. Northvale, NJ: Jason
Aronson.
Koerner, K., & Linehan, M. M. (1992). Integrative therapy for borderline personality disorder:
Dialectical behavior therapy. In J. C. Norcross and M. R. Goldfried (Eds.), Handbook of
psychotherapy integration (pp. 433–459). New York, NY: Basic Books.
Koons, C. R. (2011). The role of the team in managing telephone consultation in dialectical
behavior therapy: Three case examples. Cognitive and Behavioral Practice, 18, 168–177.
doi:10.1016/j.cbpra.2009.10.008
Lieb, K., Zanarini, M. C., Schmahl, C., Linehan, M. M., & Bohus, M. (2004). Borderline
personality disorder. Lancet, 364(9432). doi:10.1016/S0140-6736(04)16770-6
Linehan, M. M. (1993a). Cognitive-behavioral treatment of borderline personality disorder.
Linehan, M. M. (1993b). Skills training manual for treating borderline personality disorder.
Linehan, M. M. (1997). Validation and psychotherapy. In A. C. Bohart & L. S. Greenberg
(Eds.), Empathy reconsidered: New directions in psychotherapy (pp. 353–392). Washington,
DC: American Psychological Association. doi:10.1037/10226-016
Linehan, M. M., Comtois, K. A., Murray, A. M., Brown, M. Z., Gallop, R. J., Heard, H. L., &
Lindenboim, N. (2006). Two-year randomized controlled trial and follow-up of dialectical
behavior therapy vs. therapy by experts for suicidal behaviors and borderline personal-
ity disorder. Archives of General Psychiatry, 63(7), 757–766. doi:10.1001/archpsyc.63.
7.757
Linehan, M. M., Kanter, J. W., & Comtois, K. A. (1999). Dialectical behavior therapy
for borderline personality disorder: Efficacy, specificity, and cost effectiveness. In D. S.
Janowsky (Ed.), Psychotherapy indications and outcomes (pp. 93–118). Washington, DC:
American Psychiatric Association.
McMain, S. F., Links, P. S., Gnam, W. H., Guimond, T., Cardish, R. J., Korman, L., & Streiner,
D. L. (2009). A randomized trial of dialectical behavior therapy versus general psychiatric
management for borderline personality disorder. American Journal of Psychiatry, 166(12),
1365–1374. doi:10.1176/appi.ajp.2009.09010039
Miller, A. L., Muehlenkamp, J. J., & Jacobson, C. M. (2008). Fact or fiction: Diagnosing bor-
derline personality disorder in adolescents. Clinical Psychology Review, 28(6), 969–981.
doi:10.1016/j.cpr.2008.02.004
Miller, A. L., Rathus, J. H., & Linehan, M. M. (2007). Dialectical behavioral therapy with
suicidal adolescents. New York, NY: Guilford Press.
Rathus, J. H., & Miller, A. L. (2000). DBT for adolescents: Dialectical dilemmas
and secondary treatment targets. Cognitive and Behavioral Practice, 7 (4), 425–434.
doi:10.1016/S1077-7229(00)80054-1
Rathus, J. H., & Miller, A. L. (in press). Dialectical behavior therapy: Multi-family skills training
manual. New York, NY: Guilford Press.
Rogosch, F. A., & Cicchetti, D. (2005). Child maltreatment, attention networks, and poten-
tial precursors to borderline personality disorder. Development and Psychopathology, 17 ,
1071–1089. doi:10.1017/S0954579405050509
Soler, J., Pascual, J. C., Tiana, T., Cebrià, A., Barrachina, J., Campins, M. J., … Pérez, V.
(2009). Dialectical behaviour therapy skills training compared to standard group therapy in
borderline personality disorder: A 3-month randomised controlled clinical trial. Behaviour
Research and Therapy, 47 (5), 353–358. doi:10.1016/j.brat.2009.01.013
Verheul, R., van den Bosch, L. M. C., Koeter, M. W. J., de Ridder, M. A. J., Stijnen, T.,
& van den Brink, W. (2003). Dialectical behaviour therapy for women with borderline
personality disorder: 12-month randomized clinical trial in The Netherlands. British
Journal of Psychiatry, 182, 135–140. doi:10.1192/bjp.02.184
Walter, M., Berth, H., Selinger, J., Gerhard, U., Küchenhoff, J., Frommer, J., & Dammann,
G. (2009). The lack of negative affects as an indicator for identity disturbance in
borderline personality disorder: A preliminary report. Psychopathology, 42(6), 399–404.
doi:10.1159/000241196
Widiger, T. A., & Frances, A. (1985). Axis II personality disorders: Diagnostic and treatment
issues. Hospital & Community Psychiatry, 36(6), 619–627.
Winograd, G., Cohen, P., & Chen, H. (2008). Adolescent borderline symptoms in the
community: Prognosis for functioning over 20 years. Journal of Child Psychology and
Psychiatry, 49(9), 933–941. doi:10.1111/j.1469-7610.2008.01930.x
Young, J. E., Klosko, J. S., & Weishaar, M. E. (2003). Schema therapy: A practitioner’s guide.
Zanarini, M. C., Gunderson, J. G., & Frankenburg, F. R. (1989). Axis I phenomenol-
ogy of borderline personality disorder. Comprehensive Psychiatry, 30(2), 149–156.
doi:10.1016/0010-440X(89)90067-9
52
Suicidality
Erin F. Ward-Ciesielski and Marsha M. Linehan
University of Washington, United States
Few would argue with the fact that suicide is a major public health problem both
nationally and internationally. Efforts at outreach and intervention for those at risk for
suicide in the United States have had no impact on the suicide rate. In fact, since 1955
the rate of suicide in the United States has remained fairly consistent at 10.2 to 12.4
suicides per 100,000 (World Health Organization, 2010). With the most extensive
epidemiological studies indicating that for each completed suicide worldwide there are
anywhere from 10 to 40 suicide attempts (e.g., Centers for Disease Control, 2012),
there is no question that suicidal behaviors are a significant target for improvement.
With all of these data pointing to the persistence of suicidal behavior, it is necessary
that providers develop and evaluate treatments to help the individuals that comprise
these statistics. The work that has been accomplished to date forms the basis of
this chapter. We review the empirical literature related to interventions for suicidal
individuals in which a cognitive behavioral therapy (CBT) intervention is compared to
another, non-CBT intervention and then attempt to highlight patterns and similarities
across the reviewed trials. Finally, we provide some recommendations for clinicians in
the hope that we can take note of the potential mechanisms through which CBT has
been shown to affect suicidal behaviors.
In order to provide a comprehensive review and summary of the extant literature
related to interventions targeting suicidal behavior, it is principally important to
discuss a handful of significant weaknesses that impact the interpretation of each
empirical finding. Admittedly, every research arena has its unique challenges and is
charged with finding creative ways to overcome them. The field of suicide intervention
research is no different. In fact, many of the challenges facing suicide intervention
researchers are the same faced by individuals working in the community who provide
mental health services to suicidal patients (e.g., fear of litigation; Pearson, Stanley,
King, & Fisher, 2001). However, there are many challenges that are unique—or

DOI: 10.1002/9781118528563.wbcbt52
at least more central—in this domain (e.g., the low base rate of suicidal behavior;
see Pearson et al., 2001, for a review) and researchers seeking to implement CBT
interventions with this population have worked diligently to make progress in the
ability to impact suicidal behavior. However, in order to provide a context for
the studies that will be reviewed, it is imperative to begin this discussion by noting the
current weaknesses that continue to impede empirical progress.
The first limitation is the overall shortage of randomized controlled trials (RCTs)
to evaluate the efficacy and effectiveness of available or newly developed interventions
which specifically target suicidal behaviors. In order to be classified as an RCT, par-
ticipants must be randomly assigned to intervention conditions. The importance of
randomization in treatment trials cannot be overemphasized. Without the random-
ization of participants to treatment conditions, it cannot be assumed that changes that
occur during or after the implementation of the intervention are actually the result of
that intervention. Instead, the results obtained can only be thought of as correlation
(Linehan, 1997).
The RCT represents the gold standard for determining the efficacy of treatments
across disciplines, yet in the field of suicide intervention research there are only 47
trials that meet this criterion (Ward-Ciesielski & Linehan, in press). This number is
troublingly small considering that suicide remains in the top 10 causes of death in
the United States (Centers for Disease Control, 2012). This is perhaps even more
noteworthy when we look at the RCTs evaluating CBT interventions for suicidal indi-
viduals, relative to the number of RCTs that use CBT interventions to target other
populations and problem domains. For example, when searching the Cochrane Cen-
tral Register of Controlled Trials (2012) for randomized trials of CBT interventions
in which depression is a keyword, 359 are reported. For trials in which anxiety is a
keyword, 409 are reported. Certainly a percentage of these results would be excluded
following scrutiny to determine whether they were actually RCTs of CBT interven-
tions; however, the same search using suicide as a keyword yields only 32 results. If
we use as a starting place the fact that only 17 RCTs of CBT have been identified
using our criteria, we can estimate that half of the results obtained are irrelevant to the
topic at hand. This leaves nearly 180 depression trials and nearly 205 anxiety trials.
Given the persistence of the problem of suicide, the disparity is difficult to rationalize.
The second limitation, and perhaps the one most responsible for the slow rate
of progress in the field of suicide intervention research, is the lack of operational
definitions for intervention targets. A field cannot collectively work toward common
ends if each research team defines their variables and outcomes of interest indepen-
dently of other previously provided definitions. Unfortunately, such idiosyncrasy is
common throughout this area of research. During the past several decades, the field of
suicide intervention research has seen the use of terms such as nonsuicidal self-injury,
intentional self-harm, suicide attempt, parasuicide, suicidal ideation, and self-injurious
thoughts all to represent components of the larger category of suicidal behavior. Not
only are there many different terms reported by different research teams, but only a
handful of these researchers define the specific way in which they are using any one
of the terms. Thus, we are left with results that are difficult to generalize and, overall,
less meaningful to others in the field. In the 17 RCTs of CBT, the minority of studies
(seven of 17; 41%) include any sort of operational definition of the class of behaviors
Suicidality 1243
they are targeting in their treatments and measuring as an outcome. Further, within
these seven trials, even the definitions themselves are inconsistent. Throughout the
discussion of the research literature on CBT interventions for suicidal individuals,
definitions as provided by the researchers are included as available. Additionally, trials
that do not include operational definitions will be noted.
Owing to the variability of terms used by different research teams, we are very
limited in our ability to compare results from research studies by the terms that
researchers themselves have used. At times it is difficult to determine if one study’s
“suicide attempt” is the same behavior as another study’s “parasuicide” because these
terms have not been defined. In some cases, these two terms may have been meant
to be used interchangeably; however, far more frequently there are differences in
the two ranging from subtle, nuanced variations to downright conflicting definitions.
This leaves us with stilted progress by necessitating replication for the purpose not of
confirming significant results, but in order to clarify what is actually being studied and
impacted by an intervention. Thus, the field of suicide intervention research needs
to choose terms, operationally define them, and then use them consistently across
studies and across research teams. This will allow us to refine definitions if needed,
but also to clarify and generalize the results of each new trial that is conducted.
Following the limitations imposed on a field that does not use a consistent language,
the third limitation is the infrequent use of published assessment instruments that
have demonstrated reliability and validity. Although there are psychometrically sound
measures of suicide attempts and nonsuicidal self-injury, such as the Suicide Attempt
Self-Injury Interview (SASII; Linehan, Comtois, Brown, Heard, & Wagner, 2006)
and the Self-Injurious Thoughts and Behaviors Interview (SITBI; Nock, Holmberg,
Photos, & Michel, 2007) as well as measures of suicidal ideation such as the Scale
for Suicidal Ideation (SSI; Beck, Steer, & Ranieri, 1988) and the Suicidal Behaviors
Questionnaire (SBQ; Addis & Linehan, 1989; Osman et al., 2001), these measures
are rarely used in suicide intervention studies (see Brown, 2001, for a full review).
In fact, less than half of the RCTs of CBT (eight of 17; 47%) targeting suicidal
behaviors measured their primary outcome(s) with an assessment that has adequate
and published psychometric properties.
Instead of using measures such as those mentioned above, many studies develop
idiosyncratic assessments for their specific study (e.g., Hawton et al., 1987), use a
subset of items from measures that have previously been criticized for their clinical
utility (e.g., Bagby, Ryder, Schuller, & Marshall, 2004) and reliability, or simply do not
report which outcome measures they used at all (e.g., Donaldson, Spirito, & Esposito-
Smythers, 2005). Other research teams develop new measures, whether formally or
informally, that have a similar or identical purpose to those already available in the
literature (e.g., using unidentified questionnaires to gather participants’ reports of
their own behaviors; Brown et al., 2005; Hawton et al., 1987; Liberman & Eckman,
1981).
While the rationale for pointing out this limitation is not to advocate that those
measures which have previously been published and have demonstrated reliability
and validity are sufficient to assess any and all domains related to suicidal behaviors,
it is critical to underscore the importance of accurately measuring outcomes with
assessments that we know actually measure what we think they measure. Doing
so requires some basic analysis to determine whether a newly created instrument

measures what we think it measures and does so reliably. Unfortunately, even if
these nonvalidated measures are very strong and accurately assess the domains we are
interested in, we simply have no way of knowing that to be the case without the
results of the psychometric analyses. Even more unfortunately, this process remains
distressingly rare within the field of suicide intervention research. In effect, we have a
limited number of empirically grounded assessment instruments and a large number
of other instruments that are useless without the appropriate evaluation. Again, we
must spend time replicating and redoing studies in order to correct these oversights
of previous researchers, and again, our own forward movement toward developing
effective treatments for suicidal individuals is delayed.
Further, even when psychometrically sound measures are used in studies, the
reliability of assessments within individual studies is not evaluated with any consistency.
Most of the RCTs of CBT did not report the context of their assessments. Of
those that did, a fundamental tenet of clinical trials methodology—namely, blind
assessment—was reported in only seven (41%) of the RCTs. Only with the use of
blind assessment can we be sure that the results obtained were not the inadvertent
result of an assessor’s bias based on knowledge about the treatment condition assigned
(e.g., Kazdin, 1977; Rosenthal, 1966).
The fourth and final limitation is the exclusion of individuals at high risk for immi-
nent suicide from studies targeting suicidal behaviors. In most RCTs of what are now
considered evidence-based treatments (EBTs) for mental disorders, provisions are
often made in the exclusion criteria to rule out individuals deemed to be at risk of sui-
cide. Thus, although these treatments have been shown effective for disorders shown
to be correlated with suicidal behaviors (e.g., depression, anxiety disorders), we cannot
currently implement these treatments with suicidal individuals with the same diagnosis.
Research evaluating whether these EBTs are efficacious for a high-risk population has
yet to be carried out. Thus, suicidal individuals are similar to pregnant women in that
they are not only commonly excluded from clinical trials, but the ethical costs of not
learning how to treat these individuals are rarely discussed. That is, given the persis-
tence and significance of suicidal behaviors, the practice of excluding these individuals
from trials evaluating interventions for other psychological problems presents an eth-
ical dilemma that will remain as long as exclusion of these populations continues. The
question remains of whether it is ethical for a field to refuse to develop effective inter-
ventions for individuals with such a serious set of problems (i.e., suicidal behaviors),
but to be willing to develop interventions for people with less severe problems.
Even more important is the fact that intervention studies targeting suicidal behaviors
routinely exclude those at the highest risk for death by suicide. In fact, 36% (17 of
47) RCTs for suicidal interventions have excluded individuals at high risk for suicide.
Each of these 17 trials excluded individuals for at least one of the following reasons:
(a) they were in need of psychiatric treatment, (b) they were in need of inpatient
hospitalization, (c) they had been diagnosed with a mental disorder, or (d) they were
determined to need immediate treatment for suicidality. CBT intervention researchers
are similarly guilty of this exclusionary practice. Of the 17 trials reviewed here, six
(35%) excluded participants meeting one or more of these criteria. Unfortunately,
Suicidality 1245
this means that much of the research involving treatment of individuals with co-
occurring disorders and/or at very high risk of imminent suicide has yet to be carried
out. Promisingly, this trend appears to be improving in more recent studies. More
than a decade ago, Linehan (1997) commented on the fact that trials that included
the highest risk individuals had yielded a more consistently significant impact on
decreasing suicidal behaviors. This still appears to be the case and it is encouraging
that those at highest risk are being included more frequently.
As with virtually all other treatments for mental disorders or medical illnesses, no
treatment can completely eliminate the risk of the disorder or illness. The same is true
of suicide. Although some interventions have been shown to reduce specific suicidal
behaviors, no intervention has demonstrated effectiveness at eliminating the risk of
death by suicide. There is, without a doubt, much work to be done in this area. The
most productive and impactful way forward is to persevere in the use of rigorous
research methodologies and significantly to minimize the extent to which each study
leaves behind errors that will need to be remedied by future research endeavors.
There have been 47 RCTs explicitly targeting suicidal behaviors. However,
the remainder of this chapter focuses only on those RCTs that have explicitly selected
participants based on the presence of suicidal behaviors and have examined the
efficacy of a CBT-oriented intervention as the experimental condition. Therefore,
the following review focuses on 17 RCTs.
Why Try Cognitive Behavioral Therapy to Treat

Suicidal Behaviors?
Suicidal individuals have many well-documented deficits for which CBT interven-
tions appear tailor made. For instance, suicidal populations demonstrate reliable
deficits related to problem-solving abilities, especially interpersonal problem solving
(e.g., Bonner & Rich, 1988; Howat & Davidson, 2002; Linehan, Camper, Chiles,
Strosahl, & Shearin, 1987; Pollock & Williams, 1998; Schotte & Clum, 1982).
Sadowski and Kelley (1993) investigated the role of social problem solving in ado-
lescent suicide attempters as it related to suicide intent and medical lethality of the
method by which suicide was attempted. Of note is the fact that adolescents who
attempted suicide showed more problem-solving deficits than either psychiatric or
normal control participants. Additionally, Schotte and Clum (1982) reported that
poor problem-solving participants under high stress were the highest of all experimen-
tal groups on a measure of suicide intent, indicating that poor problem solving is one
important piece of the puzzle that contributes to suicidality in an individual. Further,
studies of active (a process in which the problem solver takes an active role in the reso-
lution of the problem) and passive problem-solving strategies (which are characterized
by a problem solver who relies on others or the passage of time to resolve a problem
situation) have consistently found that suicidal populations (e.g., suicide attempters)
rely more heavily on passive problem-solving strategies than both normal and psy-
chiatric control groups (Linehan et al., 1987; Pollock & Williams, 2004). Taken
together, this literature highlights the important role that targeted efforts at increasing
problem-solving capabilities may play in reducing the incidence of suicidal behaviors.
A second factor that lends itself to intervention using CBT approaches is the
interpersonal nature of many of the risk factors identified in the suicide literature.
Interpersonal stress (e.g., Davila & Daley, 2000; Joiner, Van Orden, Witte, &
Rudd, 2009), social isolation (e.g., Davidson, Wingate, Grant, Judah, & Mills, 2011;
Lamis & Malone, 2011), and social withdrawal (e.g., Stewart, Ross, Watson, James, &
Bowers, 2012) are a few of the many risk factors and warning signs of suicidal behavior
that have been identified and discussed. The extent to which the therapeutic alliance
is a central element of CBT interventions makes them particularly attractive to utilize
with a population oftentimes characterized by their detachment and interpersonal
isolation. Building a strong working relationship and using that rapport as a way to
enhance motivation to continue to do the challenging work involved in staying alive
when you want to die is paramount.
Randomized Controlled Trials of Cognitive Behavioral

Therapy Interventions
Inpatient or Partial Hospitalization

Some of the first CBT interventions were evaluated with inpatient suicidal populations.
Specifically, two trials compared variations of inpatient treatments that an individual
could receive. Liberman and Eckman (1981) selected a small sample of multiple
suicide attempters (undefined; 24 participants in total) who were admitted to the
inpatient unit following a suicide attempt. Participants were randomized to receive
behavior therapy or insight-oriented therapy during their 10-day admission. High
risk individuals were included in the study; however, two years after the treatment,
there were no significant differences between the two conditions on the number of
suicide attempts requiring medical attention (16.7% receiving behavior therapy, 25%
receiving insight-oriented therapy).
Patsiokas and Clum (1985) also selected a small sample of inpatients who were
hospitalized following suicide attempts (undefined). These participants were randomly
assigned to receive (a) cognitive therapy, (b) problem-solving skills training, or
(c) nondirective, reflective psychotherapy. Each intervention was conducted in ten
1-hour sessions over the course of the 3-week hospitalization. Similar to Liberman
and Eckman (1981), Patsiokas and Clum found no difference between the three
conditions on self-reported suicidal ideation or intent (undefined).
While Liberman and Eckman (1981) and Patsiokas and Clum (1985) targeted
adult populations and provided intervention on the inpatient unit, Rudd et al.
(1996) selected young adults (mean age 22 years) with a history of suicide attempts
(undefined) and/or suicide ideation (undefined). Participants were randomized to
receive treatment as usual (TAU) or a structured, time-limited, intensive outpatient
group therapy. Participants in the experimental condition received this treatment
for approximately 9 hours each day for 2 weeks. While both groups improved on
suicide ideation and suicidal behavior (undefined), the experimental intervention was
not significantly more effective than the TAU control relevant to repeated suicide
attempts (1.4% in the experimental condition, 0.8% in the control condition).
Suicidality 1247
Finally, Salkovskis, Atha, and Storer (1990) provided TAU with and without the
addition of a brief (five-session) cognitive behavioral problem-solving intervention.
Adult participants were admitted to an emergency room following repeated suicide
attempts (undefined) who had taken antidepressants as part of an overdose and who
scored at least a four on Buglass and Horton’s (1974) scale to predict repeated
suicidal behavior. In the CBT intervention condition, some sessions were provided
on an inpatient basis and others were provided in-home. They found that there were
significantly fewer repeated suicide attempts at 6 months in the experimental group
compared to the control condition (0% compared to 37.5%, respectively). Unfortu-
nately, the cumulative number of suicide attempts during the 18-month follow-up
was not significantly different between the groups; however, as is common with these
trials, the sample size used in this study was very small (20 participants in total).
These four trials represent the limited number of treatment development efforts
targeting suicidal populations by providing an inpatient or partial hospitalization
intervention using a CBT framework. Only one of these interventions (Salkovskis
et al., 1990) shows promise as a potential intervention for this population. Salkovskis
and colleagues’ (1990) intervention suggests that it may be possible to provide a
brief intervention with a very high risk population. However, given the previous
discussion of the lack of data supporting hospitalization as a treatment for suicidal
individuals, these results may suggest that interventions that require hospitalization
or day treatment are insufficient to impact suicidal outcomes.
Outpatient Interventions
There are several trials which can be broadly categorized as outpatient interventions
for suicidal individuals. These interventions include various strategies, which typically
include a limited number of sessions (e.g., Brown et al., 2005; Evans et al., 1999).
Unfortunately, albeit somewhat predictably, these trials yield inconsistent findings
related to their effectiveness at treating specific suicidal behaviors.
To date, three trials have evaluated manual-assisted CBT (MACT; Evans et al.,
1999; Tyrer et al., 2003; Weinberg, Gunderson, Hennen, & Cutter, 2006). Each
of these studies, however, has defined its sample, target behaviors, and intervention
slightly differently. To begin, Evans et al. (1999) recruited patients seen after an
episode of deliberate self-harm (parasuicide: “a non-fatal act in which an individual
deliberately causes self-injury or ingests a substance in excess of any prescribed or
generally recognized therapeutic dosage,” in Kreitman, 1977, p. 3) who also had a
previous history of deliberate self-harm in the past year and had a “disturbance” in
the flamboyant personality cluster (antisocial, histrionic, and borderline personality
disorders). Participants were randomly assigned to the MACT condition or TAU. The
MACT condition included between two and six sessions of structured, cognitively
oriented, problem-focused therapy based on a brief manual. Perhaps because the
sample size was so small (34 participants in total), there was no significant difference
between experimental and control conditions in the number of participants who
engaged in a suicidal act during the 4 to 6 months following treatment (56% of
participants in the MACT condition, 71% in the control).
Tyrer et al. (2003) also recruited participants following a repeated episode of

parasuicide or deliberate self-harm (parasuicide: “a non-fatal act in which an individual
deliberately causes self-injury or ingests a substance in excess of any prescribed or
generally recognized therapeutic dosage,” in Kreitman, 1977, p. 3). While Evans
et al. (1999) included high risk individuals, Tyrer et al. did not; however, they did use
a much larger sample (239 participants in the experimental condition and 241 in the
control). In this trial, participants randomly assigned to the experimental condition
received a booklet including information based on CBT principles and were offered
up to seven treatment sessions with a MACT-trained therapist. Similar to Evans
et al. (1999), Tyrer et al. (2003) did not find a significant difference between the
numbers of participants who engaged in deliberate self-harm across the two conditions
(39% of MACT participants, 46% of control participants). Additionally, there was no
difference in the number of deaths by suicide between the conditions (two in the
MACT condition, five in the control condition).
Finally, Weinberg et al. (2006) randomized women with a borderline personality
disorder diagnosis and a history of repeated deliberate self-harm (“intentional self-
inflicted injury without intent to die,” p. 482) to receive TAU with or without the
addition of MACT sessions. Despite the fact that there was no significant difference
between treatment conditions in terms of the amount of time to repeated deliberate
self-harm or suicidal ideation, individuals assigned to the MACT condition had
significantly fewer acts of deliberate self-harm than those assigned to the control
condition (mean frequency 1.98 compared to 6.69, respectively).
One potential explanation for the nonsignificant findings of the first two trials may
be that participants were given the option of not attending offered sessions. Those
participants in the Evans et al. trial (1999) only attended an average of 2.7 out of
six possible sessions. In the third trial by Weinberg et al. (2006), all participants
in the experimental condition completed the full six sessions of the intervention.
This may suggest the importance of in-person meetings to make the intervention
optimally effective, or that the dosage received by participants who do not attend
all available sessions is insufficient to obtain the full benefit of the intervention.
Additionally, Weinberg et al. (2006) excluded participants with prior suicide attempts
(“intentional act of self-inflicted injury that involves intent to die,” p. 482) while the
other two MACT trials included these participants. While this made for a less severe
sample, which can be considered a methodological weakness, in this case the increased
homogeneity obtained by excluding individuals at the severe end of the spectrum may
have made it easier to detect significant differences.
Hawton et al. (1987) randomly assigned participants admitted to the emergency
room for deliberate self-poisoning (undefined) to receive brief, problem-oriented
counseling in the clinic or a referral. The brief intervention, however, failed to
yield frequencies of repeated deliberate self-poisoning or deaths by suicide that were
significantly different between the two conditions (7.3% repeaters in the outpatient
problem-oriented counseling, 15.4% in the control condition).
McLeavey, Daly, Ludgate, and Murray (1994) took Hawton’s intervention one step
further and compared brief interpersonal problem-solving skills training to problem-
oriented counseling with a group of participants admitted to hospital following an
episode of intentional self-poisoning (undefined). However, consistent with much
Suicidality 1249
of the suicide intervention literature, McLeavey et al. used a very small sample size
and excluded participants at high risk for suicide. This may account for some of
their difficulty in detecting a significant effect of the intervention even though only
10.5% of participants in the problem-solving skills training condition repeated acts of
self-poisoning compared to 25% in the control condition.
Brown et al. (2005) recruited high risk participants who had made a suicide
attempt (“a potentially self-injurious behavior with a nonfatal outcome for which
there is evidence, either explicit or implicit, that the individual intended to kill himself
or herself,” p. 564) in the previous 48 hours. All participants received treatment
as usual in addition to intensive case management. Participants in the experimental
condition were also offered 10 sessions of CBT. This CBT intervention included
specific suicide prevention strategies and skills training to identify thoughts and
suicidal beliefs and to develop adaptive coping behaviors. Sessions were provided on
a weekly, biweekly, or as-needed basis. During the 18-month follow-up, participants
in the experimental condition made significantly fewer suicide attempts than those
in the control condition (24.1% compared to 41.6%, respectively). Unfortunately,
the absence of blind assessment somewhat reduces the certainty that we can place
on these results. It should be noted that it is not clear from the publication how
long participants were engaged in the CBT intervention in order to complete the
10-session protocol.
Utilizing a younger sample, Donaldson et al. (2005) selected adolescents in the
emergency room or inpatient unit following a suicide attempt (“any intentional,
nonfatal self-injury, regardless of medical lethality, if intent to die is indicated,”
p. 114). The experimental condition received skills-based treatment that included
problem-solving training and affect management by way of cognitive and behavioral
strategies (e.g., cognitive modification, relaxation, homework). This intervention was
compared to Brent and Kolko’s (1991) supportive relationship treatment, which
did not include any problem-solving skills training or homework. Receiving skills-
based treatment did not yield a significantly lower frequency of suicide attempts
during the 6-month follow-up when compared to the supportive relationship treat-
ment control (26.7% reattempts in problem-solving training, 12.5% in supportive
control).
Again using an adolescent sample, Wood, Trainor, Rothwell, Moore, and
Harrington (2001) evaluated an intervention for adolescents referred for deliberate
self-harm (DSH; “any intentional self-inflicted injury, irrespective of the apparent
purpose of the act,” p. 1247). The experimental intervention consisted of six acute
group sessions in conjunction with long-term group sessions combining CBT
and psychodynamic group psychotherapy strategies and a median two-and-a-half
individual sessions. They found a significantly lower mean number of acts of DSH
in the experimental when compared to the control condition (means: 0.6 and 1.8,
respectively) in addition to significantly fewer participants engaging in multiple acts
of DSH (6% compared to 32%, respectively). High risk participants (those ruled
too suicidal for ambulatory care) were excluded from the study; however, Wood
et al. did keep assessors blind to the treatment condition to which participants were
assigned. Unfortunately, in an attempt to replicate the findings of Wood et al.,
Hazell et al. (2009) were unsuccessful, which calls into question the effectiveness of
this intervention. Hazell et al. (2009) found a greater proportion of participants with
repeated episodes of DSH in the group therapy condition (88.2%) than the control
condition (67.6%).
While there is certainly great diversity in the samples and interventions grouped
together there, all of these interventions have a problem-focused, strategic approach
to treating specific suicidal behaviors. Additionally, many of these studies have
nonsignificant results and appear to have no more influence on subsequent suicidal
behaviors than control conditions. However, there are promising results to highlight.
Brown et al. (2005), Salkovskis et al. (1990), Weinberg et al. (2006), and Wood
et al. (2001) have all found significant intervention effects on subsequent suicidal
behaviors. Even more inspiring is the fact that both Brown et al. and Salkovskis et al.
included high risk individuals in their trials and were able to significantly reduce
suicide attempts beyond the level of the control condition. These studies certainly
deserve consideration for replication and validation, especially considering that neither
trial employed assessors who were blind to the treatment condition of participants.
Further, the other studies may not need to be disregarded completely. Instead, their
nonsignificant findings may be the result of insufficient power or less severe clinical
populations. More investigation would undoubtedly be a valuable addition to the
field.
To date, the intervention with the most empirical support for the reduction of
suicidal behaviors is dialectical behavior therapy (DBT; Linehan, 1993). DBT has four
randomized controlled trials demonstrating its efficacy in treating suicidal behaviors
(Koons et al., 2001; Linehan, Armstrong, Suarez, Allmon, & Heard, 1991; Linehan,
Heard, & Armstrong, 1993; Linehan et al., 2006; Verheul et al., 2003). DBT is a
principle- and protocol-based, manualized treatment that was developed specifically
for suicidal, difficult-to-treat clients. It has since been consistently shown to be an
effective intervention for suicidal and other extreme behaviors. In addition to weekly
individual therapy and phone consultation to patients, DBT includes skills training
in four primary areas of deficit: mindfulness, emotion regulation, distress tolerance,
and interpersonal effectiveness (for more information on DBT, see Chapter 51,
“Borderline Personality Disorder”).
In the first RCT of DBT, Linehan et al. (1991) recruited women meeting criteria
for borderline personality disorder who had a history of parasuicide (“any intentional,
acute self-injurious behavior with or without suicidal intent, including both suicide
attempts and self-mutilative behaviors,” p. 1060) and a recent incident within the
2 months prior to enrollment in the study. These participants were randomized to
receive DBT for one year or treatment as usual (i.e., referral to outpatient treatment).
Participants in the DBT condition had fewer episodes of self-inflicted injury (i.e.,
suicide attempts and self-inflicted injury combined) at the end of the treatment
year (63.6% compared to 95.5%, respectively). Additionally, this difference between
conditions was maintained during another year of posttreatment follow-up (26.3%
compared to 60%).
These compelling results were replicated 15 years later when Linehan et al. (2006)
again recruited borderline women with a history of suicidal behavior (“intentional,
non-fatal, self-injurious acts committed with or without intent to die,” p. 757) in
the 8 weeks prior to referral and at least one other intentional self-injury in the
Suicidality 1251
preceding year. Participants in the experimental condition again received DBT while
those in the control condition received treatment by expert non-behavioral therapists
in the community. The number of participants who attempted suicide was signifi-
cantly lower in the DBT treatment condition than in the control condition (23.1%
compared to 46%, respectively). Further, the DBT condition reduced emergency
room admissions by 53% and inpatient hospital admissions by 73%. This suggests
that DBT reduces suicidal behavior on an outpatient basis without incorporating
hospitalization.
Koons et al. (2001) provided further support for DBT in their randomized
trial with female borderline veterans. They found that participants in the DBT
condition had greater decreases in intentional self-harm (including suicide attempts)
at the follow-up assessment compared to the treatment as usual control condition
(10% compared to 20%, respectively). Finally, Verheul et al. (2003) found that
borderline women who received DBT engaged in significantly fewer self-mutilating
behaviors (undefined) during one year of treatment than participants who were
assigned to clinical management as a control condition (35% compared to 57%,
respectively).
One additional DBT trial has been conducted with a suicidal population. McMain
et al. (2009) compared DBT to general psychiatric management, which included
psychodynamically informed psychotherapy, case management, and medication man-
agement provided by therapists with expertise and interested in treating individuals
with BPD. Participants were adults meeting criteria for BPD who had engaged in
at least one suicidal or self-injurious behavior (undefined) in the last 3 months in
addition to at least one other incidence in the previous 5 years. While both treatments
significantly reduced suicidal and self-injurious behaviors during the one-year treat-
ments, there were no significant differences in suicidal outcomes between the two
conditions.
Taken in concert, these five studies—all of which utilized blind assessment and
used sample sizes adequate to detect effects of the DBT condition—provide the
strongest empirical support for any intervention targeting suicidal behaviors to date,
cognitively or behaviorally oriented or otherwise. While Koons et al. (2001) and
Verheul et al. (2003) did not specifically select participants with a history of suicidal
behavior, women with borderline personality disorder have been selected in these
studies because they represent a group with staggering suicide rates compared to
other populations (e.g., Brodsky, Groves, Oquendo, Mann, & Stanley, 2006; Soloff,
Lis, Kelly, & Cornelius, 1994). As DBT was developed for this difficult population,
it is the most compelling intervention and one that should be implemented with
complex suicidal patients. The inclusion of the highest risk suicidal patients makes
it all the more important that this treatment be considered when severe suicidality
is present. Additionally, its efficacy with suicidal patients who do not meet criteria
for borderline personality disorder should be evaluated. Finally, the nonsignificant
differences between treatment conditions in the trial conducted by McMain et al.
(2009) suggests that there is still room for improvement and additional studies
utilizing larger sample sizes may provide even more support for the use of this
treatment with suicidal populations.
An Analysis of the Critical Components

of Individual Interventions
As is clear from this brief review of the existing literature concerning RCTs in which
CBT interventions are the experimental condition, in many respects there is still a
long way to go toward finding effective interventions. CBT interventions make the
strongest showing of all interventions that have been evaluated. Given that the results
are mixed when collapsed across all these CBT interventions, it may not be sufficient
to examine these trials individually. Instead, we will attempt to look at the factors
involved in the interventions described above in order to identify the strategies that
appear to be most effective in order to move forward in our efforts to address the
problem of suicide.
While this qualitative analysis provides a starting place to further study and examine
which components of these interventions ought to be continued and expanded upon
and which may be better left out of future intervention endeavors, there are limitations
to taking such an approach. Specifically, the ideas presented here are based on the data
of varied studies using iterations of CBT interventions and are meant to provide one
interpretation of the various significant and nonsignificant findings in the literature.
Thus, the common elements we highlight are simply hypotheses about what may or
may not be important when trying to treat a suicidal population. Owing to the varied
nature of the different interventions we are attempting to synthesize in this review, we
believe our approach is more appropriate for this stage in the development of effective
interventions given the extant literature.
Significant Trials
Of the 17 trials described above, only eight found a significant difference between
the experimental (CBT) intervention and the control condition in outcomes related
to suicide and suicidal behaviors. Of these eight trials, three CBT interventions are
designed to be short-term, individual interventions (i.e., Brown et al., 2005; Salkovskis
et al., 1990; Weinberg et al., 2006), one is an intensive outpatient group intervention
for adolescents (i.e., Wood et al., 2001), and the remaining four are trials evaluating
the effectiveness of one year of DBT (i.e., Koons et al., 2001; Linehan et al., 1991;
Linehan et al., 2006; Verheul et al., 2003).
These eight trials have a number of potentially important elements in common.
First, they are all delivered on an outpatient basis. While two of the nonsignificant
trials described were conducted as inpatient interventions (i.e., Liberman & Eckman,
1981; Patsiokas & Clum, 1985), all of the trials with significant effects on suicidal
behavior were delivered in an outpatient setting. Overall, these two trials of inpatient
interventions raise important questions about the efficacy of hospitalization for
individuals who are suicidal. Without going too far afield, this issue is critically
important since not only is it possible to involuntarily hospitalize individuals in every
state in the United States, but also because there is compelling evidence that prior
inpatient treatment is a factor that heightens risk for suicide both immediately after the
hospitalization and in the long term (Combs & Romm, 2007; Kallert, Glockner, &
Suicidality 1253
Schutzwohl, 2008). Importantly, two additional inpatient trials (van der Sande et al.,
1997; Waterhouse & Platt, 1990) have been conducted to evaluate other, non-CBT
interventions compared to treatment as usual outside the inpatient unit. Both of these
additional trials have also failed to find support for inpatient hospitalization. While it
may be the case that patient characteristics that pre-date hospitalization are responsible
for these high postdischarge rates of suicide, we must also consider the possibility that
hospitalization of suicidal individuals is actually iatrogenic. The problem we are trying
to highlight here is that as the data stand, we cannot say one way or the other. While
it may be the case that heightened risk of suicidality is driving the high rates of suicide
following inpatient hospitalization discharge, we have to consider the alternative (that
hospitalization is actually iatrogenic) and collect the data to answer this important
question.
Second, based on the descriptions provided by the researchers in their publications,
each of the effective interventions emphasizes coping skills acquisition in some way.
In effect, there is an emphasis on learning new, adaptive coping behaviors to replace
suicidal ones. Importantly, most of the interventions specify teaching problem-solving
skills to participants. Whether this is done explicitly, as in Brown et al.’s (2005) time-
limited CBT intervention or Linehan’s (1993) DBT, or in a more indirect way as
in Weinberg et al.’s (2006) MACT intervention (which also utilized a subset of
skills from the DBT skills training curriculum) or Wood et al.’s (2001) adolescent
group treatment, participants receiving the experimental interventions are exposed to
discussions and specific teaching on problem-solving strategies and alternative ways to
cope with interpersonal problems, difficult emotions, or other stressors that may arise.
Further, given the previously discussed problem-solving deficits of suicidal individuals
(e.g., using passive problem-solving strategies; Linehan et al., 1987), the inclusion
of didactic teaching and interactive practice to develop problem-solving skills is not
surprising.
Third, five of the trials (the DBT trials and the adolescent trial) incorporate group
psychotherapy in addition to (or instead of) individual therapy. The primary aim of
these groups in DBT is the acquisition of behavioral skills, including those already
mentioned, to cope more effectively with situations where suicidal behaviors have
previously been utilized. Wood et al. (2001) also used the group format of their
intervention in order to target specific problems in the lives of the adolescent group
members and come up with ways to solve them. While Wood et al. continued with a
long-term psychodynamically oriented group after the acute group problem-solving
program ended, during this acute phase of the intervention, problem solving and other
relevant domains of concern (e.g., depression, peer relationships, family problems,
etc.) were targeted for improvement.
Fourth, most of the trials in which the experimental (i.e., CBT) intervention
outperformed the control condition place particular emphasis on the therapeutic
relationship. In DBT, there is a focus on the therapeutic relationship as an indicator of
what is happening outside therapy in the patient’s life and attachment to the provider
is used as a mechanism to keep the person alive. Similarities between in-session and
out-of-session patterns are highlighted and the therapy relationship is used as a vehicle
for change. The attachment and rapport created in the relationship is also brought in
as a protective factor to keep the person alive. Similarly, Wood et al. (2001) utilized the
therapeutic relationship to provide a positive and corrective environment from which

adolescents could grow through the difficulties they encounter. Although the two
remaining effective trials do not specify particular focus on the therapeutic relationship
in the description of their interventions, given that the therapeutic alliance is a central
component of any CBT treatment (see Chapter 1, “The Therapeutic Relationship”),
we can guess that the relationship is a focal point.
Finally, it is important to note the commonalities across the four DBT trials,
which are considered standard DBT practices. Several of these practices that may
be most important in this treatment’s repeated efficacy with suicidal populations
are: (a) targeting suicidal behavior, (b) focusing on creating a life worth living, (c)
balancing problem-oriented (change) techniques with acceptance techniques, and
(d) behavioral chain analysis. Additionally, DBT clinicians often become experts in
managing and treating suicidal behavior by virtue of their extensive training while
learning the treatment.
DBT is a principle-driven treatment that has specific protocols for use depending
on what behaviors have occurred between and within sessions. From the outset,
DBT therapy sessions are structured around a target hierarchy, which prioritizes life-
threatening behaviors above other therapy-interfering or quality-of-life-interfering
behaviors. From this organization, DBT providers explicitly focus on suicidality and
target it for change. Given this explicit emphasis on suicidal behavior as the target for
change, rather than other conceptualizations of suicidal behavior which place these
behaviors as merely symptoms of an underlying disorder (e.g., depression), it appears
that this foundational organization of DBT is necessary—although likely insufficient
in isolation—to impact the incidence of suicidal behavior.
Another important factor in the framework of DBT is the goal of building a life
worth living, rather than preventing suicide, per se. This is a critical underpinning of
the treatment and, in essence, highlights that a more effective way to keep someone
alive is to help them create a life that they want to live and do not want to give up
through suicide. While assessment and management of suicidal crises, precipitating
factors, and coping skills are also fundamental components of the treatment, it is a
unique worldview to focus not on, for example, removing lethal means alone, but also
simultaneously to work to figure out what the individual’s life would need to be like
in order for it to be one that the person wants to continue living and then to work on
bringing that life into existence.
The central dialectical tension in DBT is that of attempting to balance acceptance
and change. This means that at any moment in treatment, the therapist is providing
what is needed in that particular instance, rather than following some proscribed “if X
happens, then do Y” protocol. This means that DBT is not purely a change-focused
treatment at the expense of alienating the patient nor is it a purely acceptance-focused
treatment at the expense of not making the necessary changes in life in order to reduce
suicidality. Instead, the treatment represents a synthesis of these two poles in which
the therapist will, at times, alternate between supporting the patient by validating and
conveying understanding of where he or she is and the pain and difficulties in his or her
life and teaching, modeling, encouraging, and pushing the patient to do more, work
harder, and make difficult changes in order to create a life worth living. Many different
treatments for various disorders now discuss the importance of acceptance. Often this
Suicidality 1255
is achieved by incorporating mindfulness into the treatment (e.g., acceptance and

commitment therapy [Hayes & Wilson, 1994], mindfulness-based cognitive therapy
[Williams et al., 2000], etc.). However, DBT was the first and remains the only
treatment in which this is applied to suicidal populations. Especially considering that
much of the work related to the effectiveness of DBT with suicidal populations has
been conducted using patients who meet criteria for borderline personality disorder,
and who might reasonably be considered some of the most complicated and complex
suicidal patients, providing a treatment that simultaneously emphasizes acceptance
and change could be the factor within the treatment that has made it so consistently
effective. While many of the interventions reviewed here emphasize problem solving,
far fewer underscore the importance of also supporting and accepting patients where
they are while in the midst of suicidal crises or recurrent suicidal behaviors. DBT
is also the only treatment reviewed here to underscore the critical role of teaching
clients to accept themselves.
Behavioral chain analysis is a method for detailed, moment-by-moment assessment
of problematic target behaviors that includes attending to prompting events leading
up to the problematic behavior, the behavior itself, and positive and negative conse-
quences that follow the behavior in time. The goal of conducting a chain analysis is
both to make previously unnoticed contingencies clear and to identify and problem
solve other potential coping skills or strategies that could have been implemented to
prevent the target behavior from occurring. Owing to the deficits in recalling specific
events that have been demonstrated with suicidal populations (Pollock & Williams,
2001), conducting such an analysis serves the added benefit of elucidating increased
detail about the event (J. M. Williams, personal communication, 1991) as well as
diversifying the range of possible locations in the chain of events for new behavior to
be inserted.
Finally, suicide expertise may be more important than any of the other factors
discussed so far. Looking closely at the one study of DBT with a suicidal population
in which DBT did not outperform the control condition (McMain et al., 2009), the
providers in the control condition were selected because they were experts at treating
suicide. This suggests that expertise in suicide risk assessment, management, and
treatment may be the superordinate factor in determining whether a given treatment
will effectively target and reduce suicidal behaviors.
While these commonalities seen across trials with significant treatment effects are
encouraging and provide us with the beginning of a framework from which to move
forward, it is also critically important to underline the components of those CBT
interventions which have not been shown to have superior outcomes to control
conditions. Somewhat confusingly, many of these commonalities are reminiscent of
(or, in fact, identical to) those just outlined in reference to the effective interventions.
This certainly complicates the picture and is worth analysis.
Nonsignificant Trials
Of the 17 trials outlined here, nine found no difference between their CBT exper-
imental intervention and the control condition. While five trials found significant
reductions in suicidal outcomes (i.e., Donaldson et al., 2005; Liberman & Eckman,
1981; McMain et al., 2009; Patsiokas & Clum, 1985; Rudd et al., 1996), these
trials did not find significant differences between conditions. While it is admittedly an
oversimplification of the empirical findings of these trials, for ease of discussion they
will be referred to henceforth as “ineffective” interventions given that each of these
trials did not find a significant difference which would have suggested the effectiveness
of the experimental intervention. As with those trials with significant findings, it is
similarly valuable to examine the common factors across these nine interventions to
determine what elements of CBT-based interventions may be possible to eliminate
from future treatment development endeavors. First, as previously mentioned, two of
the trials utilized inpatient interventions (i.e., Liberman & Eckman, 1981; Patsiokas
& Clum, 1985). Additionally, one trial was provided in a partial or day hospital format
(i.e., Rudd et al., 1996). While the six remaining interventions were provided on an
outpatient basis, perhaps further consideration of the context in which interventions
for suicidal individuals are provided is warranted.
Second, with few exceptions, this subset of interventions is comprised almost entirely
of interventions that are brief in duration. The two most intensive interventions were
the one provided by Liberman and Eckman (1981) in the inpatient unit, comprising
a total of 32 hours of therapy (over an 8-day period) and the one provided by
Rudd et al. (1996) which included 90 hours of treatment (over a 2-week period).
Compared to the one year of treatment provided in each of the five DBT trials
(including both individual therapy and group skills training, averaging approximately
180 hours of treatment in total over a one-year period), these interventions are
much shorter. In fact, most of these interventions have 10 sessions or fewer (i.e.,
Donaldson et al., 2005; Evans et al., 1999; Hawton et al., 1987; McLeavey et al.,
1994; Patsiokas & Clum, 1985; Tyrer et al., 2003). Certainly, three of the effective
trials (i.e., Brown et al., 2005; Salkovskis et al., 1990; Weinberg et al., 2006) also
utilized very brief interventions (i.e., interventions with a very limited number of
sessions); however, it is noteworthy that the proportion of trials that utilized brief
interventions is much larger in this noneffective subset. Perhaps it is possible to see
improvement right away with CBT interventions, but attachment to the provider
may be a more important variable than previously realized for maintained treatment
gains.
While these trends seem to indicate potential factors that differentiate the effective
from the ineffective interventions, there are several factors that obscure the picture.
Perhaps most critically, all of the interventions that were not superior to the control
conditions against which they were evaluated also emphasize teaching problem-solving
and other coping skills. For instance, Evans et al. (1999) and Tyrer et al. (2003) used
bibliotherapy (the same as used by Weinberg et al., 2006), which included chapters
on problem solving and basic strategies for managing emotions. More directly, other
interventions were designed specifically to target problem-solving deficits and emotion
regulation (i.e., Donaldson et al., 2005; Hawton et al., 1987; Liberman & Eckman,
1981; Patsiokas & Clum, 1985; Rudd et al., 1996). The manner in which skills
training was incorporated in the intervention (e.g., in an individual or group setting,
using chapters for self-study, specific steps for effective problem-solving, or discussing
alternative coping strategies in the context of previous suicidal behaviors) varies across
all of these interventions. At this point, it is not possible to determine whether
Suicidality 1257
one method is superior for targeting suicidal behavior given that some methods are
utilized in both significant and nonsignificant trials. However, given the previous
discussion of the potential importance of balancing change (i.e., problem solving)
with acceptance seen in the DBT trials, this may provide additional support for the
inclusion of a more dialectical and principle-driven stance than that seen in some
of the ineffective interventions. Additionally, given the relative effectiveness of the
longer interventions compared to the briefer ones, perhaps it takes longer to learn
problem-solving and other coping skills than it does to teach them. While they can
be presented and taught in a very brief amount of time, patients may not be able to
learn and use them independently with the same speed.
A second obscuring factor is the importance placed on the therapeutic alliance. At
least one of the ineffective interventions explicitly notes the use of the therapeutic
relationship to assist in bringing about change (i.e., Hawton et al., 1987) and, as
previously highlighted, the therapeutic alliance is of relatively universal import in
CBT. This begs the question of why both effective and ineffective interventions
both emphasize this relationship. Again, we can refer back to the way in which
the relationship is used in treatment. In treatments such as DBT, the therapeutic
relationship is a vehicle for change as well as a useful mechanism used to keep the
person alive. However, this is not ubiquitous across CBT interventions. While few
CBT practitioners would deny that the therapeutic alliance is an important element
that improves treatment outcomes and, as such, must be attended to throughout
the therapy process, these therapists may or may not actually use the therapeutic
relationship they have worked to cultivate as both a marker of what kinds of behaviors
or problems are showing up outside the therapy room and as a practice space to
start changing them. Hawton et al. (1987) do, in fact, describe their intervention
as involving attempts to link past experiences to current ones that are occurring in
the therapy session, but this is the only one of these nine ineffective interventions
to note this. Perhaps this is the critical element lacking from the other ineffective
interventions.
Also of note is the fact that DBT providers place special attention on not reinforcing
suicidal behaviors within the therapeutic relationship. For instance, DBT therapists
encourage phone coaching outside of session in order to generalize skills acquisition
to the real world, but this coaching is done strategically to ensure that the client is
not necessarily getting more attention and caring displays from the therapist when he
or she is suicidal, but also at times when suicidality is not elevated. This prevents the
patient from necessarily being suicidal in order to receive additional support from a
caring therapist.
Summary and Recommendations
The literature reviewed in this chapter suggests that CBT interventions are at the
forefront of treatment development efforts to manage suicidal behavior in clinical
practice. Interestingly, the nonsignificant trials have provided important information
to guide future research and clinical endeavors just as much as the significant trials
have provided guidance for which empirical and clinical avenues to pursue. Clearly,
outpatient interventions currently hold a monopoly on the effective interventions,

and providing intervention in an inpatient or day-treatment setting requires further
study before being utilized as an EBT. Additionally, caution should be used when
implementing brief interventions given the inconsistent results supporting their
effectiveness for this population. At this point in time, the data suggest that long-term
interventions may be more suitable to yield long-term and lasting effects on suicidal
behaviors.
Furthermore, coping skills are an integral part of the effective treatments reviewed
here, as is the therapeutic relationship. The value of group psychotherapy needs to
be further elaborated in future research as the current review suggests that group
interventions may hold particular promise for this population. Further, the replicated
effectiveness of DBT at reducing suicidal behavior should be underscored. Regardless
of whether the specific strategies and procedures outlined here are correctly identifying
the central components that make the treatment effective, or if expertise in suicide
is really the driving force behind the significant results, DBT is the most empirically
supported treatment available for suicide.
Taken in concert, the results of this review suggest that CBT interventions show
considerable promise and, in the case of DBT, convincing evidence that they can and
should be used to treat suicidality. There is much more work to be done in order
to understand fully what elements of these interventions are most critical and which
components drive reductions in suicidal behaviors; however, the field continues to
progress and the CBT interventions reviewed here have provided a solid foundation
upon which future research endeavors can build.
References
Addis, M., & Linehan, M. M. (1989, November). Predicting suicidal behavior: Psychometric
properties of the Suicidal Behaviors Questionnaire. Poster session presented at the Annual
Meeting of the Association for the Advancement Behavior Therapy, Washington, DC.
Bagby, R. M., Ryder, A. G., Schuller, D. R., & Marshall, M. B. (2004). The Hamilton
Depression Rating Scale: Has the gold standard become a lead weight? American Journal
of Psychiatry, 161, 2163–2177. doi:10.1176/appi.ajp.161.12.2163
Beck, A. T., Steer, R. A., & Ranieri, W. (1988). Scale for Suicide Ideation: Psychome-
tric properties of a self-report version. Journal of Clinical Psychology, 44, 449–505.
doi:10.1002/1097-4679(198807)44:4<499::AID-JCLP2270440404>3.0.CO;2-6
Bonner, R. L., & Rich, A. R. (1988). Negative life stress, social problem-solving self-appraisal,
and hopelessness: Implications for suicide research. Cognitive Therapy and Research, 12,
549–556. doi:10.1007/BF01205009
Brent, D. A., & Kolko, D. J. (1991). Supportive relationship treatment manual. Pittsburg, PA:
University of Pittsburgh/WPIC, Department of Psychiatry.
Brodsky, B. S., Groves, S. A., Oquendo, M. A., Mann, J. J., & Stanley, B. (2006). Interpersonal
precipitants and suicide attempts in borderline personality disorder. Suicide & Life-
Threatening Behavior, 36, 313–322. doi:10.1521/suli.2006.36.3.313
Brown, G. K. (2001). A review of suicide assessment measures for intervention research with
adults and older adults. Washington, DC: American Association of Suicidology.
Suicidality 1259
Brown, G. K., Ten Have, T., Henriques, G. R., Xie, S. X., Hollander, J. E., & Beck, A. T.
(2005). Cognitive therapy for the prevention of suicide attempts: A randomized con-
trolled trial. Journal of the American Medical Association, 294, 563–570. doi:10.1001/
jama.294.5.563
Buglass, D., & Horton, J. (1974). A scale for predicting subsequent suicidal behavior. British
Journal of Psychiatry, 124, 573–578. doi:10.1192/bjp.124.6.573
Centers for Disease Control. (2012, January). Deaths: Final data for 2009. National Vital
Statistics Reports, 60. Retrieved from http://www.cdc.gov/nchs/data/nvsr/nvsr60/
nvsr60_03_tables.pdf
Cochrane Central Register of Controlled Trials. (2012). Retrieved on April 5, 2012, from
http://mrw.interscience.wiley.com/cochrane/cochrane_clcentral_articles_fs.html
Combs, H., & Romm, S. (2007). Psychiatric inpatient suicide: A literature review. Primary
Davidson, C. L., Wingate, L. R., Grant, D. M., Judah, M. R., & Mills, A. C. (2011).
Interpersonal suicide risk and ideation: The influence of depression and social anxiety.
Journal of Social and Clinical Psychology, 30, 842–855. doi:10.1521/jscp.2011.30.8.842
Davila, J., & Daley, S. E. (2000). Studying interpersonal factors in suicide: Perspectives from
depression research. In T. E. Joiner & M. Rudd (Eds.), Suicide science: Expanding the
boundaries (pp. 175–200). New York, NY: Kluwer Academic/Plenum.
Donaldson, D., Spirito, A., & Esposito-Smythers, C. (2005). Treatment for adolescents
following a suicide attempt: Results of a pilot trial. Journal of the American Academy
of Child and Adolescent Psychiatry, 44, 113–120. doi:10.1097/00004583-200502000-
00003
Evans, K., Tyrer, P., Catalan, J., Schmidt, U., Davidson, K., Dent, J., … Thompson, S. (1999).
Manual-assisted cognitive-behaviour therapy (MACT): A randomized controlled trial of
a brief intervention with bibliotherapy in the treatment of recurrent deliberate self-harm.
Psychological Medicine, 29, 19–25. doi:10.1017/S003329179800765X
Hawton, K., McKeown, S., Day, A., Martin, P., O’Connor, M., & Yule, J. (1987). Evaluation
of outpatient counseling compared with general practitioner care following overdoses.
Hayes, S. C., & Wilson, K. G. (1994). Acceptance and commitment therapy: Altering the
verbal support for experiential avoidance. Behavior Analyst, 17 , 289–303.
Hazell, P. L., Martin, G., McGill, K., Kay, T., Wood, A., Trainor, G., & Harrington, R. (2009).
Group therapy for repeated deliberate self-harm in adolescents: Failure of replication of a
randomized trial. Journal of the American Academy of Child & Adolescent Psychiatry, 48,
662–670. doi:10.1097/CHI.0b013e3181aOacec
Howat, S., & Davidson, K. (2002). Parasuicidal behaviour and interpersonal problem solv-
ing performance in older adults. British Journal of Clinical Psychology, 41, 375–386.
doi:10.1348/014466502760387498
Joiner, T. E., Jr., Van Orden, K. A., Witte, T. K., & Rudd, M. D. (2009). The interpersonal
theory of suicide: Guidance for working with suicidal clients. Washington, DC: American
Kallert, T. W., Glockner, M., & Schutzwohl, M. (2008). Involuntary vs. voluntary hospi-
tal admission: A systematic literature review on outcome diversity. European Archives
of Psychiatry and Clinical Neuroscience, 258, 195–209. doi:10.1007/s00406-007-
0777-4
Kazdin, A. E. (1977). Artifact, bias, and complexity of assessment: The ABCs of reliability.
Journal of Applied Behavior Analysis, 10, 141–150. doi:10.1901/jaba.1977.10-141
Koons, C. R., Robins, C. J., Tweed, J. L., Lynch, T. R., Gonzalez, A. M., Morse, J. Q., …
Bastian, L. A. (2001). Efficacy of dialectical behavior therapy in women veterans with
borderline personality disorder. Behavior Therapy, 32, 371–390. doi:10.1016/S0005-
7894(01)80009-5
Kreitman, N. (1977). Parasuicide. Chichester, England: John Wiley & Sons, Ltd.
Lamis, D. A., & Malone, P. S. (2011). Alcohol-related problems and risk of suicide among
college students: The mediating roles of belongingness and burdensomeness. Suicide &
Life-Threatening Behavior, 41, 543–553. doi:10.1111/j.1943-278X.2011.00052.x
Liberman, R. P., & Eckman, T. (1981). Behavior therapy vs. insight-oriented ther-
apy for repeated suicide attempters. Archives of General Psychiatry, 38, 1126–1130.
doi:10.1001/archpsyc.1981.01780350060007
Linehan, M. M. (1993). Cognitive behavioral treatment of borderline personality disorder. New
Linehan, M.M. (1997). Behavioral treatments of suicidal behaviors: Definitional obfuscation
and treatment outcomes. In D. M. Stoff & J. J. Mann (Eds.), Neurobiology of suicide:
From the bench to the clinic (pp. 302–328). New York, NY: Annals of the New York
Academy of Sciences.
Linehan, M. M., Armstrong, H. E., Suarez, A., Allmon, D., & Heard, H. L. (1991). Cognitive-
behavioral treatment of chronically parasuicidal borderline patients. Archives of General
Linehan, M. M., Camper, P., Chiles, J. A., Strosahl, K., & Shearin, E. (1987). Inter-
personal problem solving and parasuicide. Cognitive Therapy and Research, 11, 1–12.
doi:10.1007/BF01183128
Linehan, M. M., Comtois, K. A., Brown, M. Z., Heard, H. L., & Wagner, A. (2006). Suicide
Attempt Self-Injury Interview (SASII): Development, reliability, and validity of a scale to
assess suicide attempts and intentional self-injury. Psychological Assessment, 18, 303–312.
doi:10.1037/1040-3590.18.3.303
Linehan, M. M., Comtois, K. A., Murray, A. M., Brown, M. Z., Gallop, R. J., Heard, H. L., …
Lindenboim, N. (2006). Two-year randomized controlled trial and follow-up of dialectical
behavior therapy vs. therapy by experts for suicidal behaviors and borderline personality
disorder. Archives of General Psychiatry, 63, 757–766. doi:10.1001/archpsyc.63.7.757
Linehan, M. M., Heard, H. L., & Armstrong, H. E. (1993). Naturalistic follow-up of a
behavioral treatment for chronically parasuicidal borderline patients. Archives of General
McLeavey, B. C., Daly, R. J., Ludgate, J. W., & Murray, C. M. (1994). Interpersonal
problem-solving skills training in the treatment of self-poisoning patients. Suicide &
Life-Threatening Behavior, 24, 382–394.
McMain, S. F., Links, P. S., Gnam, W. H., Guimond, T., Cardish, R. J., Korman, L., & Streiner,
D. L. (2009). A randomized trial of dialectical behavior therapy versus general psychiatric
management for borderline personality disorder. American Journal of Psychiatry, 166,
1365–1374. doi:10.117/appi.ajp.2009.09010039
Nock, M. K., Holmberg, E. B., Photos, V. I., & Michel, B. D. (2007). The Self-Injurious
Thoughts and Behaviors Interview: Development, reliability, and validity in an adolescent
sample. Psychological Assessment, 19, 309–317. doi:10.1037/1040-3590.19.3.309
Osman, A., Bagge, C. L., Gutierrez, P. M., Konick, L. C., Kopper, B. A., & Barrios, F. X.
(2001). The Suicidal Behaviors Questionnaire-Revised (SBQ-R): Validation with clinical
and nonclinical samples. Assessment, 8, 443–454. doi:10.1177/107319110100800409
Patsiokas, A. T., & Clum, G. A. (1985). Effects of psychotherapeutic strategies in the treatment
of suicide attempters. Psychotherapy, 22, 281–290. doi:10.1037/h0085507
Suicidality 1261
Pearson, J. L., Stanley, B., King, C. A., & Fisher, C. B. (2001). Intervention research with
persons at high risk for suicidality: Safety and ethical considerations. Journal of Clinical
Pollock, L. R., & Williams, J. M. G. (1998). Problem solving and suicidal behavior. Suicide &
Life-Threatening Behavior, 28, 375–387.
Pollock, L. R., & Williams, J. G. (2001). Effective problem solving in suicide attempters
depends on specific autobiographical recall. Suicide & Life-Threatening Behavior, 31,
386–396. doi:10.1521/suli.31.4.386.22041
Pollock, L. R., & Williams, J. M. G. (2004). Problem-solving in suicide attempters. Psychological
Medicine, 34, 163–167. doi:10.1017/S0033291703008092
Rosenthal, R. (1966). Experimenter effects in behavioral research. New York, NY: Appleton-
Century-Crofts.
Rudd, M. D., Rajab, M. H., Orman, D. T., Stulman, D. A., Joiner, T., & Dixon, W. (1996).
Effectiveness of an outpatient intervention targeting suicidal young adults: Preliminary
results. Journal of Consulting and Clinical Psychology, 64, 179–190. doi:10.1037//0022-
006X.64.1.179
Sadowski, C., & Kelley, M. L. (1993). Social problem solving in suicidal adolescents. Journal
of Consulting and Clinical Psychology, 61, 121–127. doi:10.1037//0022.006X.61.1.121
Salkovskis, P. M., Atha, C., & Storer, D. (1990). Cognitive-behavioural problem solving in the
treatment of patients who repeatedly attempt suicide: A controlled trial. British Journal of
Psychiatry, 157 , 871–876. doi:10.1192/bjp.157.6.871
Schotte, D. E., & Clum, G. A. (1982). Suicide ideation in a college population: A test of a
model. Journal of Consulting and Clinical Psychology, 50, 690–696. doi:10.1037//0022-
006X.50.5.690
Soloff, P. H., Lis, J. A., Kelly, T., & Cornelius, J. R. (1994). Risk factors for suicidal behavior
in borderline personality disorder. American Journal of Psychiatry, 151, 1316–1323.
Stewart, D., Ross, J., Watson, C., James, K., & Bowers, L. (2012). Patient characteristics
and behaviors associated with self-harm and attempted suicide in acute psychiatric wards.
Journal of Clinical Nursing, 21, 1004–1013. doi:10.1111/j.1365-2702.2011.03832.x
Tyrer, P., Thompson, S., Schmidt, U., Jones, V., Knapp, M., Davidson, K., … Wessely, S.
(2003). Randomized controlled trial of brief cognitive behaviour therapy versus treatment
as usual in recurrent deliberate self-harm: The POPMACT study. Psychological Medicine,
33, 969–976.
van der Sande, R., van Rooijen, L., Buskens, E., Allart, E., Hawton, K., van der Graaf, Y., &
van Engeland, H. (1997). Intensive in-patient and community intervention versus routine
care after attempted suicide: A randomized controlled intervention study. British Journal
of Psychiatry, 171, 35–41. doi:10.1192/bjp.171.1.35
Verheul, R., van den Bosch, L. M. C., Koeter, M. W. J., de Ridder, M. A. J., Stijnen, T.,
& van den Brink, W. (2003). Dialectical behaviour therapy for women with borderline
personality disorder: 12-month, randomized clinical trial in the Netherlands. British
Journal of Psychiatry, 182, 135–140. doi:10.1192/bjp.182.2.135
Ward-Ciesielski, E. F., & Linehan, M. M. (in press). Psychological treatment of suicidal
behaviors. In M. Nock (Ed.), Suicide and self-injury. New York, NY: Oxford University
Press.
Waterhouse, J., & Platt, S. (1990). General hospital admission in the management of para-
suicide: A randomized controlled trial. British Journal of Psychiatry, 156, 236–242.
doi:10.1192/bjp.156.2.236
Weinberg, I., Gunderson, J. G., Hennen, H., & Cutter, C. J., Jr. (2006). Manual assisted
cognitive treatment for deliberate self-harm in borderline personality disorder patients.
Journal of Personality Disorders, 20, 482–492. doi:10.1521/pedi.2006.20.5.482
Williams, J. G., Teasdale, J. D., Segal, Z. V., & Soulsby, J. (2000). Mindfulness-based cognitive
therapy reduces overgeneral autobiographical memory in formerly depressed patients.
Journal of Abnormal Psychology, 109, 150–155. doi:10.1037//0021-843X.109.1.150
Wood, A., Trainor, G., Rothwell, J., Moore, A., & Harrington, R. (2001). Randomized trial
of group therapy for repeated deliberate self-harm in adolescents. Journal of the American
200111000-00003
World Health Organization. (2010). WHO Statistical Information System (WHOSIS). Geneva,
Switzerland: Author.
53
Antisocial Personality Disorder
Christopher J. Patrick and Lindsay D. Nelson
Florida State University, United States
Among the various disorders of personality, antisocial personality disorder (ASPD)

and its diagnostic cousin, psychopathy (psychopathic personality), stand as unique in
terms of the costly toll they exact on society. Because of this, these disorders have long
held the fascination of the public at large as well as that of investigators in the scientific
community. Our goal in this chapter is to review what is currently known about the
nature and causal bases of ASPD, highlighting ways in which it resembles and differs
from psychopathy, and discuss currently available and potentially new approaches to
the treatment of ASPD in light of this existing knowledge base. In reviewing what is
known about ASPD, we consider relationships that ASPD has with phenomena in the
domains of personality and psychopathology more broadly and consider what these
relationships might tell us about psychological mechanisms and maintaining factors
that can serve as targets for intervention.
The chapter begins with an historical overview of the construct of ASPD,
highlighting its links to the concept of psychopathy. The next section summarizes
contemporary conceptual perspectives and empirical findings on ASPD. Here, our
emphasis is on placing ASPD into a broader conceptual framework that encompasses
other impulse control disorders (e.g., conduct disorder, alcohol dependence, and
drug dependence) with which ASPD is closely associated. Specifically, drawing on
recent research findings, we argue that ASPD comprises one phenotypic manifestation
of a broader genotypic disposition toward disinhibitory (externalizing) problems.
The next section discusses physiological (including brain response) correlates of
ASPD in relation to what is known about corresponding correlates of externalizing
proneness and of psychopathy. This is followed by a section on currently available
treatments for ASPD, focusing in particular on behavioral and cognitive behavioral
methods, and a further section on possible alternative approaches to intervention
suggested by recent developments in the empirical literature.

DOI: 10.1002/9781118528563.wbcbt53
Conceptualizing and Assessing Antisocial Personality Disorder
Historical Overview
Early conceptions. The earliest accounts of the condition that came to be known as
ASPD emphasized extreme behavioral deviance in the context of intact reasoning
and communicative abilities. French physician Philippe Pinel (1801) described cases
of individuals who engaged repeatedly in impulsive acts injurious to themselves
and others despite recognizing at a verbal/conceptual level the irrationality of
such acts. The label Pinel used for this condition was manie sans delire (“insanity
without delirium”). Around the same time in the United States, Benjamin Rush
(1812) documented similar cases, but postulated moral weakness (i.e., incapacity
for guilt or shame in relation to actions and potential consequences) as the root
cause. In his account, Rush highlighted the manipulative, deceitful nature of such
individuals.
Reflecting a perspective similar to Rush’s, British physician J. C. Pritchard (1835)
applied the term “moral insanity” to cases of this type. However, Pritchard applied
this term much more broadly than Rush, for conditions ranging from drug or alco-
hol addiction to sexual deviations to mood disorders, along with conditions that
would be classified today as mental retardation or schizophrenia. The alternative
term “psychopathic” was introduced by German psychiatrist J. L. Koch (1891) to
denote conditions of a chronic nature presumed to have an underlying organic (phys-
ical, brain-based) cause. Like Pritchard, Koch applied this term to a much broader
array of clinical conditions than would be encompassed by current conceptions of
ASPD or psychopathy. Operating from a similar etiologic perspective, Emil Kraepelin
(1915) used the term “psychopathic personalities” for a somewhat narrower range of
conditions including impulse-related problems, sexual deviations, obsessional disor-
ders, and other “degenerative” personalities. The latter category included antisocial
(callous-destructive) and quarrelsome (hostile-alienated) subgroups that would be
classifiable today as APSD.
Reversing the trend toward broad application of the term “psychopathic,” Hervey
Cleckley (1976; original edition, 1941) proposed that the label be reserved for a
specific condition with a distinct set of diagnostic features. Cleckley’s diagnostic
criteria focused on three sets of features: (a) indications of psychological stability
(i.e., good intelligence and social charm, absence of delusions/irrationality, absence
of nervousness, and suicide rarely carried out); (b) tendencies toward emotional
underresponsiveness and superficial/insincere relationships with others (i.e., deceit-
fulness, poverty in affective reactions, self-centeredness and incapacity for love, lack of
reciprocity in social relations, lack of insight); and (c) persistent behavioral deviance in
the form of repeated antisocial acts (often without obvious motives), irresponsibility,
promiscuity, and absence of any clear life plan. According to Cleckley, the overt
presentation of psychological stability in such individuals functioned as a convinc-
ing “mask of sanity,” concealing their affective-interpersonal deficits and behavioral
deviancy.
Antisocial Personality Disorder 1265
Emergence of the concept of antisocial personality disorder. The first edition of

the Diagnostic and Statistical Manual of Mental Disorders (DSM-I; American
Psychiatric Association [APA], 1952) included a category of mental disorders termed
“sociopathic personality disturbance.” Following early conceptions of psychopathy,
this designation encompassed a broad array of clinical phenomena including sexual
deviations of various types, addictions, and a condition referred to as “sociopathic
personality disturbance: antisocial reaction,” entailing persistent aggressive and
criminally deviant behavior. In the next edition (DSM-II; APA, 1968), the term
“reaction” was eliminated as a descriptor for disorders, and sexual deviations,
addictions, and delinquent personality types were grouped together in the category
of “personality disorders and other non-psychotic mental disorders,” which included
an “antisocial personality” designation resembling the syndrome of psychopathy
described by Cleckley (i.e., with features including defective socialization, selfishness,
callousness, untrustworthiness, and absence of guilt).
However, a serious limitation of the DSM-II (as with the DSM-I) was that diagnoses
were assigned on the basis of prototypic descriptions of disorders rather than through
use of specific behavioral criteria. As a result, the reliability of diagnoses using
the DSM-II was poor (APA, 1980). This problem was addressed in the DSM-III
(APA, 1980) by specifying more explicit, behaviorally oriented criteria for diagnoses.
The criteria for ASPD in the DSM-III were strongly influenced by the work of Lee
Robins (1966), who undertook longitudinal research to investigate the developmental
course of “sociopathy.” Following Cleckley, Robins’s initial criteria for sociopathy
included items relating to lack of guilt, remorse, and shame, but (due in part to
weak reliability) these criteria showed weak discrimination in her work and thus were
discarded as indicators. In line with this, the criteria for ASPD adopted in the DSM-III
focused exclusively on behavioral indicants of deviance in childhood and adulthood,
including such things as truancy, delinquency, stealing, vandalism, irresponsibility,
aggressiveness, impulsivity, recklessness, and lying.
As a function of this change, the DSM-III diagnosis of ASPD proved highly reliable.
However, prominent researchers (e.g., Frances, 1980; Hare, 1983) challenged the
validity of the diagnosis on the grounds that it excluded many of the features
identified by Cleckley as essential to psychopathy, including superficial charm, absence
of anxiety, lack of remorse or empathy, and general poverty of affect. Some effort
was made to address these criticisms in the revised third edition (DSM-III-R; APA,
1987) by adding lack of remorse (i.e., “feels justified in having hurt, mistreated, or
stolen from another”; p. 346) as an adult criterion for ASPD. Despite an extensive
field trial (Widiger et al., 1996) that provided for evaluation of alternative criterion
sets including a 10-item version of Hare’s (1991) Psychopathy Checklist-Revised
(PCL-R), intended to provide greater coverage of affective-interpersonal features of
psychopathy, the diagnostic criteria for ASPD in the DSM-IV (APA, 1994, 2000)
remain much the same as those in the DSM-III.
Current DSM Conception of Antisocial Personality Disorder

Clinical features. Table 53.1 summarizes the diagnostic criteria for ASPD in the
current fourth edition of the DSM (DSM-IV-TR; APA, 2000). As with other disorders,
Table 53.1 Summary of Diagnostic Criteria for DSM-IV Antisocial Personality Disorder
Criterion category Summary description of criterion
A. Adult antisocial behavior 1. repeated participation in illegal acts

(3 or more of the 2. deceitfulness
following since age 15): 3. impulsiveness or failure to make plans in advance
4. hostile-aggressive behavior
5. engagement in actions that endanger self or others
6. frequent irresponsible behavior
7. absence of remorse
B. Age criterion: Current age at least 18
C. Evidence of child conduct Aggression toward people or animals:
disorder (3 or more of 1. frequent bullying, threatening, or intimidation of others
the following before age 2. frequent initiation of physical fights
15, resulting in impaired 3. use of dangerous weapons
social, academic, or 4. physical cruelty toward people
occupational function):a 5. physical cruelty toward animals
6. theft involving victim confrontation
7. forced sexual contact
Destroying property:
8. deliberate fire setting with intent to cause damage
9. deliberate destruction of property
Deceptiveness or stealing:
10. breaking/entering (house, building, or vehicle)
11. frequent lying to acquire things or to avoid duties
12. nontrivial theft without victim confrontation
Serious rule violations:
13. frequent violations of parental curfew, starting before age 13
14. running away from home
15. frequent truancy, starting before age 13
D. Comorbidity criterion: Antisocial behavior does not occur exclusively during episodes
of schizophrenia or mania
Notes. a The DSM-IV criteria for conduct disorder require the occurrence of three or more of these behavioral
symptoms before age 15. Criterion C for antisocial personality disorder (ASPD) is vague as to the number
of child symptoms needing to be met, specifying only “evidence of Conduct Disorder with onset before
age 15 years.” Some approaches to assessing ASPD, for example the Structured Clinical Interview for
DSM-IV Axis II Personality Disorders (SCID-II; First, Gibbon, Spitzer, Williams, & Benjamin, 1997),
interpret “evidence of” as denoting a lower threshold (i.e., occurrence of two child symptoms, as opposed
to three). Adapted from American Psychiatric Association (2000).
the criteria for ASPD are polythetic. That is, because only a portion of designated
child and adult criteria need to be met, individuals can achieve the diagnosis in
many different ways, subject to fulfilling inclusionary requirements (i.e., age 18 or
older, antisocial behavior not attributable to mania or psychosis). As shown in Table
53.1, the child criteria for ASPD include aggressive and destructive behaviors on one
hand, and deceitfulness/theft and nonaggressive rule breaking on the other. Formal
factor-analytic investigations of the child criteria (e.g., Frick et al., 1991; Tackett,
Krueger, Sawyer, & Graetz, 2003) have established that the aggressive and rule-
breaking symptoms define separate, albeit correlated, factors. Tackett et al. (2003)
reported that these two conduct disorder factors showed discriminative associations
with aggressive behavior syndrome and delinquent behavior syndrome, respectively,
as defined by scores on the Child Behavior Checklist (Achenbach, 1991).
An implication of this work is that there may be distinct variants of child antisocial
deviance with different etiologic underpinnings. Along these lines, Moffitt (1993)
proposed a distinction between adolescence-limited and life-course-persistent sub-
groups of delinquent individuals. The former was distinguished by a later onset and
predominantly nonaggressive forms of deviancy and rule breaking, the latter by early
age of onset, aggressive-destructive as well as nonaggressive delinquent behaviors, and
continuation of child and adolescent deviancy into adulthood. Moffitt postulated that
the early-onset, aggressive subtype of delinquency may have a stronger underlying
neurobiological basis (see also Lynam, 1997).
Tackett, Krueger, Iacono, and McGue (2005) further examined the structure of
conduct disorder symptoms in a male twin sample, permitting an analysis of etiologic
contributions to aggressive versus nonaggressive subfactors. Their results indicated
that these two components of conduct disorder have common as well as distinctive
etiologic underpinnings. Additive genetic influences and nonshared environment (i.e.,
experiences unique to the individual) contributed significantly to both components,
with the proportion of symptom variance attributable to genes somewhat higher for
the aggressive than the nonaggressive component (35% vs. 28%). In addition, a sig-
nificant contribution of shared environment (i.e., influences common to two siblings
growing up in the same household) was found for the nonaggressive component
only. Recently, Kendler, Aggen, and Patrick (2013) extended this work by present-
ing behavioral genetic evidence that (a) aggressive and rule-breaking components of
conduct disorder reflect differing sources of genetic influence, and (b) the shared envi-
ronmental contribution to the rule-breaking component is concentrated in a distinct
subset of symptoms reflecting covert delinquent acts (e.g., stealing, telling lies).
The adult criteria for ASPD include deceitfulness, impulsivity, irresponsibility,
irritability and aggressiveness, reckless disregard for safety of self or others, lack of
remorse, and failure to conform to norms with respect to lawful behaviors. As with
child conduct disorder symptoms, evidence exists for differing etiological influences
underlying aggressive and nonaggressive antisocial behavior patterns in adulthood.
In a study involving adult twins, Kendler, Aggen, and Patrick (2012) reported two
distinct factors emerging from a structural analysis of the adult criteria for ASPD,
one (labeled disinhibition) reflecting tendencies toward impulsivity, irresponsibility,
and deceitfulness, and the other (labeled aggressive-disregard) reflecting irritabil-
ity/aggressiveness and behaviors indicative of recklessness and lack of concern for
oneself and others. Paralleling what has been reported for distinct factors of con-
duct disorder (Kendler et al., 2013; Tackett et al, 2005), these authors found that
nonaggressive and aggressive facets of antisociality in adulthood were associated with
differing sources of genetic influence.
Other evidence in the literature also supports the idea that aggressive forms of
adult antisocial behavior have unique neurobiological underpinnings. For example,
published studies have reported consistent evidence for reduced levels of the neu-
rotransmitter serotonin (indexed by concentrations of the serotonin metabolite
5-Hydroxyindoleacetic acid [5-HIAA] in cerebrospinal fluid) in antisocial individ-
uals exhibiting severe episodes of impulsive aggressive behavior (for a review, see
Minzenberg & Siever, 2006). Evidence of reduced brain serotonin has also been
reported in antisocial individuals who engage in impulsive suicidal acts (Linnoila &
Virkkunen, 1992), which have been conceptualized as an alternative, self-directed
expression of impulsive aggressive tendencies (Verona & Patrick, 2000).
Notably, findings demonstrating distinct aggressive and nonaggressive (disin-
hibitory or rule-breaking) components of antisocial behavior in childhood and
adulthood dovetail with findings of recent research on the structure of impulse-related
(externalizing) problems more broadly (Krueger, Markon, Patrick, Benning, &
Kramer, 2007). As discussed in more detail later in this chapter, this work has yielded
evidence of separate disinhibitory and callous-aggression factors (along with a third
substance-addiction factor) underlying this domain of problems. Given these various
converging lines of evidence, it will be valuable in future research to evaluate (through
longitudinal investigations) the temporal stability of these distinct symptomatic
facets of antisocial behavior from childhood to adulthood. For example, it might be
hypothesized that the aggressive facet would exhibit greater stability across time than
the disinhibitory/rule-breaking facet (cf. Moffit, 1993; Tackett et al., 2005).
Antisocial personality disorder in the DSM-5. The fifth edition of the DSM (DSM-5;
APA, 2013), includes an important change to the diagnosis of conduct disorder and
an alternative dimensional approach to characterizing adult personality pathology
that accommodate the foregoing developments along with emerging perspectives
on the distinction between externalizing proneness and psychopathy (see the section
on “Antisocial Personality Disorder and Psychopathy”). The change to the diagnosis
of conduct disorder entails the addition of a “limited prosocial emotions” specifier
to distinguish between variants with and without callous unemotional tendencies (cf.
Frick & Marsee, 2006). Research has demonstrated the callous unemotional variant to
be characterized in particular by proactive aggressive tendencies and disregard for the
feelings and welfare of others. With regard to adult personality disorders, categorical
definitions remain the same as in DSM-IV, but a supplementary dimensional system
now appears in Section III of the DSM-5 (“Emerging Models”). This system includes
an alternative trait-based definition of ASPD that characterizes the disorder in terms
of high levels of traits from two distinct domains: antagonism, reflecting callousness,
hostility, manipulativeness, and deceitfulness; and disinhibition, reflecting impulsivity,
irresponsibility, and risk-taking. The inclusion of antagonism-related traits in this
dimensional characterization of ASPD parallels the demarcation of a distinct variant of
conduct disorder entailing callous-unemotional traits. Additionally, the dimensional
approach to characterizing ASPD in the DSM-5 includes a specifier for distinguishing

a classically psychopathic variant of ASPD, marked by low anxiousness and social
assertiveness.
Comorbidity with other DSM disorders. ASPD shows well-documented patterns of

comorbidity with other disorders in the DSM, most notably substance use disorders.
In the Epidemiologic Catchment Area study (Robins & Regier, 1991), the base rate of
substance use disorders of any type among individuals diagnosed with ASPD exceeded
80%. Earlier studies employing DSM-III criteria reported similar high rates of alcohol
and drug problems among individuals diagnosed with ASPD (e.g., Koenigsberg,
Kaplan, Gilmore, & Cooper, 1985; Lewis, Rice, & Helzer, 1983). ASPD has also been
shown to be associated with greatly enhanced risk for alcohol and drug use disorders
in more recent comorbidity studies (e.g., Grant et al., 2004; Kessler & Walters, 2002).
The fact that substance use disorders co-occur with ASPD to a much greater extent
than would be expected if each occurred by chance, given their respective popu-
lation prevalence rates, implies that something systematic underlies the association
between the two. This hypothesis has been supported by factor-analytic investigations
of the diagnostic overlap among common disorders within the DSM. For example,
employing diagnostic data from the National Comorbidity Survey (Kessler & Walters,
2002), Krueger (1999a) reported evidence for two broad factors underlying the most
common Axis I disorders: an “externalizing” factor encompassing ASPD, alcohol
dependence, and drug dependence, and an “internalizing” dimension encapsulating
the mood and anxiety disorders (see also Krueger, Caspi, Moffitt, & Silva, 1998; Volle-
bergh et al., 2001). One possible explanation for the systematic association between
ASPD and substance use disorders is that it reflects overlap between the criteria for the
two types of disorders. For example, it could be argued that some of the behaviors that
define ASPD (e.g., irresponsibility, recklessness, aggressiveness) are common sequelae
of alcohol or drug abuse, so that increased rates of such behaviors would be expected
among individuals with substance use problems. However, this seems unlikely to
explain the systematic association between ASPD and substance use disorders. For
one thing, the onset of ASPD typically precedes that of substance use problems in
cases where the two are comorbid. In addition, the relationship between ASPD and
substance abuse problems is asymmetric, due to the higher population prevalence of
the latter—that is, whereas most individuals diagnosed with ASPD also show evidence
of substance use disorders, the majority of individuals from the general community
diagnosed with substance abuse or dependence do not meet criteria for ASPD.
Another possibility is that ASPD and substance use problems arise from a com-
mon diathesis—that is, a common underlying trait factor that predisposes individuals
toward the development of both types of disorders. Consistent with this possibility,
behavior genetic (twin) studies have revealed evidence of shared genetic factors under-
lying ASPD and substance use disorders (e.g., Pickens, Svikis, McGue, & LaBuda,
1995; Slutske et al., 1998). More recent quantitative analyses of etiologic factors
contributing to the broad externalizing factor representing the systematic covariance
among these disorders have revealed that this factor is substantially heritable (Kendler,
Prescott, Myers, & Neale, 2003; Krueger et al., 2002; Young, Stallings, Corley,
Krauter, & Hewitt, 2000). This work is described in more detail later in this chapter.
Personality correlates. Two personality trait variables in particular, represented in

differing models of personality, have been shown to be related to ASPD. One is
impulsiveness, represented in the five-factor model (FFM; cf. Digman, 1990) by
the conscientiousness factor (reversed) and in Tellegen’s (2003) Multidimensional
Personality Questionnaire (MPQ) model by the higher-order factor of constraint
(reversed). The other is aggressiveness, represented in the FFM by the agreeableness
factor (reversed) and in the MPQ by the lower-order trait of aggression. Notably, these
same personality variables (impulsivity and aggression) show reliable associations with
substance use disorders (Casillas & Clark, 2002; Krueger, 1999b; Lynam, Leukefeld,
& Clayton, 2003; Trull & Sher, 1994).
These observed relations between personality trait variables and clinical disorders
have been interpreted in various ways. One perspective is that traits indexed by per-
sonality scales reflect basic individual difference processes from which mental disorder
symptoms arise; another is that deviations in personality emerge as a consequence
of psychopathology (Widiger, Verheul, & van den Brink, 1999). A third perspective
is that psychopathology symptoms and personality trait variables correlate with one
another because they are indicators of a shared underlying (latent) individual differ-
ences factor. With regard to ASPD and substance dependence, this perspective would
suggest that these disorders are related to one another and in turn to personality traits
of impulsivity and aggression because all of these variables are manifest indicators of a
shared underlying externalizing factor. Krueger et al. (2002) evaluated this hypothesis
for the broad MPQ factor of constraint by including this personality variable along
with child and adult symptoms of ASPD and alcohol and drug dependence symptoms
in a joint-factor analysis. Consistent with the aforementioned hypothesis, the analysis
revealed the presence of a single latent factor on which constraint loaded significantly
together with all four symptom variables.
Krueger et al. (2007) extended this work by undertaking a fine-grained analysis
of traits and problem behaviors within the domain of externalizing psychopathology
to elucidate the scope and structure of this spectrum more fully. They began by
identifying various constructs embodied in the DSM definitions of the disorders
included in the Krueger et al. (2002) analysis, and then developed self-report items to
tap these constructs. They also surveyed the literature to identify other behavioral and
trait constructs related empirically or conceptually to externalizing psychopathology
and developed additional items to index these constructs. Across multiple rounds of
data collection and analysis, item response modeling and factor analysis were used to
refine the overall item set and thereby clarify the nature of constructs associated with
the broad externalizing factor.
Employing this strategy, Krueger et al. (2007) arrived at a final set of 23 constructs,
each operationalized by a unique subscale. These constructs included alcohol, mari-
juana, and other drug use and problems; aggression of various sorts; impulsiveness;
irresponsibility; rebelliousness; excitement seeking; and blame externalization. Struc-
tural analyses of these 23 subscales yielded evidence of one broad superordinate factor
(externalizing) on which all subscales loaded (the strongest indicators being “irrespon-
sibility” and “problematic impulsivity”) and two subordinate factors accounting for
residual variance in specific subscales—a callous-aggression factor marked by subscales
indexing aggression (all forms), callousness, and excitement seeking, and a substance
abuse factor marked by subscales indexing excessive use and problems with alcohol,
marijuana, and other drugs. These findings provide support for the idea that problem
behaviors and affiliated personality traits within this domain are indicators of a shared
underlying factor (externalizing). In addition, consistent with results from structural
analyses of the child and adult symptom criteria for ASPD, this more comprehensive
analysis of constructs within the externalizing domain revealed evidence of distinctive
aggressive and nonaggressive expressions of this general factor.
Neurobiological correlates. A variety of neurobiological correlates of ASPD have been

identified. For example, as noted earlier, antisocial individuals—in particular, those
displaying impulsive aggressive behavior—show evidence of reduced levels of the
neurotransmitter serotonin in the brain. Other research has consistently demonstrated
that low resting heart rate is a correlate of antisocial deviance, with prospective studies
showing that low heart rate in childhood predicts later antisocial behavior (Ortiz
& Raine, 2004). This finding has been interpreted as indicating that physiological
hypoarousal confers liability to antisocial behavior by promoting sensation-seeking
behavior (Raine, 2002).
Neuropsychological studies provide evidence of deficits in frontal brain function
in individuals diagnosed as antisocial. Morgan and Lilienfeld (2000) reported meta-
analytic evidence for deficits on frontal lobe tasks in individuals exhibiting conduct
disorder and adult antisocial behavior. Notably, individuals at risk for alcoholism by
virtue of a positive parental history also show evidence of impairment on neuropsy-
chological tests of frontal lobe function (Peterson & Pihl, 1990; Tarter, Alterman, &
Edwards, 1985). Iacono, Carlson, and Malone (2000) suggested that impairments in
frontal brain function may be generally characteristic of individuals with externalizing
problems.
There is also evidence that reduced amplitude of the P3 brain potential response,
long known to be an indicator of risk for alcohol problems (Polich, Pollock, & Bloom,
1994), may be a marker of externalizing problems more generally, including ASPD.
A number of studies have reported evidence of reduced P3 brain response amplitude
in individuals with ASPD (Bauer, Hesselbrock, O’Connor, & Roberts, 1994; Bauer,
O’Connor, & Hesselbrock, 1994; Costa et al., 2000; Iacono, Carlson, Malone, &
McGue, 2002). Reduced P3 response amplitude has also been found in individuals
with other impulse control problems, including nicotine dependence (Anokhin et al.,
2000; Iacono et al., 2002), child conduct disorder (Bauer & Hesselbrock, 1999a,
1999b, 2002; M. S. Kim, Kim, & Kwon, 2001), and attention-deficit/hyperactivity
disorder (ADHD; Johnstone & Barry, 1996; Klorman, 1991). The implication is that
reduced P3 amplitude could be an indicator of the general externalizing factor that
these disorders share.
Patrick et al. (2006) evaluated this possibility in a sample of 969 males recruited
from the community by examining the association between reduced P3 amplitude and
scores on the externalizing factor, defined as the primary component derived from
a principal components analysis of symptoms of various DSM-III-R impulse control
disorders (i.e., conduct disorder, adult antisocial behavior, and alcohol, drug, and
nicotine dependence). These investigators found a highly significant negative associa-
tion between scores on the externalizing factor and P3 brain response amplitude (i.e.,
higher externalizing scores, reflecting a greater number of impulse problems, were

associated with smaller P3 amplitude). Moreover, significant associations between
each individual diagnostic variable and P3 amplitude were accounted for entirely by
the externalizing factor—that is, after controlling for scores on this common factor,
all associations for individual disorders dropped to nonsignificance. These results
indicate that reduced P3 amplitude represents a neural indicator of general proneness
to externalizing problems, rather than an indicator of ASPD per se (or of other specific
disorders, such as alcohol dependence).
Etiologic perspectives on antisocial personality disorder. A variety of etiologic models of

ASPD have been proposed, some of them based on the aforementioned neurobiolog-
ical findings (for reviews, see Raine, 1997; Zuckerman, 1999). Most of these models
focus on the underpinnings of ASPD as a distinctive syndrome, without consider-
ing its relations to other forms of psychopathology (e.g., substance use disorders).
However, recent efforts have been made to develop integrative etiologic models that
accommodate ASPD’s associations with other disorders and distinctive personality
traits by conceptualizing ASPD as one facet of a broader spectrum of traits and
problem behaviors. An example of this is the hierarchical spectrum model proposed
by Krueger et al. (2002).
The essence of the hierarchical spectrum model is that there is a broad dispositional
factor that disorders within a spectrum share, along with unique etiologic influences
that determine the unique symptomatic expression of each disorder. The database
on which the model was based consisted of symptom scores on four diagnostic
variables (child conduct disorder, adult antisocial behavior, alcohol dependence, and
drug dependence) along with a trait measure of impulsiveness (the broad Constraint
scale of the MPQ) for a sample of male and female twins recruited from the
community (N = 1,048). A biometric structural analysis revealed a large common
factor (“externalizing”) on which all of these diagnostic variables loaded substantially
(.58–.78); more than 80% of the variance in this common factor was attributable to
additive genetic influence (see also Kendler et al., 2003; Young et al., 2000). The
remaining variance in each disorder not accounted for by the broad externalizing
factor was attributable primarily to nonshared environmental influence—although for
conduct disorder there was also a significant contribution of shared environment.
Based on these findings, Krueger et al. (2002) proposed that a general constitutional
factor contributes to the development of various disorders in this spectrum, but that
the precise expression of this underlying vulnerability (i.e., as antisocial deviance or
substance problems of different kinds) is determined by disorder-specific etiologic
influences. Although the analysis pointed to unique environmental experience as
the main determinant of diagnostic specificity (with some contribution of family
environment for conduct disorder), owing to the somewhat modest sample size and
large confidence intervals around parameters in the model, the authors acknowledged
that specific genetic factors might also contribute to the uniqueness of certain
disorders. Indeed, Kendler et al. (2003) presented evidence for this possibility in
a subsequent study. As noted earlier, Krueger et al. (2007) extended the work of
Krueger et al. (2002) by providing a more comprehensive analysis of traits and
problem behaviors within the externalizing spectrum. However, an etiologic analysis
of this newer, more comprehensive model remains to be undertaken. In particular,

it will be important to evaluate differences in etiologic contributions to the two
subordinate factors (callous-aggression, substance abuse) identified by Krueger et al.
(2007) in comparison with those for the broad externalizing factor (for a discussion of
possible neurobiological mechanisms, see Patrick & Bernat, 2006; Patrick, Drislane,
& Strickland, 2012).
Antisocial Personality Disorder and Psychopathy:

Overlap and Distinctiveness
Psychopathy has been conceptualized in diverse ways historically, and contemporary
assessment instruments such as the interview-based Psychopathy Checklist-Revised
(PCL-R; Hare, 1991, 2003) and the self-report-based Psychopathic Personality
Inventory (PPI; Lilienfeld & Andrews, 1996; Lilienfeld & Widows, 2005) differ in
the types of features they use to identify psychopathic individuals. A model that
was recently advanced to reconcile differing conceptions of psychopathy, and clarify
its relationship with ASPD, is the Triarchic Model (Patrick, Fowles, & Krueger,
2009). This model conceives of psychopathy as encompassing three distinguishable
symptomatic components—disinhibition, meanness, and boldness—that represent
thematic building blocks for alternative conceptions of psychopathy.
Disinhibition entails tendencies toward impulsiveness, deficient behavioral restraint,
and difficulty in regulating emotion. Impulse-related problems of differing types,
including child and adult antisocial behavior and substance-related disorders, feature
disinhibition as a strong common element. Meanness as defined in the Triarchic
Model is marked by deficient empathy, low social connectedness, exploitativeness,
excitement-seeking, and empowerment through cruelty. In contrast with disinhibi-
tion, which reflects general proneness to problems of impulse control, meanness entails
more specific tendencies toward callous insensitivity, instrumental use of aggression,
destructive fun-seeking, and predatory manipulation of others. The third compo-
nent of the Triarchic Model, boldness, entails social efficacy, calmness under pressure
and rapid recovery from stressors, and high tolerance for unfamiliarity and danger.
Correlates of boldness include confidence, interpersonal assertiveness, narcissism and
thrill-seeking behavior, and low anxiety and depression (Benning, Patrick, Blonigen,
Hicks, & Iacono, 2005).
Alternative instruments for assessing psychopathy provide differing coverage of
disinhibition, meanness, and boldness in their item content. The PCL-R, designed
for use with adult offenders, assesses psychopathy in terms of two distinct factors,
an affective-interpersonal factor reflecting a blend of meanness and boldness (Hall,
Benning, & Patrick, 2004; Venables & Patrick, 2012) and an antisocial-deviance
factor reflecting a blend of disinhibition and meanness (Patrick, Hicks, Nichol, &
Krueger, 2007; Venables & Patrick, 2012). The PPI, developed for use with adults
from the general community, assesses psychopathy in terms of a fearless-dominance
factor that predominantly reflects boldness (Patrick et al., 2009; Sellbom & Phillips,
2013) and an impulsive-antisociality factor that reflects disinhibition and to a lesser
extent meanness (Sellbom & Phillips, 2013; Venables & Patrick, 2012); the PPI
also contains one subscale, Coldheartedness, that is distinct from its two factors and
that appears to tap meanness specifically (Sellbom & Phillips, 2013). The Antisocial
Process Screening Device (Frick & Hare, 2001), designed for use with children
and younger adolescents exhibiting conduct problems, assesses psychopathy in terms
of impulsive-externalizing and callous-unemotional factors that show contrasting
relations with external criterion variables (Frick & Marsee, 2006; Frick, O’Brien,
Wooten, & McBurnett, 1994; Frick & White, 2008); inspired by this work, the
newly released DSM-5 includes a specifier for the diagnosis of conduct disorder that
distinguishes between variants with and without callous-unemotional traits. ASPD
as carried over from DSM-IV to the main Personality Disorders section of DSM-5
emphasizes disinhibition and to a lesser extent meanness (Venables & Patrick, 2012),
with negligible coverage of boldness (Patrick, Venables, & Drislane, 2012). However,
as emphasis on traits related to meanness (i.e., antagonism) in the diagnosis.
Available research findings point to differing causal factors underlying the disinhibi-
tion and meanness components of psychopathy that comprise its points of overlap with
ASPD, and the boldness component that distinguishes psychopathy most from ASPD
(Patrick et al., 2012). As noted in earlier sections, biometric analyses of child and
adult criteria for ASPD point to differing sources of genetic influence for aggressive
and nonaggressive symptom components. Behavior genetic research on the etiologic
bases of the fearless-dominance (akin to boldness) and impulsive-antisociality factors
of the PPI (Blonigen et al., 2005) likewise demonstrates distinct sources of genetic
influence for the two. With regard to brain mechanisms, disinhibition is hypothesized
to reflect dysfunction in anterior brain systems—including the prefrontal cortex and
anterior cingulate cortex—that operate to guide decision making and action and
regulate emotional reactivity. As a result, highly disinhibited individuals operate in
the present moment, failing to moderate their actions and reactions as a function of
past experiences or anticipated future outcomes.
Different neurobiological processes have been hypothesized to contribute to the
meanness (callous-aggression) component of psychopathy, which is represented to
some extent also in ASPD. One of these is a weakness in regions of the brain that
govern fear reactivity (Fowles & Dindo, 2009; Frick & Marsee, 2006), or perhaps
emotional responsiveness more generally (Blair, 2006). As evidence of this, high scores
on the callousness-unemotional factor of the Antisocial Process Screening Device are
associated with low levels of reported anxiety, lack of responsiveness to distressing
stimuli, impaired ability to learn from punishment, and affinity for activities entailing
novelty and risk. Beyond this, it seems likely that impairments in biological systems
underlying caring (nurturance) and affiliative capacity also contribute to the expression
of meanness. For example, disturbances in the function of neuromodulatory hormones
such as oxytocin and vasopressin, which are known to influence a range of social
phenomena including social bonding, altruism, cooperation versus competition, and
recognition of others’ emotional displays (e.g., Domes, Heinrichs, Michel, Berger,
& Herpertz, 2007; Gobrogge, Liu, Jia, & Wang, 2007; Kosfeld, Heinrichs, Zak,
Fischbacher, & Fehr, 2005; Lim et al., 2004), may contribute to the emergence and
maintenance of callous-aggressive tendencies.
The third component of the Triarchic Model, boldness, has been conceptualized as
reflecting the behavioral (phenotypic) expression of an underlying fearless disposition
(genotype; Fowles & Dindo, 2009; Lykken, 1995; Patrick et al., 2009). Boldness
entails a more straightforward, adaptive expression of low fear than meanness; as just
noted, the expression of fearlessness as meanness may entail co-occurring disturbances
in systems underlying social connectedness and caring. Individual differences in the
functioning of the brain’s defensive motivational system, including the amygdala
and affiliated structures, have been posited to play a role in boldness (Kramer,
Patrick, Krueger, & Gaspari, 2012; Patrick et al., 2009). Consistent with this pers-
pective, individuals high on the fearless-dominance factor of the PPI show reduced
responsiveness to affective visual (including aversive) stimuli (Benning, Patrick, &
Iacono, 2005; Gordon, Baird, & End, 2004). Additionally, experiential factors that
promote a sense of personal efficacy and effective top-down regulatory control of
emotion may also contribute to individual differences in boldness.
Treatment of Antisocial Personality Disorder
Contemporary Perspectives and Approaches

The symptoms of ASPD and its effects on others present unique challenges for
treatment, as a number of elements inherent to the disorder, and its typical pathways
to treatment, stand in stark contrast to many theoretically based and empirically
supported tenets of effective psychotherapy. For example, a client’s internal motivation
for change is considered by many to be a prerequisite for successful intervention
(Olver, Stockdale, & Wormith, 2011; Ryan, Plant, & O’Malley, 1995), yet the
impetus for initiating treatment with ASPD clients often comes from external sources
(i.e., the courts). Relatedly, whereas addressing patient-relevant goals is known to
enhance motivation and thereby improve treatment outcomes (Michalek, Klappheck,
& Kosfelder, 2004; Ryan & Deci, 2008), the primary goal of treatment with antisocial
individuals has traditionally been to protect society rather than help these individuals
achieve personal goals (Andrews, Bonta, & Hoge, 1990; Skeem & Manchak, 2008;
Skeem, Polascheck, & Manchak, 2009). Moreover, while a strong therapeutic alliance
can enhance treatment adherence and outcome irrespective of other factors (Martin,
Garske, & Davis, 2000), characteristics common to antisocial individuals (e.g.,
dishonesty, low motivation for treatment; APA, 2000; Reid & Gacono, 2000) and
their providers (e.g., pessimism regarding the potential for change; Salekin, 2002) can
hinder development of effective therapist–client relationships. Alliances are especially
complex in mandated treatment, where the therapist’s dual role (both to care for and
control the client) further complicates this tenuous but crucial relationship (Skeem,
Eno Louden, Manchak, Vidal, & Haddad, 2009; Skeem, Eno Louden, Polaschek, &
Camp, 2007).
These challenges are compounded by the fact that researchers and practitioners have
historically been cynical about the potential for successful treatment of individuals
with psychopathy in particular (e.g., Salekin, 2002), and of criminal offenders more
generally (Bailey, 1966; Reid & Gacono, 2000; Robison & Smith, 1971). Up to
the 1970s, the field of criminology viewed the potential to rehabilitate offenders
in a positive light, but then underwent a paradigm shift in part due to reviews of
intervention studies indicating that existing methods of treatment had “no appreciable
effect on recidivism” (Martinson, 1974, p. 25). Two competing perspectives on

criminal justice policy emerged at this time, each of which contributed to the
devaluation of rehabilitation efforts: On the one hand, “left wing” criminologists
rejected the possibility that psychological characteristics of individuals could motivate
the occurrence of criminal behaviors, advocating for changes in social structures as the
best means for reducing recidivism; on the other hand, “right wing” criminologists
advocated for a “just deserts” approach (i.e., punishment rather than treatment) for
addressing the behavior of offenders (Cooke & Philip, 2000).
Fortunately, the pessimism expressed by these and other groups sparked a new
wave of research that has generated a more hopeful outlook regarding prospects for
successful treatment of antisocial individuals. Even opponents of rehabilitation, such
as Martinson (1974), have acknowledged the pervasive methodological weaknesses
in traditional research on treatment of offenders: “It is just possible that some of
our treatment programs are working to some extent, but that our research is so bad
that it is incapable of telling” (p. 49). Since the 1980s, increases in well-controlled
studies and meta-analytic reviews of such studies have challenged longstanding beliefs
about the stability of crime-relevant personality traits and the potential for antisocial
individuals to undergo change (e.g., Rogers, Jackson, Sewell, & Johansen, 2004). In
light of these developments, criminal justice agencies have shifted from the viewpoint
that “nothing works” to an emphasis on determining “what works.” Beyond adapting
traditional psychotherapeutic techniques for use with antisocial populations, advances
in understanding of the neurobiological underpinnings and developmental pathways
of antisocial behavior have inspired new perspectives on treatment that focus on
dispositional and environmental factors underlying the development and maintenance
of antisocial tendencies, and on developing alternative interventions for distinct
subsets of antisocial individuals with unique treatment needs (Frick, 2001; Patrick,
Drislane, & Strickland, 2012; Seto & Quinsey, 2006).
Cognitive behavioral interventions. At present, cognitive behavioral therapy (CBT)

methods comprise the most widely accepted approaches to treatment of antisocial
offenders. In general, treatments of this type for offenders emphasize the teaching of
cognitive skills theorized to be deficient in these individuals and considered causally
relevant to criminal behavior (e.g., Friendship, Blud, Erikson, Travers, & Thornton,
2003; Lipsey, Chapman, & Landenberger, 2001; Samenow, 1991; Yochelson &
Samenow, 1976, 1977).
Reasoning and rehabilitation therapy. Although many variants of CBT have been
employed with antisocial (particularly offender) populations, arguably the best-known
and most widely used method is the reasoning and rehabilitation (R&R) program,
developed in the 1980s and now used across a range of settings in various countries
(Polaschek, 2011; Robinson & Porporino, 2000). Also referred to as cognitive skills
training, R&R is a structured, multifaceted intervention that focuses on criminogenic
beliefs and thinking patterns and the role they play in maintaining offense behavior.
Because of its focus on behavior patterns as well as affiliated thought processes, R&R
is considered a cognitive behavioral treatment as opposed to a more purely cognitive
intervention (Antonowitz, 2005; Fernandez, Shingler, & Marshall, 2006).
R&R was developed in response to evidence that offenders exhibit cognitive deficits
relevant to interpersonal problem solving and social interactions, including tendencies
to think concretely, fail to consider the consequences of behavior, and disregard
or misapprehend others’ behavior, thoughts, and feelings (Ross, Fabiano, & Ewles,
1988). The R&R approach contains a number of components designed to address
such problems, including modules directed at social perspective taking, interpersonal
problem solving, and assertiveness (i.e., nonaggressive ways to communicate), along
with training in self-control, critical reasoning, and consideration of values (Robinson
& Porporino, 2000; Ross et al., 1988). Typically administered over multiple 2-hour
sessions involving groups of six to 12 individuals, and requiring extensive training
on the part of therapists (referred to as “trainers” or “coaches”), R&R emphasizes
development of skills in a step-wise manner, through repetition, and from diverse
learning modalities entailing active participation (e.g., role playing, games) to engage
offenders’ attention and accommodate a range of client learning styles. A further
feature of the R&R approach is that it seeks to enhance motivation on the part of
participants by framing the training as an opportunity to develop new skills or ways
of thinking that individuals can choose to use outside the training context (Robinson
& Porporino, 2000).
Moral reconation therapy. Another well-known treatment for offenders is moral

reconation therapy (MRT). Developed in the 1980s for the purpose of improving
offenders’ behavior through improvements in moral and social capacities (Little &
Robinson, 1988; Wilson, Bouffard, & MacKenzie, 2005), MRT is also considered
cognitive behavioral in orientation. However, in contrast with R&R, it draws specifi-
cally on ideas from Kohlberg’s (1976) theory of moral development and places distinct
emphasis on development of individual identity and self-concept and on drawing con-
nections between moral reasoning and behavior. MRT views offenders as entering
therapy with “low levels of moral development, strong narcissism, low ego/identity
strength, poor self-concept, low self-esteem, inability to delay gratification, relatively
strong defense mechanisms, and relative strong resistance to change and treatment”
(Little & Robinson, 1988, p. 135).
Like R&R, MRT is a structured, manualized program administered in treatment
groups, typically including 10–15 offenders, with sessions lasting 1–2 hours and
offered twice per week. The program revolves around use of a workbook that calls
for engagement in a variety of tasks, including identifying goals, exploring good and
bad times in one’s life, recognizing behaviors that lead to negative outcomes, and
recognizing and discussing sources of unhappiness (Little & Robinson, 1988; Wilson
et al., 2005).
Other cognitive behavioral approaches. Other CBT-oriented approaches to the

treatment of antisocial individuals include Thinking for a Change, developed by the
National Institute of Corrections for use with adult offenders on probation (Golden,
Gatchel, & Cahill, 2006), and aggression replacement therapy, designed for use
with persistently aggressive youth (Glick & Goldstein, 1987). Despite procedural
differences, these and other variants of CBT all emphasize training-based acquisition
of thinking skills directed at enhancing self-control and interpersonal relations.

This commonality of emphasis might be expected to translate into similar levels of
effectiveness for differing treatments of this type. Consistent with this, a recent review
of alternative approaches to the treatment of offenders (Landenberger & Lipsey,
2005) found no evidence of differential effectiveness for “brand name” as compared
to “generic” forms of CBT with clientele of this type.
Effectiveness of cognitive behavioral therapy for antisocial populations. Various

qualitative and quantitative reviews of the empirical literature on treatments for anti-
social behavior have converged on the conclusion that cognitive behavioral interven-
tions produce modest but stable reductions in recidivism for offending populations
(e.g., Andrews et al., 1990; Antonowitz & Ross, 1994; Friendship et al., 2003;
Garrett, 1985; Izzo & Ross, 1990; Landenberger & Lipsey, 2005; Lipsey et al.,
2001; Whitehead & Lab, 1989; Wilson et al., 2005). Meta-analyses, in which data
from multiple studies are aggregated quantitatively (Rosenthal & DiMatteo, 2001),
have been particularly valuable due to their ability to provide composite indices
of treatment impact (effect sizes) and identify moderating variables (variables that
interact with antisocial status to determine the effectiveness of treatment).
Overall, meta-analytic reviews have established that, on average, offender rehabili-
tation programs reduce reoffending by approximately 10% (Lösel, 1996). Although
small in absolute terms, this level of effect is considered valuable from financial and
social standpoints given the heavy costs associated with reoffending—including court,
legal, and incarceration-related fees as well as negative effects on victims. Consistent
with this, numerous cost–benefit analyses of cognitive behavioral and other intensive
treatment programs have reported that programs of these types reduce costs over
the long term relative to traditional punishment or inappropriate treatments (e.g.,
Robertson, Grimes, & Rogers, 2001; Romani, Morgan, Gross, & McDonald, 2012).
Beyond improvements in the standard outcome criterion of recidivism, interventions
with offenders also appear to produce reliable effects on more clinically relevant indices
of improvement such as psychological, community, and vocational adjustment as well
as academic performance (Garrett, 1985; Lipsey, 1995).
Factors that moderate effectiveness of treatment. Several factors have been

shown to moderate the effectiveness of treatments for antisocial behavior across
studies and sites. Some of these are highlighted in the risk–need–responsivity (RNR)
model, the dominant conceptual framework guiding treatment of adolescent and
adult offenders (Andrews et al., 1990). The RNR model articulates a set of broad
principles distilled from reviews of the empirical literature for designing rehabilitation
services based on relevant characteristics of individual clients, namely: risk (i.e.,
likelihood of reoffending in more vs. less severe ways), criminogenic needs (i.e.,
underlying motives for antisocial behavior that represent targets for treatment),
and abilities and learning styles that affect responsivity to treatment (e.g., general
intellect). Although these principles have been subject to debate (e.g., risk level and
intensiveness of service can be defined in varying ways; Polaschek, 2011) and may be
difficult to translate into practice in some cases, they provide useful guidelines that
appear to enhance outcomes (e.g., reduce recidivism) when followed (Andrews et al.,
1990; Lowenkamp, Latessa, & Smith, 2004).
Beyond the RNR model components, researchers have identified other specific
factors that contribute to treatment effectiveness through additional studies of offender
populations. One of these is quality of program implementation (Landenberger &
Lipsey, 2005; Lowenkamp et al., 2004)—which poses distinct challenges given that
most programs for treatment of offenders reviewed by Lowenkamp et al. (2004)
were classified as having “unsatisfactory” adherence to RNR principles. Another
factor that has been increasingly recognized as a moderator of treatment success
consists of provider characteristics that affect therapist–client (or staff–offender)
relationships. Specifically, providers with “firm but fair” or authoritative (as opposed
to authoritarian) styles appear most effective in fostering positive alliances that enhance
treatment outcomes (Skeem et al., 2007; Skeem, Eno Louden, et al., 2009).
Other therapeutic approaches. Other change techniques that have been used with
offenders include psychodynamic therapy and traditional behavior therapies (e.g.,
token economies; Pearson, Lipton, Cleland, & Yee, 2002). In the case of psychody-
namic therapy, evidence for effectiveness is decidedly mixed (Cooke & Philip, 2000),
with some studies reporting worse outcomes for treated versus untreated offenders
(Andrews et al., 1990; Antonowicz & Ross, 1994). Interestingly, strict behavior
modification techniques appear to be less effective than cognitive behavioral interven-
tions for juvenile and adult offenders, according to findings of a meta-analysis of 58
experimental and quasi-experimental studies reported by Landenberger and Lipsey
(2005).
Another common approach in the literature is the therapeutic community, a term
that has been applied both to psychoanalytically oriented treatments for offenders
with serious mental illness used in the United Kingdom and to nonpsychoanalytic
treatments used in the United States for offenders with comorbid substance use
problems. Empirical findings for approaches of these types are less encouraging, with
some prominent studies reporting evidence of adverse effects with certain offender
populations (e.g., studies by Ogloff, Wong, & Greenwood, 1990, and Rice, Harris,
& Cormier, 1992, have demonstrated worse outcomes for psychopathic offenders
undergoing therapeutic community intervention; but see Skeem, Polaschek, Patrick,
& Lilienfeld, 2011, for a critique of these studies).
Summary of Existing Treatments of Antisocial Personality Disorder

As a whole, available evidence supports the use of R&R and other cognitive behav-
ioral treatment approaches with offender populations (e.g., Friendship et al., 2003;
Landenberger & Lipsey, 2005; Lipsey et al., 2001; Wilson et al., 2005). However, a
number of questions remain regarding the essential components of these treatments
and how to maximize their effectiveness with more severely antisocial individuals and
those exhibiting prominent psychopathic features. Although compelling arguments
have been made for the use of multimodal interventions with antisocial clients (Frick,
2001), findings indicating that some treatment approaches may produce adverse
effects with certain subgroups of offenders (e.g., psychopaths; Harris & Rice, 2006)
suggest caution in implementing treatments of this kind on a widespread basis.

Findings of this kind also highlight the need for further research directed at evaluating
the effectiveness of customized interventions for distinct subtypes of individuals in
the broader antisocial population (i.e., those exhibiting particular symptomatic fea-
tures; see the next section). Another question requiring further research is whether
positive findings reported for treatments of antisocial individuals (including cognitive
behavioral interventions) simply reflect preexisting characteristics of those individuals
who appear willing to complete treatment as opposed to effects of the treatments
per se. This question is not resolvable through existing literature, because the major-
ity of published studies have used no-treatment control groups and not accounted
adequately for dropout. In fact, evidence indicating that individuals who stay in
treatment tend to be those with lower severity/risk raises the possibility of inflation
of estimates of treatment effectiveness in many studies, and suggests that currently
available treatments may not be reaching those individuals who need it most (Olver
et al., 2011; Olver & Wong, 2010).
Toward the Future: Interventions for Separable Facets of

Antisocial Personality Disorder that Reflect Distinct
Underlying Processes
Lessons from the Treatment of Child Conduct Problems

The literature on childhood precursors to ASPD offers some useful insights that can
help to guide efforts to improve adult treatment. Within the domain of “Disruptive,
Impulse Control, and Conduct Disorders” in the DSM-5, conditions diagnosable in
childhood include oppositional defiant disorder (ODD), characterized by unusual dis-
obedience and defiance, and conduct disorder (CD), involving more severe behavioral
symptoms than ODD and considered the child precursor to adult ASPD. In addition
to these established diagnoses, research over the past 15 years has highlighted the
diagnostic importance of callous-unemotional (CU) traits for evaluating behavioral
risk and treatment amenability in children with conduct problems. This influential
body of research has led to inclusion of a “limited prosocial emotions” specifier in
the DSM-5 to distinguish variants of CD entailing the presence versus absence of
traits of this kind, which are considered to be indicative of psychopathy (Frick, 2006;
Frick & Ellis, 1999). Because of significant overlap between conduct problems and
attentional deficits (up to 90% of children with CD or ODD also have a diagnosis
of ADHD; Abikoff & Klein, 1992), research on children with ADHD and multiple
disruptive behavior diagnoses is also relevant. Furthermore, the fact that the course
of ADHD appears more chronic in children with as opposed to without co-occurring
conduct problems (Barkley, Fischer, Smallish, & Fletcher, 2002; Broidy et al., 2003)
calls for separate consideration of individuals with differing levels of comorbidity in
deciding among alternative methods of intervention.
Currently, four approaches to the treatment of child conduct disorder are considered
well-supported: behavioral (contingency) management strategies, parent training,
cognitive behavioral programs, and stimulant medications. Behavioral management
strategies entail setting concrete behavioral goals relevant to a child’s problem behav-
ior, establishing reinforcement and punishment contingencies in order to gradually
shape behavior in more appropriate directions, and providing for effective ongoing
monitoring of children’s behavior and treatment progress (Abramowitz & O’Leary,
1991). Parent training programs, the best-supported intervention for children with
severe CD, teach parents to run contingency management programs within the
home and emphasize improving the quality of parent–child relationships (Kazdin &
Whitley, 2003). Similar to adult CBT interventions, cognitive behavioral programs
for conduct problems address children’s social-cognitive and social problem-solving
deficits (e.g., through procedures directed at overriding tendencies to attribute hostile
intent in others and strengthening ability to inhibit impulsive responding). Stimulant
medications are well supported for children with comorbid ADHD and are widely
used (Hinshaw, 1991; Hinshaw, Heller, & McHale, 1992).
Considering Individual Differences within the Antisocial Population

Two lessons from this literature are perhaps most relevant to future work on the
treatment of ASPD. The first is that there appear to be individual differences among
children diagnosed with CD (i.e., subgroups within this diagnostic category) that
warrant special consideration in determining treatment. In particular, CU traits and
comorbidity with ADHD appear particularly relevant to understanding individual
prognoses and treatment needs. A number of studies have reported that CD children
with CU traits have more persistent conduct problems (Frick & Ellis, 1999), more
difficulties in academic, social, and other areas of functioning (e.g., Pettit, Bates, &
Dodge, 1993; Sanders, Dadds, Johnston, & Cash, 1992), and poorer response to
standard treatments than CD children without CU traits (Hawes & Dadds, 2005).
For example, Hawes and Dadds (2005) found that boys high in CU traits showed less
affective reactivity to discipline involving time-outs and as such responded less well
to this form of behavioral intervention. Similarly, Haas et al. (2011) found time-outs
to be less effective for CD children with CU traits, and in addition, reported that
children high in CU traits responded more disruptively to time-outs than those low
in CU traits.
Another study that focused on children with comorbid CD and ADHD found
that those high in CU traits (CU+) fared worse than those low in CU traits
(CU–) in a behavioral-only intervention (Waschbush, Carrey, Willoughby, King, &
Andrade, 2007). By contrast, outcomes for CU– and CU+ groups were largely
comparable for a combined intervention approach including stimulant medication
along with behavioral treatment. This finding suggests that while behavioral therapy
in itself is ineffective with ADHD/CD children exhibiting high levels of CU traits,
these higher-risk children can be effectively treated with more intensive combined
treatments. Despite evidence for a prominent genetic contribution to CU traits
(Viding, Blair, Moffitt, & Plomin, 2005) and relative stability of these traits over
time (Waller et al., 2012), other work has shown that comprehensive and structured
treatments can produce improvements in high-CU/psychopathic children (Hawes &
Dadds, 2007; Kolko et al., 2009; McDonald, Dodson, Rosenfield, & Jouriles, 2011).
Notably, just as high-risk CD children appear responsive to more intensive treat-

ment, adolescents and adults with severe antisocial and psychopathic features appear
capable of responding to more intensive forms of appropriate treatment (Skeem,
Polaschek, & Manchak, 2009). But despite these promising findings, the fact remains
that a relatively high proportion of antisocial children and adults who enter treatment
(in particular, those with prominent psychopathic features) fail to complete it, or
do not respond appreciably even though they do (e.g., Brestan & Eyberg, 1998).
Moreover, generalizability of treatment gains across settings and maintenance of
treatment gains over time tend to be poor for such individuals (e.g., Kimonis &
Frick, 2012). Taken together, these findings suggest that, rather than viewing “of-
fenders” as a broad population with common deficits, subsets of antisocial individuals
with particular symptomatic (phenotypic) patterns may require distinct treatment
approaches.
In thinking about how CBT-oriented methods might be applied to the treatment
of particular subgroups of antisocial individuals, it is useful to consider components
of existing treatments in relation to models of disinhibitory (externalizing) psycho-
pathology. For example, the Externalizing Spectrum Model (ESM; Krueger et al.,
2007) delineates a range of interrelated problems and traits, some involving more
antisocial-aggressive expressions and others more addiction-proneness. Certain com-
ponents of existing treatments like R&R may be more effective for addressing some
elements of externalizing relative to others. In teaching offenders to be more reflective
(vs. reactive) and more systematic in pursuing actions and goals, modules focusing on
aspects of externalizing relevant to inhibitory control (e.g., planful control, problem-
atic impulsivity, impatient urgency) are likely to be especially valuable. Components
aimed at improving perspective taking and flexibility of thought may be particularly
useful in modifying interpersonal biases or deficits (e.g., alienation, externalization of
blame, deficient empathy, relational aggression, and other tendencies involving hos-
tility toward or lack of consideration for others). By contrast, the R&R intervention
approach does not directly target alcohol or drug problems, which are considered part
of the externalizing spectrum and co-occur frequently with ASPD, nor does it include
modules directed at boredom proneness or tendencies toward excitement seeking.
Targeting and evaluating change in specific facets of disinhibition/externalizing such
as these would contribute to understanding of the mechanisms by which existing
treatments effect change, and also to new approaches for targeting elements of
antisociality not addressed by current interventions.
Designing Structured yet Individualized Interventions

The second major lesson to be learned from the child literature is that treatments can
be structured and empirically sound while also being tailored to meet the unique needs
of individuals. CD (and, by extension, ASPD) appears to develop via multiple pathways
(genetic, environmental), affects children across numerous domains/contexts (school,
home, community), and is maintained by diverse factors within affected children (e.g.,
temperament characteristics, social-cognitive deficits) and their environments (Frick,
2006). As such, researchers are increasingly recognizing the need for interventions
to be comprehensive and individualized in order to be maximally effective with this
heterogeneous population. One intervention that appears to fulfill these criteria is

multisystemic therapy (MST). Based on a systems-oriented perspective on family
therapy, MST is inherently comprehensive in that it views child adjustment as embed-
ded within a broader familial, social, and cultural context (Kimonis & Frick, 2010).
Importantly, while explicitly tailoring interventions to meet differing needs of individ-
ual children, MST in general has garnered strong empirical support (e.g., Henggeler,
Melton, & Smith, 1992; Sawyer & Borduin, 2011), setting an example for how treat-
ments can achieve a balance between programmatic implementation and flexibility.
Although adherence to general principles of effective treatment is important to
the success of specific intervention approaches (Landenberger & Lipsey, 2005;
Lowenkamp et al., 2004), the degree to which CBT and other treatments are manual-
ized and highly structured limits their ability to accommodate the treatment needs of
individuals. The literature reviewed in this chapter suggests that considering client-
specific variables is important and that components of treatment may need to be
tailored to patterns of strengths and weaknesses on the part of individuals (e.g.,
intellectual level, personality and temperament characteristics, environmental risk and
protective factors) in order to maximize the efficacy of adult therapies in the broader
antisocial population.
Future Directions for Treatment of Antisocial Personality

Disorder: Incorporating Neuroscientific
Concepts and Findings
Another potential avenue for development of improved treatments entails application

of findings from research on the neural substrates of ASPD and affiliated conditions,
with the aim of more directly targeting cognitive and affective processing deficits char-
acteristic of antisocial and psychopathic individuals (Patrick, Drislane, & Strickland,
2012; Seto & Quinsey, 2006). Child and adult externalizing problems, which show a
close relationship with disinhibitory personality traits (Iacono, Carlson, Taylor, Elkins,
& McGue, 1999; Krueger et al., 2002), appear to be associated with dysfunction in
anterior brain systems critical for monitoring and regulating behavior. For example,
integrative reviews have described evidence for impairments in the functioning of the
prefrontal and temporal lobes in violent offenders (Davidson, Putnam, & Larson,
2000; Patrick, 2008; Raine & Yang, 2006). Other work has reported impairments in
brain event-related potential (ERP) responses, including the P3 (Iacono et al., 2002;
Patrick et al., 2006) and the error-related negativity (ERN; Dikman & Allen, 2000;
Hall, Bernat, & Patrick, 2007), in individuals with antisocial-externalizing tendencies.
Of particular note, the ERN, which occurs following behavioral errors in performance
tasks, has direct conceptual relevance to impulse control problems because it directly
reflects the extent to which individuals monitor their own actions as they occur.
Pharmacologic interventions may prove useful as an adjunct to forms of CBT in the
treatment of antisocial behavior problems. As suggested by the abovementioned work
of Waschbush et al. (2007), induction of changes in the functioning of underlying
neural systems through pharmacological means may facilitate the effectiveness of
cognitive and behavioral interventions in modifying maladaptive behaviors associated

with ASPD and psychopathy. Along these lines, evidence exists for the effectiveness of
drug treatments for various impulse-related problems, including impulsive aggression
(e.g., lithium, selective serotonin reuptake inhibitors; Minzenberg & Siever, 2006),
alcoholism (e.g., acamprosate, naltrexone; O’Malley, Croop, Wroblewski, Labriola,
& Volpicelli, 1995; Paille et al., 1995), sexual deviancy (e.g., antiandrogens; Briken,
Hill, & Berner, 2003), and pathological gambling (e.g., naltrexone; S. W. Kim &
Grant, 2001). That certain drug treatments (e.g., naltrexone) show effectiveness with
differing impulse control disorders accords with the idea of a common neurobiological
liability underlying problems of this type. From the standpoint of the hierarchical
model of externalizing problems (Krueger et al., 2002, 2007), particular pharmaco-
logical treatments may prove effective in ameliorating neurocognitive impairments
associated with general externalizing proneness, whereas others may be needed to
address distinct cognitive and affective processing deviations associated with aggressive
and addictive expressions of externalizing.
Other treatment approaches could also be developed to address brain-based pro-
cessing deviations. For example, behavioral or brain feedback interventions could
be used to train individuals to augment internal self-monitoring processes critical to
regulation of behavior. Recent work showing that the ERN deficiency characteristic
of high-externalizing individuals can be normalized through a feedback-learning pro-
cedure (Nelson, Bernat, & Patrick, 2012) provides a demonstration of this approach.
Another demonstration is provided by recent research showing that activation in the
anterior cingulate cortex (the neural source of the ERN) can be modulated through
functional magnetic resonance imaging-based brain biofeedback (Weiskopf et al.,
2003).
Beyond cognitive-attentional deficits characteristic of impulse-related problems,
antisocial individuals diagnosable as psychopathic show distinct deficits in interper-
sonal relations and emotional sensitivity. Specialized intervention strategies may be
needed to address the lack of empathic concern, exploitativeness, and social dis-
connectedness that appear central to callous-unemotionality (or “meanness”; Patrick
et al., 2009). Features of this sort present obvious, direct obstacles to forming ther-
apeutic alliances. In addition, some portion of individuals meeting criteria for ASPD
will exhibit features of dominance, stress immunity, and fearlessness associated with
the boldness component of psychopathy (Patrick et al., 2009). Characteristics of these
types, entailing strong perceptions of self-efficacy and a lack of concern about the
effects of one’s behavior on others, are likely to interfere with treatment success by
compromising motivation for change.
Neurobiologically, individuals high in affective-interpersonal features of psychopa-
thy (callousness/meanness, boldness) appear to have a heightened threshold for
activation of the brain’s defensive (fear) system, such that threatening cues must
be particularly salient to evoke fear (Levenston, Patrick, Bradley, & Lang, 2000;
Patrick, 2007). This is hypothesized to reflect in part dysfunction of the amygdala, a
subcortical brain structure crucial to fear and other emotional reactions (Blair, 2006;
LeDoux, 2000). Consistent with this perspective, a well-documented finding in the
research literature is that antisocial offenders high in affective-interpersonal features
of psychopathy show reduced potentiation of the noise-elicited startle reflex during
viewing of threatening stimuli (e.g., Patrick, 1994; Vaidyanathan, Hall, Patrick, &
Bernat, 2011)—an effect believed to be mediated by activation of the amygdala
(Davis, Walker, & Lee, 1997; Lang, Bradley, & Cuthbert, 1990). Relatedly, chil-
dren high in callous-unemotional traits showed diminished amygdala reactivity to
depictions of fear faces (Jones et al., 2009; Marsh et al., 2008).
Pharmacologic or feedback-based procedures could potentially be used to augment
responsiveness in brain regions such as the amygdala that appear underreactive in
psychopathic individuals. Alternatively, variants of attentional retraining, a newer
class of treatment that has proven effective with clinical conditions of differing types
including anxiety disorders (Hakamata et al., 2010), might be developed to enhance
emotional sensitivity in psychopathic individuals. In contrast to individuals with
anxiety, however, psychopathic individuals would be trained to enhance attentional
processing of stimuli indicative of threat to oneself or distress on the part of others
(cf. Patrick, Drislane, & Strickland, 2012).
Conclusion
ASPD as defined in the DSM can be seen as one behavioral expression (facet) of
a broader underlying propensity to problems of impulse control. Among disorders
within the externalizing spectrum, ASPD is characterized in particular by irritabil-
ity and aggressiveness along with impulsiveness and irresponsibility. Psychopathy as
defined by Hare’s (1991) PCL-R intersects with ASPD through its social deviance
(Factor 2) component, which taps the broad externalizing factor of which ASPD is
an indicator. However, in addition to impulsive-externalizing tendencies, the diag-
nostic criteria for psychopathy include affective-interpersonal features that reflect
emotional insensitivity and interpersonal detachment. Available evidence suggests
that this component of psychopathy may reflect different neurobiological mechanisms
(i.e., dysfunction in brain circuits underlying defensive/fear reactivity and affilia-
tion/attachment) from the externalizing component (i.e., impairments in anterior
regulatory circuitry).
Ultimately, to achieve satisfactory levels of effectiveness, therapeutic interventions
for ASPD will need to recognize and contend with the heterogeneity of the disorder.
Multifaceted treatment programs that employ cognitive behavioral techniques and
brain-oriented training procedures (potentially in conjunction with pharmacologic
manipulations) to target specific processing impairments associated with distinct
symptomatic features—including general impulsiveness, callous aggression, addictive
urges, and insouciant narcissism—may in time offer the best hope for dealing with
these challenging and costly disorders (cf. Seto & Quinsey, 2006).
Acknowledgement
Preparation of this chapter was supported by grants MH52384 and MH089727 from
the National Institute of Mental Health.
References
Abikoff, H., & Klein, R. G. (1992). Attention-deficit hyperactivity disorder and conduct
disorder: Comorbidity and implications for treatment. Journal of Consulting and Clinical
Psychology, 60, 881–892. doi:10.1037/0022-006X.60.6.881
Abramowitz, A. J., & O’Leary, S. G. (1991). Behavioral interventions for the classroom:
Implications for students with ADHD. School Psychology Review, 20, 220–234.
Achenbach, T. M. (1991). Manual for the Child Behavior Checklist/4–18 and 1991 profile.
Burlington, VT: University of Vermont.
(1st ed.). Washington, DC: Author.
Andrews, D. A., Bonta, J., & Hoge, R. D. (1990). Classification for effective rehabilitation:
Rediscovering psychology. Criminal Justice and Behavior, 17 , 19–52. doi:10.1177/
0093854890017001004
Anokhin, A. P., Vedeniapin, A. B., Sirevaag, E. J., Bauer, L. O., O’Connor, S. J., Kuperman,
S., … Rohrbaugh, J. W. (2000). The P300 brain potential is reduced in smokers.
Psychopharmacology, 149, 409–413. doi:10.1007/s002130000387
Antonowitz, D. H. (2005). The reasoning and rehabilitation program: Outcome evaluations
with offenders. In M. Murran & J. McGuire (Eds.), Social problem solving and offending:
Evidence, evaluation and evolution (pp. 163–181). Chichester, England: John Wiley &
Sons, Ltd.
Antonowitz, D. H., & Ross, R. R. (1994). Essential components of successful rehabilitation
programs for offenders. International Journal of Offender Therapy and Comparative
Criminology, 38, 97–104. doi:10.1177/0306624X9403800202
Bailey, W. C. (1966). Correctional outcome: An evaluation of 100 reports. Journal of Criminal
Law, Criminology, and Police Science, 57 , 153–160. doi:10.2307/1141289
Barkley, R. A., Fischer, M., Smallish, L., & Fletcher, K. (2002). The persistence of attention-
deficit/hyperactivity disorder into young adulthood as a function of reporting source and
definition of disorder. Journal of Abnormal Psychology, 111, 279–289. doi:10.1037/0021-
843X.111.2.279
Bauer, L. O., & Hesselbrock, V. M. (1999a). P300 decrements in teenagers with conduct prob-
lems: Implications for substance abuse risk and brain development. Biological Psychiatry,
46, 263–272. doi:10.1016/S0006-3223(98)00335-7
Bauer, L. O., & Hesselbrock, V. M. (1999b). Subtypes of family history and conduct
disorder: Effects on P300 during the Stroop test. Neuropsychopharmacology, 21, 51–62.
doi:10.1016.S0893-133X(98)00139-0
Bauer, L. O., & Hesselbrock, V. M. (2002). Brain maturation and subtypes of conduct
disorder: Interactive effects on P300 amplitude and topography in male adolescents.
doi:10.1097/00004583-200301000-00017
Bauer, L. O., Hesselbrock, V. M., O’Connor, S., & Roberts, L. (1994). P300 differences
between non-alcoholic young men at average and above-average risk for alcoholism: Effects
of distraction and task modality. Progress in Neuro-Psychopharmacology and Biological
Psychiatry, 18, 263–277. doi:10.1016/0278-5846(94)90058-2
Bauer, L. O., O’Connor, S., & Hesselbrock, V. M. (1994). Frontal P300 decrements in antiso-
cial personality disorder. Alcoholism: Clinical and Experimental Research, 18, 1300–1305.
doi:10.1111/j.1530-0277.1994.tb01427.x
Benning, S. D., Patrick, C. J., Blonigen, D. M., Hicks, B. M., & Iacono, W. G. (2005).
Estimating facets of psychopathy from normal personality traits: A step toward community-
epidemiological investigations. Assessment, 12, 3–18. doi:10.1177/1073191104271223
Benning, S. D., Patrick, C. J., & Iacono, W. G. (2005). Fearlessness and underarousal in
psychopathy: Startle blink modulation and electrodermal reactivity in a young adult
male community sample. Psychophysiology, 42, 753–762. doi:10.1111/j.1469-8986.
2005.00353.x
Blair, R. J. R. (2006). Subcortical brain systems in psychopathy: The amygdala and associated
structures. In C. J. Patrick (Ed.), Handbook of psychopathy (pp. 296–312). New York,
NY: Guilford Press.
Blonigen, D. M., Hicks, B. M., Patrick, C. J., Krueger, R. F., Iacono, W. G., & McGue, M. K.
(2005). Psychopathic personality traits: Heritability and genetic overlap with internalizing
and externalizing psychopathology. Psychological Medicine, 35, 1–12. doi:10.1017/
S0033291704004180
Brestan, E. V., & Eyberg, S. M. (1998). Effective psychosocial treatments for conduct
disordered children and adolescents. Journal of Clinical Child Psychology, 27 , 180–189.
doi:10.1207/s15374424jccp2702_5
Briken, P., Hill, A., & Berner, W. (2003). Pharmacotherapy of paraphilias with long-acting
agonists of luteinizing hormone-releasing hormone: A systematic review. Journal of
Clinical Psychiatry, 64, 890–897. doi:10.4088/JCP.v64n0806
Broidy, L. M., Nagin, D. S., Tremblay, R. E., Bates, J. E., Brame, B., & Dodge, K. A.
(2003). Developmental trajectories of childhood disruptive disorders and adolescent
delinquency: A six-site, cross-national study. Developmental Psychology, 39, 222–245.
doi:10.1037/0012–1649.39.2.222
Casillas, A., & Clark, L. A. (2002). Dependency, impulsivity, and self-harm: Traits hypothesized
to underlie the association between Cluster B personality and substance use disorders.
Journal of Personality Disorders, 16, 424–436. doi:10.1521/pedi.16.5.424.22124
Cleckley, H. (1976). The mask of sanity (5th ed.). St Louis, MO: Mosby.
Cooke, D. J., & Philip, L. (2000). To treat or not to treat? An empirical perspective. In C.
R. Hollin (Ed.), Handbook of offender assessment and treatment (pp. 18–34). New York,
NY: John Wiley & Sons, Inc.
Costa, L., Bauer, L., Kuperman, S., Porjesz, B., O’Connor, S., Hesselbrock, V., … Begleiter,
H. (2000). Frontal P300 decrements, alcohol dependence, and antisocial personality
disorder. Biological Psychiatry, 47 , 1064–1071. doi:10.1016/S0006-3223(99)00317-0
Davidson, R. J., Putnam, K. M., & Larson, C. L. (2000). Dysfunction in the neural cir-
cuitry of emotion regulation: A possible prelude to violence. Science, 289, 591–594.
doi:10.1126/science.289.5479.591
Davis, M., Walker, D. L., & Lee, Y. (1997). Roles of the amygdala and bed nucleus of the stria
terminalis in fear and anxiety measured with the acoustic startle reflex. Annals of the New
York Academy of Sciences, 831, 305–331.
Digman, J. M. (1990). Personality structure: Emergence of the five-factor model. Annual

Review of Psychology, 41, 417–440. doi:10.1146/annurev.ps.41.020190.002221
Dikman, Z. V., & Allen, J. J. (2000). Error monitoring during reward and avoidance learning
in high- and low-socialized individuals. Psychophysiology, 37 , 43–54.
Domes, G., Heinrichs, M., Michel, A., Berger, C., & Herpertz, S. C. (2007). Oxytocin
improves “mind-reading” in humans. Biological Psychiatry, 61, 731–733. doi:10.1017/
S0048577200980983
Fernandez, Y. M., Shingler, J., & Marshall, W. L. (2006). Putting “behavior” back into
cognitive-behavioral treatment of sexual offenders. In W. L. Marshall, Y. M. Fernandez,
L. E. Marshall, & G. A. Serran (Eds.), Sexual offender treatment: Controversial issues (pp.
211–224). New York, NY: John Wiley & Sons, Inc.
First, M. B., Gibbon, M., Spitzer, R. L., Williams, J. B. W., & Benjamin, L. S. (1997). Structured
clinical interview for DSM-IV Axis II personality disorders (SCID-II). Washington, DC:
American Psychiatric Press, Inc.
Fowles, D. C., & Dindo, L. (2009). Temperament and psychopathy: A dual-pathway
model. Current Directions in Psychological Science, 18, 179–183. doi:10.1111/j.1467-
8721.2009.01632.x
Frances, A. J. (1980). The DSM-III personality disorders section: A commentary. American
Journal of Psychiatry, 137 , 1050–1054.
Frick, P. J. (2001). Effective interventions for children and adolescents with conduct disorder.
Canadian Journal of Psychiatry, 46, 597–608.
Frick, P. J. (2006). Developmental pathways to conduct disorder. Child and Adolescent
Psychiatric Clinics of North America, 15, 311–331. doi:10.1016/j.chc.2005.11.003
Frick, P. J., & Ellis, M. (1999). Callous-unemotional traits and subtypes of conduct
disorder. Clinical Child and Family Psychology Review, 2, 149–168. doi:10.1023/
A:1021803005547
Frick, P. J., & Hare, R. D. (2001). Antisocial process screening device. Toronto, Canada:
Multi-Health Systems.
Frick, P. J., Lahey, B. B., Loeber, R., Stouthamer-Loeber, M., Green, S., Hart, E. L., &
Christ, M. G. (1991). Oppositional defiant disorder and conduct disorder in boys:
Patterns of behavioral covariation. Journal of Clinical Child Psychology, 20, 202–208.
doi:10.1207/s15374424jccp2001_12
Frick, P. J., & Marsee, M. A. (2006). Psychopathy and developmental pathways to antisocial
behavior in youth. In C. J. Patrick (Ed.), Handbook of psychopathy (pp. 353–374). New
Frick, P. J., O’Brien, B. S., Wooten, J. M., & McBurnett, K. (1994). Psychopathy
and conduct problems in children. Journal of Abnormal Psychology, 103, 700–707.
doi:10.1037/0021–843X.103.4.700
Frick, P. J., & White, S. F. (2008). The importance of callous-unemotional traits for devel-
opmental models of aggressive and antisocial behavior. Journal of Child Psychology and
Psychiatry, 49, 359–375. doi:10.1111/j.1469–7610.2007.01862.x
Friendship, C., Blud, L., Erikson, M., Travers, R., & Thornton, D. (2003). Cognitive-
behavioural treatment for imprisoned offenders: An evaluation of HM Prison Ser-
vice’s cognitive skills programmes. Legal and Criminological Psychology, 8, 103–114.
doi:10.1348/135532503762871273
Garrett, C. J. (1985). Effects of residential treatment on adjudicated delinquents: A meta-
analysis. Journal of Research on Crime and Delinquency, 22, 287–308. doi:10.1177/
0022427885022004002
Glick, B., & Goldstein, A. P. (1987). Aggression replacement training. Journal of Counseling
and Development, 65, 356–362. doi:10.1002/j.1556-6676.1987.tb00730.x
Gobrogge, K. L., Liu, Y., Jia, X., & Wang, Z. (2007). Anterior hypothalamic neural activation
and neurochemical associations with aggression in pair-bonded male prairie voles. Journal
of Comparative Neurology, 502, 1109–1122. doi:10.1002/cne.21364
Golden, L. S., Gatchel, R. J., & Cahill, M. A. (2006). Evaluating the effectiveness of the National
Institute of Corrections’ “Thinking for a Change” program among probationers. Journal
of Offender Rehabilitation, 43, 55–73. doi:10.1300/J076v43n02_03
Gordon, H. L., Baird, A. A., & End, A. (2004). Functional differences among those
high and low on a trait measure of psychopathy. Biological Psychiatry, 56, 516–521.
doi:10.1016/j.biopsych.2004.06.030
Grant, B. F., Stinson, F. S., Dawson, D. A., Chou, S. P., Ruan, W. J., & Pickering, R. P. (2004).
Co-occurrence of 12-month alcohol and drug use disorders and personality disorders in
the United States: Results from the National Epidemiologic Survey on Alcohol and
Related Conditions. Archives of General Psychiatry, 61, 361–368.
Haas, S. M., Waschbusch, D. A., Pelham, W. E., King, S., Andrade, B. F., & Carrey, N. J.
(2011). Treatment response in CP/ADHD children with callous/unemotional traits.
Journal of Abnormal Child Psychology, 39, 541–552. doi:10.1007/s10802-010-9480-4
Hakamata, Y., Lissek, S., Bar-Haim, Y., Britton, J. C., Fox, N. A., Leibenluft, E., &
Pine, D. S. (2010). Attention bias modification treatment: A meta-analysis toward
the establishment of novel treatment for anxiety. Biological Psychiatry, 68, 982–990.
doi:10.1016/j.biopsych.2010.07.021
Hall, J. R., Benning, S. D., & Patrick, C. J. (2004). Criterion-related validity of the three-factor
model of psychopathy: Personality, behavior, and adaptive functioning. Assessment, 11,
4–16. doi:10.1177/1073191103261466
Hall, J. R., Bernat, E. M., & Patrick, C. J. (2007). Externalizing psychopathology and
the error-related negativity. Psychological Science, 18, 326–333. doi:10.1111/j.1467-
9280.2007.01899.x
Hare, R. D. (1983). Diagnosis of antisocial personality disorder in two prison populations.
Hare, R. D. (1991). The Hare psychopathy checklist—revised. Toronto, Canada: Multi-Health
Systems.
Hare, R. D. (2003). The Hare psychopathy checklist—revised (2nd ed.). Toronto, Canada:
Multi-Health Systems.
Harris, G. T., & Rice, M. E. (2006). Treatment of psychopathy: A review of empirical findings.
In C. J. Patrick (Ed.), Handbook of psychopathy (pp. 555–572). New York, NY: Guilford
Press.
Hawes, D. J., & Dadds, M. R. (2005). The treatment of conduct problems in children with
callous–unemotional traits. Journal of Consulting and Clinical Psychology, 73, 737–741.
doi:10.1037/0022-006X.73.4.737
Hawes, D. J., & Dadds, M. R. (2007). Stability and malleability of callous-unemotional
traits during treatment for childhood conduct problems. Journal of Clinical Child and
Adolescent Psychology, 36, 347–355. doi:10.1080/15374410701444298
Henggeler, S. W., Melton, G. B., & Smith, L. A. (1992). Family preservation using multi-
systemic therapy: An effective alternative to incarcerating juvenile offenders. Journal of
Hinshaw, S. P. (1991). Stimulant medication and the treatment of aggression in children
with attention deficits. Journal of Clinical Child Psychology, 20, 301–312. doi:10.1207/
s15374424jccp2003_9
Hinshaw, S. P., Heller, T., & McHale, J. P. (1992). Covert antisocial behavior in boys with
attention-deficit hyperactivity disorder: External validation and effects of methylphenidate.
Journal of Consulting and Clinical Psychology, 60, 274–281. doi:10.1037.0022-

006X.60.2.274
Iacono, W. G., Carlson, S. R., & Malone, S. M. (2000). Identifying a multivariate endophe-
notype for substance use disorders using psychophysiological measures. International
Journal of Psychophysiology, 38, 81–96.
Iacono, W. G., Carlson, S. R., Malone, S. M., & McGue, M. (2002). P3 event-related
potential amplitude and risk for disinhibitory disorders in adolescent boys. Archives of
General Psychiatry, 59, 750–757. doi:10–1001/pubs.Arch Gen Psychiatry-ISSN-0003-
990x-59-8-yoa10128
Iacono, W. G., Carlson, S. R., Taylor, J., Elkins, I. J., & McGue, M. (1999). Behav-
ioral disinhibition and the development of substance-use disorders: Findings from
the Minnesota Twin Family Study. Development and Psychopathology, 11, 869–900.
doi:10.1017/S0954579499002369
Izzo, R. L., & Ross, R. R. (1990). Meta-analysis of rehabilitation programs for juve-
nile delinquents: A brief report. Criminal Justice and Behavior, 17 , 134–142.
doi:10.1177/0093854890017001008
Johnstone, S. J., & Barry, R. J. (1996). Auditory event-related potentials to a two-tone auditory
discrimination paradigm in attention deficit hyperactivity disorder. Psychiatry Research,
64, 179–192. doi:10.1016/S0165-1781(96)02893-4
Jones, A. P., Laurens, K. R., Herba, C. M., Barker, G. J., & Viding, E. (2009). Amygdala
hypoactivity to fearful faces in boys with conduct problems and callous-unemotional traits.
Kazdin, A. E., & Whitley, M. K. (2003). Treatment of parental stress to enhance therapeu-
tic change among children referred for aggressive and antisocial behavior. Journal of
Kendler, K. S., Aggen, S. H., & Patrick, C. J. (2012). A multivariate twin study of the
DSM-IV criteria for antisocial personality disorder. Biological Psychiatry, 71, 247–253.
doi:10.1016/j.biopsych.2011.05.019
Kendler, K. S., Aggen, S. H., & Patrick, C. J. (2013). Familial influences on conduct disorder
criteria in males reflect two genetic factors and one shared environmental factor: A
population-based twin study. JAMA Psychiatry, 70, 78–86.
Kendler, K. S., Prescott, C. A., Myers, J., & Neale, M. C. (2003). The structure of genetic and
environmental risk factors for common psychiatric and substance use disorders in men and
women. Archives of General Psychiatry, 60, 929–937. doi:10.1001/archpsyc.60.9.929
Kessler, R. C., & Walters, E. E. (2002). The National Comorbidity Survey. In M. T.
Tsuang & M. Tohen (Eds.), Textbook in psychiatric epidemiology (2nd ed., pp. 343–362).
New York, NY: John Wiley & Sons, Inc.
Kim, M. S., Kim, J. J., & Kwon, J. S. (2001). Frontal P300 decrement and executive dysfunction
in adolescents with conduct problems. Child Psychiatry and Human Development, 32,
93–106. doi:10.1023/A:1012299822274
Kim, S. W., & Grant, J. E. (2001). An open naltrexone treatment study in patho-
logical gambling disorder. International Clinical Psychopharmacology, 16, 285–289.
doi:10.1097/00004850-200109000-00006
Kimonis, E. R., & Frick, P. J. (2010). Oppositional defiant disorder and conduct dis-
order grown-up. Journal of Developmental and Behavioral Pediatrics, 31, 244–254.
doi:10.1097/DBP.0b013e3181d3d320
Kimonis, E. R., & Frick, P. J. (2012). Externalizing disorders of childhood and adolescence.
In J. E. Maddux & B. A. Winstead (Eds.), Psychopathology: Contemporary issues, theory,
and research (3rd ed., pp. 443–472). Mahwah, NJ: Erlbaum.
Klorman, R. (1991). Cognitive event-related potentials and in attention deficit disorder.

Journal of Learning Disabilities, 24, 130–140. doi:10.1177/002221949102400301
Koch, J. L. (1891). Die psychopathischen minderwertigkeiten. Ravensburg, Germany: Maier.
Koenigsberg, H. W., Kaplan, R. D., Gilmore, M. M., & Cooper, A. M. (1985). The relation
between syndrome and personality disorder in DSM-III: Experience with 2,412 patients.
Kohlberg, L. (1976). Moral stages and moralization: The cognitive-developmental approach.
In T. Lickona (Ed.), Moral development and behavior (pp. 31–55). New York, NY: Holt,
Rinehart, & Winston.
Kolko, D. J., Dorn, L. D., Bukstein, O., Pardini, D. A., Holden, E. A., & Hart, J. (2009).
Community vs. clinic-based modular treatment of children with early-onset ODD or CD:
A clinical trial with 3-year follow-up. Journal of Abnormal Child Psychology, 37 , 591–609.
doi:10.1007/s10802-009-9303-7
Kosfeld, M., Heinrichs, M., Zak, P. J., Fischbacher, U., & Fehr, E. (2005). Oxytocin increases
trust in humans. Nature, 435, 673–676. doi:10.1038/nature03701
Kraepelin, E. (1915). Psychiatrie: Ein lehrbuch (8th ed.). Leipzig, Germany: Barth.
Kramer, M. D., Patrick, C. J., Krueger, R. F., & Gasperi, M. (2012). Delineating physiological
defensive reactivity in the domain of self-report: Phenotypic and etiologic structure of
dispositional fear. Psychological Medicine, 42, 1305–1320.
Krueger, R. F. (1999a). The structure of common mental disorders. Archives of General
Psychiatry, 56, 921–926. doi:10-1001/archpsyc.56.10.921
Krueger, R. F. (1999b). Personality traits in late adolescence predict mental disorders in
early adulthood: A prospective-epidemiological study. Journal of Personality, 67 , 39–65.
doi:10.1111/1467-6494.00047
Krueger, R. F., Caspi, A., Moffitt, T. E., & Silva, P. A. (1998). The structure and stability of
common mental disorders (DSM-III-R): A longitudinal-epidemiological study. Journal
of Abnormal Psychology, 107 , 216–227. doi:10.1037/0021-843X.107.2.216
Krueger, R. F., Hicks, B., Patrick, C. J., Carlson, S., Iacono, W. G., & McGue, M. (2002).
Etiologic connections among substance dependence, antisocial behavior, and personality:
Modeling the externalizing spectrum. Journal of Abnormal Psychology, 111, 411–424.
doi:10.1037/0021-843X.111.3.411
Krueger, R. F., Markon, K. E., Patrick, C. J., Benning, S. D., & Kramer, M. (2007). Linking
antisocial behavior, substance use, and personality: An integrative quantitative model
of the adult externalizing spectrum. Journal of Abnormal Psychology, 116, 645–666.
doi:10.1037/0021-843X.116.4.645
Landenberger, N. A., & Lipsey, M. W. (2005). The positive effects of cognitive-behavioral
programs for offenders: A meta-analysis of factors associated with effective treatment.
Journal of Experimental Criminology, 1, 451–476. doi:10.1007/s11292-005-3541-7
Lang, P. J., Bradley, M. M., & Cuthbert, B. N. (1990). Emotion, attention, and the startle
reflex. Psychological Review, 97 , 377–398. doi:10.1037/0033-295X.97.3.377
LeDoux, J. E. (2000). Emotion circuits in the brain. Annual Review of Neuroscience, 23,
155–184. doi:10.1146/annurev.neuro.23.1.155
Levenston, G. K., Patrick, C. J., Bradley, M. M., & Lang, P. J. (2000). The psychopath as
observer: Emotion and attention in picture processing. Journal of Abnormal Psychology,
109, 373–385. doi:10.1037/0021-843X.109.3.373
Lewis, C. E., Rice, J., & Helzer, J. E. (1983). Diagnostic interactions: Alcoholism
and antisocial personality. Journal of Nervous and Mental Disease, 171, 105–113.
doi:10.1097/00005053-198302000-00007
Lilienfeld, S. O., & Andrews, B. P. (1996). Development and preliminary validation of a

self-report measure of psychopathic personality traits in noncriminal populations. Journal
of Personality Assessment, 66, 488–524. doi:10.1207/s15327752jpa6603_3
Lilienfeld, S. O., & Widows, M. R. (2005). Psychopathic Personality Inventory–Revised (PPI–R)
professional manual. Odessa, FL: Psychological Assessment Resources.
Lim, M. M., Wang, Z., Olazabal, D. E., Ren, X., Terwilliger, E. F., & Young, L. J. (2004).
Enhanced partner preference in a promiscuous species by manipulating the expression of
a single gene. Nature, 429, 754–757. doi:10.1038/nature02539
Linnoila, M., & Virkkunen, M. (1992). Aggression, suicidality, and serotonin. Journal of
Lipsey, M. W. (1995). What do we learn from 400 studies on the effectiveness of treatment
with juvenile delinquents? In J. McGuire (Ed.), What works: Reducing reoffending (pp.
63–78). Chichester, England: John Wiley & Sons, Ltd.
Lipsey, M. W., Chapman, G. L., & Landenberger, N. A. (2001). Cognitive-behavioral
programs for offenders. Annals of the American Academy of Political and Social Science,
578, 144–157. doi:10.1177/000271620157800109
Little, G. L., & Robinson, K. D. (1988). Moral reconation therapy: A systematic step-by-
step treatment system for treatment-resistant clients. Psychological Reports, 62, 135–151.
doi:10.2466/pr0.1988.62.1.135
Lösel, F. (1996, September). Effective correctional programming: What empirical research tells
us and what it doesn’t. Forum on Corrections Research, 6, 33–37.
Lowenkamp, C. T., Latessa, E. J., & Smith, P. (2004). Does correctional program quality really
matter? The impact of adhering to the principles of effective intervention. Criminology
and Public Policy, 5, 575–594. doi:10.1111/j.1745-9133.2006.00388.x
Lykken, D. T. (1995). The antisocial personalities. Hillsdale, NJ: Erlbaum.
Lynam, D. R. (1997). Childhood psychopathy: Capturing the fledgling psychopath in a
nomological net. Journal of Abnormal Psychology, 106, 425–438.
Lynam, D. R., Leukefeld, C., & Clayton, R. R. (2003). The contribution of personality to the
overlap between antisocial behavior and substance use/misuse. Aggressive Behavior, 29,
316–331. doi:10.1002/ab.10073
Marsh, A. A., Finger, E. C., Mitchell, D. G., Reid, M. E., Sims, C., Kosson, D. S., … Blair, R.
J. (2008). Reduced amygdala response to fearful expressions in children and adolescents
with callous-unemotional traits and disruptive behavior disorders. American Journal of
Psychiatry, 165, 712–720. doi:10.1176/appi.ajp.2007.07071145
Martin, D. J., Garske, J. P., & Davis, M. K. (2000). Relation of the therapeutic alliance with
outcome and other variables: A meta-analytic review. Journal of Consulting and Clinical
Psychology, 68, 438–450. doi:10.1037/0022-006X.68.3.438
Martinson, R. (1974). What works?: Questions and answers about prison reform. Public
Interest, 10, 22–54.
McDonald, R., Dodson, M. C., Rosenfield, D., & Jouriles, E. N. (2011). Effects of a parenting
intervention on features of psychopathy in children. Journal of Abnormal Child Psychology,
39, 1013–1023. doi:10.1007/s10802-011-9512-8
Michalek, J., Klappheck, M. A., & Kosfelder, J. (2004). Personal goals of psychotherapy
patients: The intensity and the “why” of goal-motivated behavior and their implications for
the therapeutic process. Psychotherapy Research, 14, 193–209. doi:10.1093/ptr/kph017
Minzenberg, M. J., & Siever, L. J. (2006). Neurochemistry and pharmacology of psychopathy

and related disorders. In C. J. Patrick (Ed.), Handbook of psychopathy (pp. 251–277).
Moffitt, T. E. (1993). Adolescence-limited and life-course-persistent antisocial behavior:
A developmental taxonomy. Psychological Review, 100, 674–701. doi:10.1037/0033-
295X.100.4.674
Morgan, A. B., & Lilienfeld, S. O. (2000). A meta-analytic review of the relation between
antisocial behavior and neuropsychological measures of executive function. Clinical
Psychology Review, 20, 113–136. doi:10.1016.S0272-7358(98)00096-8
Nelson, L. D., Bernat, E. M., & Patrick, C. J. (2012). Feedback training normalizes brain-based
error monitoring in high-externalizing individuals: Implications for treatment of impulse
control disorders. Manuscript submitted for publication.
Ogloff, J. R. P., Wong, S., & Greenwood, A. (1990). Treating criminal psychopaths in
a therapeutic community program. Behavioral Sciences and the Law, 8, 181–190.
doi:10.1002/bsl.2370080210
Olver, M. E., Stockdale, M. E., & Wormith, J. S. (2011). A meta-analysis of predictors of
offender treatment attrition and its relationship to recidivism. Journal of Consulting and
Olver, M. E., & Wong, S. (2010). Predictors of sex offender treatment dropout: Psychopathy,
sex offender risk, and responsivity implications. Psychology, Crime, & Law, 17 , 457–471.
O’Malley, S. S., Croop, R. S., Wroblewski, J. M., Labriola, D. F., & Volpicelli, J. R. (1995).
Naltrexone in the treatment of alcohol dependence: A combined analysis of two trials.
Ortiz, J., & Raine, A. (2004). Heart rate level and antisocial behavior in children and
adolescents: A meta-analysis. Journal of the American Academy of Child & Adolescent
Psychiatry, 43, 154–162. doi:10.1097/00004583-200402000-00010
Paille, F. M., Guelfi, J. D., Persons, A. C., Royer, R. J., Steru, L., & Parot, P. (1995). Double
blind randomized multicentre trial of acamprosate in maintaining abstinence from alcohol.
Alcohol and Alcoholism, 30, 239–247.
Patrick, C. J. (1994). Emotion and psychopathy: Startling new insights. Psychophysiology, 31,
319–330. doi:10.1111/j.1469-8986.1994.tb02440.x
Patrick, C. J. (2007). Getting to the heart of psychopathy. In H. F. Hervé and J. C. Yuille
(Eds.), Psychopathy: Theory, research, and social implications (pp. 207–252). Hillsdale, NJ:
Erlbaum.
Patrick, C. J. (2008). Psychophysiological correlates of aggression and violence: An integra-
tive review. Philosophical Transactions of the Royal Society B (Biological Sciences), 363,
2543–2555. doi:10.1098/rstb.2008.0028
Patrick, C. J., & Bernat, E. (2006). The construct of emotion as a bridge between personality
and psychopathology. In R. F. Krueger & J. Tackett (Eds.), Personality and psychopathology
Patrick, C. J., Bernat, E., Malone, S. M., Iacono, W. G., Krueger, R. F., & McGue,
M. K. (2006). P300 amplitude as an indicator of externalizing in adolescent males.
Psychophysiology, 43, 84–92. doi:10.1111/j.1469-8986.2006.00376.x
Patrick, C. J., Drislane, L. E., & Strickland, C. (2012). Conceptualizing psychopathy in triarchic
terms: Implications for treatment. International Journal of Forensic Mental Health, 11,
253–266.
Patrick, C. J., Fowles, D. C., & Krueger, R. F. (2009). Triarchic conceptualization of psy-
chopathy: Developmental origins of disinhibition, boldness, and meanness. Development
and Psychopathology, 21, 913–938. doi:10.1017/S0954579409000492
Patrick, C. J., Hicks, B. M., Nichol, P. E., & Krueger, R. F. (2007). A bifactor approach
to modeling the structure of the Psychopathy Checklist-Revised. Journal of Personality
Disorders, 21, 118–141. doi:10.1521/pedi.2007.21.2.118
Patrick, C. J., Venables, N. C., & Drislane, L. E. (2012). The role of fearless dominance
in differentiating psychopathy from antisocial personality disorder. Personality Disorders
Theory, Research, and Treatment. doi:10.1037/a0027173
Pearson, F. S., Lipton, D. S., Cleland, C. M., & Yee, D. S. (2002). The effects of behavioral/
cognitive-behavioral programs on recidivism. Crime and Delinquency, 48, 476–496.
doi:10.1177/001112870204800306
Peterson, J. B., & Pihl, R. O. (1990). Information processing, neuropsychological function,
and the inherited predisposition to alcoholism. Neuropsychology Review, 1, 343–369.
doi:10.1007/BF01109029
Pettit, G. S., Bates, J. E., & Dodge, K. A. (1993). Family interaction patterns and children’s
conduct problems at home and school: A longitudinal perspective. School Psychology
Review, 22, 403–420.
Pickens, R. W., Svikis, D. S., McGue, M., & LaBuda, M. C. (1995). Common genetic mecha-
nisms in alcohol, drug, and mental disorder comorbidity. Drug and Alcohol Dependence,
39, 129–138. doi:10.1016/0376-8716(95)01151-N
Pinel, P. (1801). Traité médico-philosophique sur l’liénation mentale ou la manie [Medico-
philosophical treatise on mental alienation or mania]. (Trans. 1962 by D. Davis, as A
treatise on insanity). New York, NY: Hafner.
Polaschek, D. L. L. (2011). Many sizes fit all: A preliminary framework for conceptualizing the
development and provision of cognitive-behavioral rehabilitation programs for offenders.
Aggression and Violent Behavior, 16, 20–35. doi:10.1016/j.avb.2010.10.002
Polich, J., Pollock, V. E., & Bloom, F. E. (1994). Meta-analysis of P300 amplitude from males at
risk for alcoholism. Psychological Bulletin, 115, 55–73. doi:10.1037/0033-2909.115.1.55
Pritchard, J. C. (1835). A treatise on insanity and other disorders affecting the mind. London,
England: Sherwood, Gilbert & Piper.
Raine, A. (1997). Antisocial behavior and psychophysiology: A biosocial perspective and a
prefrontal dysfunction hypothesis. In D. M. Stoff, J. Breiling, & J. D. Maser (Eds.),
Handbook of antisocial behavior (pp. 289–303). New York, NY: John Wiley & Sons, Inc.
Raine, A. (2002). Biosocial bases of antisocial and violent behavior in children and adults: A
review. Journal of Abnormal Child Psychology, 30, 311–326.
Raine, A., & Yang, Y. (2006). The neuroanatomical bases of psychopathy: A review of
brain imaging findings. In C. J. Patrick (Ed.), Handbook of psychopathy (pp. 278–295).
Reid, W. H., & Gacono, C. (2000). Treatment of antisocial personality, psychopathy, and other
characterologic antisocial syndromes. Behavioral Sciences and the Law, 18, 647–662.
Rice, M. E., Harris, G. T., & Cormier, C. A. (1992). An evaluation of a maximum security
therapeutic community for psychopaths and other mentally disordered offenders. Law
and Human Behavior, 16, 399–412. doi:10.1007/BF02352266
Robertson, A. A., Grimes, P. W., & Rogers, K. E. (2001). A short-run cost-benefit analysis
of community-based interventions for juvenile offenders. Crime and Delinquency, 47 ,
265–284. doi:10.1177/0011128701047002006
Robins, L. N. (1966). Deviant children grown up. Baltimore, MD: Williams & Wilkins.
Robins, L. N., & Regier, D. A. (1991). Psychiatric disorders in America: The epidemiological
catchment area study. New York, NY: Free Press.
Robinson, D., & Porporino, F. J. (2000). Programming in cognitive skills: The Reasoning and
Rehabilitation Programme. In C. R. Hollin (Ed.), Handbook of offender assessment and
treatment (pp. 179–193). New York, NY: John Wiley & Sons, Inc.
Robison, J., & Smith, G. (1971). The effectiveness of correctional programs. Crime &
Delinquency, 17 , 67–80. doi:10.1177/001112877101700108
Rogers, R., Jackson, R. L., Sewell, K. W., & Johansen, J. (2004). Predictors of treatment
outcome in dually-diagnosed antisocial youth: An initial study of forensic inpatients.
Behavioral Sciences and the Law, 33, 215–222. doi:10.1002/bsl.558
Romani, C. J., Morgan, R. D., Gross, N. R., & McDonald, B. R. (2012). Treating criminal
behavior: Is the bang worth the buck? Psychology, Public Policy, and Law, 18, 144–165.
doi:10.1037/a0024714
Rosenthal, R., & DiMatteo, M. R. (2001). Meta-analysis: Recent developments in quantitative
methods for literature reviews. Annual Review of Psychology, 52, 59–82. doi:10.1146/
annurev.psych.52.1.59
Ross, R. R., Fabiano, E. A., & Ewles, C. D. (1988). Reasoning and rehabilitation. International
Journal of Offender Therapy and Comparative Criminology, 32, 29–35. doi:10.1177/
0306624X8803200104
Rush, B. (1812). Medical inquiries and observations upon the diseases of the mind. Philadelphia,
PA: Kimber & Richardson.
Ryan, R. M., & Deci, E. J. (2008). A self-determination theory approach to psychotherapy:
The motivational basis for effective change. Canadian Psychology, 39, 186–193.
doi:10.1037/a0012753
Ryan, R. M., Plant, R. W., & O’Malley, S. (1995). Initial motivations for alcohol treatment:
Relations with patient characteristics, treatment involvement, and dropout. Addictive
Behaviors, 20, 279–297. doi:10.1016/0306-4603(94)00072-7
Salekin, R. T. (2002). Psychopathy and therapeutic pessimism: Clinical lore or clinical reality?
Clinical Psychology Review, 22, 79–112. doi:10.1016/S0272-7358(01)00083-6
Samenow, S. E. (1991). Correcting errors in thinking in the socialization of offenders. Journal
of Correctional Education, 42, 56–58.
Sanders, M. R., Dadds, M. R., Johnston, B. M., & Cash, R. (1992). Childhood depression
and conduct disorder: I. Behavioral, affective, and cognitive aspects of family problem-
solving interactions. Journal of Abnormal Psychology, 101, 495–504. doi:10.1037/0021-
843X.101.3.495
Sawyer, A. M., & Borduin, C. M. (2011). Effects of multisystemic therapy through midlife: A
21.9-year-follow-up to a randomized clinical trial with serious and violent juvenile offend-
ers. Journal of Consulting and Clinical Psychology, 79, 643–652. doi:10.1037/a0024862
Sellbom, M., & Phillips, T. R. (2013). An examination of the Triarchic conceptualization of
psychopathy in incarcerated and non-incarcerated samples. Journal of Abnormal Psychology,
122, 208–214.
Seto, M. C., & Quinsey, V. L. (2006). Toward the future: Translating basic research into
prevention and treatment strategies. In C. J. Patrick (Ed.), Handbook of psychopathy (pp.
Skeem, J., Eno Louden, J., Manchak, S., Vidal, S., & Haddad, E. (2009). Social networks and
social control of probationers with co-occurring mental and substance abuse problems.
Law and Human Behavior, 33, 122–135. doi:10.1007/s10979-008-9140-1
Skeem, J. L., Eno Louden, J., Polaschek, D., & Camp, J. (2007). Assessing relationship quality
in mandated community treatment: Blending care with control. Psychological Assessment,
19, 397–410. doi:10.1037/1040-3590.19.4.397
Skeem, J. L., & Manchak, S. (2008). Back to the future: From Klockars’ model of effective
supervision to evidence-based practice on probation. Journal of Offender Rehabilitation,
47 , 220–247. doi:10.1080/10509670802134069
Skeem, J., Polascheck, D., & Manchak, S. (2009). Appropriate treatment works, but how?
Rehabilitating general, psychopathic, and high risk offenders. In J. L. Skeem, K. S.
Douglas, and S. L. Lilienfeld (Eds.), Psychological science in the courtroom: Consensus and
controversies (pp. 358–384). New York, NY: Guilford Press.
Skeem, J., Polaschek, D., Patrick, C., & Lilienfeld, S. (2011). Psychopathic personality:
Bridging the gap between scientific evidence and public policy. Psychological Science in the
Public Interest, 12, 95–162.
Slutske, W. S., Heath, A. C., Dinwiddie, S. H., Madden, P. A. F., Bucholz, K. K., Dunne,
M. P., … Martin, N. G. (1998). Common genetic risk factors for conduct disorder and
alcohol dependence. Journal of Abnormal Psychology, 107 , 363–374. doi:10.1037/0021-
843X.107.3.363
Tackett, J. L., Krueger, R. F., Iacono, W. G., & McGue, M. (2005). Symptom-based
subfactors of DSM-defined conduct disorder: Evidence for etiologic distinctions. Journal
of Abnormal Psychology, 114, 483–487. doi:10.1037/0021-843X.114.3.483
Tackett, J. L., Krueger, R. F., Sawyer, M. G., & Graetz, B. W. (2003). Subfactors of
DSM-IV conduct disorder: Evidence and connections with syndromes from the child
behavior checklist. Journal of Abnormal Child Psychology, 31, 647–654. doi:10.1023/
A:1026214324287
Tarter, R., Alterman, A., & Edwards, K. (1985). Vulnerability to alcoholism in men: A
behavior-genetic perspective. Journal of Studies on Alcohol, 46, 259–261.
Tellegen, A. (2003). Multidimensional Personality Questionnaire-276 (MPQ-276): Test booklet.
Minneapolis, MN: University of Minnesota Press.
Trull, T. J., & Sher, K. J. (1994). Relationship between the five-factor model of personality and
Axis I disorders in a nonclinical sample. Journal of Abnormal Psychology, 103, 350–360.
doi:10.1037/0021-843X.103.2.350
Vaidyanathan, U., Hall, J. R., Patrick, C. J., & Bernat, E. M. (2011). Clarifying the role of
defensive reactivity deficits in psychopathy and antisocial personality using startle reflex
methodology. Journal of Abnormal Psychology, 12, 253–258. doi:10.1037/a0021224
Venables, N. C., & Patrick, C. J. (2012). Validity of the Externalizing Spectrum Inventory in a
criminal offender sample: Relations with disinhibitory psychopathology, personality, and
psychopathic features. Psychological Assessment, 24, 88–100. doi:10.1037/a0024703
Verona, E., & Patrick, C. J. (2000). Suicide risk in externalizing syndromes: Temperamental
and neurobiological underpinnings. In T. E. Joiner (Ed.), Suicide science: Expanding the
boundaries (pp. 137–173). Boston, MA: Kluwer Academic.
Viding, E., Blair, R. J., Moffitt, T. E., & Plomin, R. (2005). Evidence for substantial genetic risk
for psychopathy in 7-year-olds. Journal of Child Psychology and Psychiatry, 46, 592–597.
doi:10.1111/j.1469-7610.2004.00393.x
Vollebergh, W. A. M., Iedema, J., Bijl, R. V., de Graaf, R., Smit, F., & Ormel, J. (2001).
The structure and stability of common mental disorders: The NEMESIS study. Archives
of General Psychiatry, 58, 597–603. doi:10.1001/archpsyc.58.6.597
Waller, R., Gardner, F., Hyde, L. W., Shaw, D. S., Dishion, T. J., & Wilson, M. N.
(2012). Do harsh and positive parenting predict parent reports of deceitful-callous
behavior in early childhood? Journal of Child Psychology and Psychiatry, 53, 946–953.
doi:10.1111/j.1469-7610.2012.02550.x
Waschbush, D. A., Carrey, N. J., Willoughby, M. T., King, S., & Andrade, B. F. (2007).
Effects of methylphenidate and behavior modification on the social and academic behav-
ior of children with disruptive behavior disorders: The moderating role of callous/
unemotional traits. Journal of Clinical Child and Adolescent Psychology, 36, 629–644.
doi:10.1080/15374410701662766
Weiskopf, N., Veit, R., Erb, M., Mathiak, K., Grodd, W., Goebel, R., & Birbaumer, N.
(2003). Physiological self-regulation of regional brain activity using real-time functional
magnetic resonance imaging (fMRI): Methodology and exemplary data. NeuroImage, 19,
577–586. doi:10.1016/S1053-8119(03)00145-9
Whitehead, J. T., & Lab, S. P. (1989). A meta-analysis of juvenile correctional treat-
ment. Journal of Research on Crime and Delinquency, 26, 276–295. doi:10.1177/
0022427889026003005
Widiger, T. A., Cadoret, R., Hare, R., Robins, L., Rutherford, M., Zanarini, M., … Francis, A.
(1996). DSM-IV antisocial personality disorder field trial. Journal of Abnormal Psychology,
105, 3–16. doi:10.1037/0021-843X.105.1.3
Widiger, T. A., Verheul, R., & van den Brink, W. (1999). Personality and psychopathology. In
L. A. Pervin & O. John (Eds.), Handbook of personality: Theory and research (2nd ed., pp.
Wilson, D. B., Bouffard, L. A., & MacKenzie, D. L. (2005). A quantitative review of
structured, group-oriented, cognitive-behavioral programs for offenders. Criminal Justice
and Behavior, 32, 172–204. doi:10.1177/0093854804272889
Yochelson, S., & Samenow, S. E. (1976). The criminal personality: Vol. 1. A profile for change.
New York, NY: Jason Aronson.
Yochelson, S., & Samenow, S. E. (1977). The criminal personality: Vol. 2. The change process.
New York, NY: Jason Aronson.
Young, S. E., Stallings, M. C., Corley, R. P., Krauter, K. S., & Hewitt, J. K. (2000). Genetic
and environmental influences on behavioral disinhibition. American Journal of Medical
Genetics (Neuropsychiatric Genetics), 96, 684–695.
Zuckerman, M. (1999). Vulnerability to psychopathology: A biosocial model. Washington, DC:
54
Tobacco Dependence
Daniel S. McGrath
Mount Allison University, Canada
Sherry H. Stewart
Dalhousie University, Canada
Tobacco smoking remains the most prevalent cause of preventable death worldwide
(World Health Organization, 2011). Recent estimates indicate that between 5 and
6 million deaths each year are directly attributable to tobacco, with this number
expected to rise to as many as 8 to 10 million by 2030 (Jha et al., 2006; World
Health Organization, 2011). Approximately one-half to about two-thirds of current
long-term smokers will eventually succumb to tobacco-related disease (Doll, Peto,
Boreham, & Sutherland, 2004). Moreover, tobacco use has been implicated as one
of the leading contributors to numerous cancers (e.g., Botteri et al., 2008; Gandini
et al., 2008; Hymowitz, 2011) as well as a host of chronic illnesses such as coronary
artery disease (Pipe, Papadakis, & Reid, 2010), chronic obstructive pulmonary disease
(COPD; Forey, Thornton, & Lee, 2011), and stroke (Shah & Cole, 2010). In
addition to its direct human toll on smokers, tobacco also places a substantial
economic burden on society in the form of increased health care expenditure and
lost productivity (Lightwood, Collins, Lapsley, & Novotny, 2000), as well as the
health hazards associated with second-hand smoke (Centers for Disease Control and
Prevention, 2002). Given the considerable harms associated with tobacco use, it is
perhaps unsurprising that 69% of adult smokers report wanting to quit, with over half
(52%) actually attempting to quit in the past year. However, very few smokers (6.2%)
are ultimately successful in achieving tobacco abstinence (Centers for Disease Control
and Prevention, 2011).
Cognitive behavioral therapy (CBT) is among the most commonly researched and
adopted forms of psychotherapy. A large body of evidence supports the efficacy of CBT
for a wide range of psychological disorders (Butler, Chapman, Forman, & Beck, 2006)
including substance use disorders (SUDs; O’Connor & Stewart, 2010). The CBT
approach to smoking cessation, specifically, involves changing cognitions surrounding
tobacco use as well as altering behaviors to avoid or manage smoking temptations

DOI: 10.1002/9781118528563.wbcbt54
(Niaura, 2008). The overarching goal of these interventions is to provide smokers

with skills training to modify their smoking behavior and to cope with the challenges
they often face (e.g., craving and relapse) following cessation (Perkins, Conklin,
& Levine, 2007; Vidrine, Cofta-Woerpel, Daza, Wright, & Wetter, 2006). CBT
interventions typically involve therapy sessions consisting of face-to-face interactions
between a smoker/smokers and a smoking cessation counselor, clinician, or health
care worker. Therapy can vary in format (e.g., individual vs. group) as well as in level
of intensity (e.g., intensive vs. brief) (Lancaster & Stead, 2005; Mottillo et al., 2009;
Niaura, 2008).
The goal of this chapter is to provide a review of the most recent literature pertaining
to the effectiveness of CBT in the treatment of tobacco dependence. For this review,
CBT is broadly defined as any psychotherapy intervention which employs behavioral
skills training, operant/classical/vicarious conditioning or social learning principles,
or cognitive techniques for the purposes of helping the smoker achieve smoking
cessation or reduction in tobacco intake. First, we briefly describe the most common
CBT techniques employed for tobacco dependent clients and discuss their proposed
underlying mechanisms of action as applied to smoking cessation/reduction. We then
focus on the most recent empirical literature pertaining specifically to the effectiveness
of CBT-based interventions designed to increase rates of tobacco abstinence in
smokers. The literature cited in this chapter was compiled through keyword searches
using several electronic databases including PubMed, PsycINFO, and the Cochrane
Library. Wherever possible, we cite the pooled evidence from studies examining the
effectiveness of CBT-based interventions from recent meta-analyses, review papers,
and Cochrane Reviews. Finally, we conclude the chapter by offering our interpretation
of the sum of this evidence and provide suggestions for future research on CBT for
tobacco dependence.
Cognitive Behavioral Therapy Interventions
Numerous variations of CBT have been developed and applied to smoking cessation.
While the goal of modifying problematic cognitions/behavior may be similar, the
approach used to achieve these results often differs across interventions. We briefly
describe the structure and theoretical underpinnings of some of the more commonly
used CBT interventions for tobacco cessation.
Cognitive Therapies
Cognitive therapy is based on the principle that emotions and behavior are determined
by thoughts, and that feelings and behavior can be changed by restructuring thoughts
(Meichenbaum, 1977). For those who are tobacco dependent, thoughts about
smoking might facilitate the maintenance of smoking behavior. For instance, thought
patterns such as, “I’m not able cope with my urges to smoke,” or, “If I were to
smoke right now, then I would feel less tense,” would contribute to continued use of
tobacco. Various types of cognitions have been identified as potentially contributing
to smoking. However, considerable focus has been given to the influence of smoking
Tobacco Dependence 1301
outcome expectancies (beliefs about the positive or negative effects of smoking)

(Brandon, Juliano, & Copeland, 1999; Glock, Unz, & Kovacs, 2012; Hendricks &
Brandon, 2005) as well as smoking abstinence self-efficacy expectancies (beliefs about
one’s own ability to successfully abstain from smoking in various high-risk situations)
(Hendricks, Wood, & Hall, 2009). These underlying beliefs are said to be activated
in the form of automatic thoughts when the smoker is exposed to smoking-related
cues or high risk for smoking situations (Tiffany, 1990; Waters, Shiffman, Bradley, &
Mogg, 2003). In cognitive restructuring, clients are taught to identify their automatic
thoughts that promote smoking behavior, and to challenge these thoughts so as to
replace them with more adaptive ways of thinking that are less likely to promote
smoking behavior (Perkins et al., 2007).
Behavioral Therapies
Based on the principles of classical and operant conditioning theories, smoking is
triggered by exposure to external or internal cues that have been frequently paired
with smoking in the past (e.g., drinking coffee or alcohol; negative mood states)
(Carter & Tiffany, 1999; Ferguson & Shiffman, 2009), and maintained through
its positive consequences (e.g., social approval by smoking peers; short-term ten-
sion reduction; mood enhancement) (Benowitz, 2008; Epstein, Griffin, & Botvin,
2000). In most behavioral approaches to smoking cessation, prior to the smoking
cessation attempt, clients are taught about the antecedent, behavior, consequences
(ABC) sequence, and are asked to self-monitor their smoking behavior in order
to identify their own unique triggers (or high risk for smoking situations) and
consequences (reinforcers of smoking). This information is used in treatment plan-
ning. For example, if triggers involve anxious emotions for a particular client, he
or she may be taught relaxation strategies. Triggers may at times be avoided,
or the client may be encouraged to engage in exposure and response preven-
tion (ERP) exercises in order to extinguish the urge to smoke in the presence
of the smoking-related cue (Ferguson & Shiffman, 2009; Hammersley, 1992). In
terms of identifying the unique consequences (reinforcers) that may be maintain-
ing smoking in an individual client, this information is useful in finding alternative
reinforcers (healthy alternatives to smoking) that meet these same needs for a given
client.
Mindfulness/Urge Surfing
While mindfulness has its roots in Eastern philosophies and healing practices, in
recent years it has been adopted by CBT practitioners as part of their treatment
package. Mindfulness is a way of relating directly to what is happening in one’s
life by consciously and systematically working with discomfort and stress (urges or
withdrawal, in the case of smoking cessation). The practice of applying mindfulness in
the clinical setting originated with the work of Jon Kabat-Zinn (1984). Mindfulness
was introduced as a clinical tool in the CBT addiction treatment field by the late
Alan Marlatt, who originally coined the term “urge surfing” (Marlatt & Gordon,
1985) to describe a mindfulness-based relapse prevention technique that has since
been applied successfully in the smoking cessation area (Bowen & Marlatt, 2009). It
is often introduced to CBT clients following cognitive restructuring as an alternative
to thought challenging. With the urge surfing technique, clients are taught simply to
remain curious about their thoughts and feelings and to continue to experience them
fully in the present moment without judgment. Through the practice of mindful urge
surfing, the client learns that uncomfortable urges and tobacco withdrawal sensations
dissipate naturally “like a wave” if one does not give in to the urge to smoke or try
to escape from the discomfort in some other manner (Bowen, Chawla, & Marlatt,
2011).
Relapse Prevention
Relapse frequently occurs following treatment of an addictive behavior and has been
described as an outcome of behavioral change whereby an individual returns to a
problematic behavior pattern following a lapse (Hsu & Marlatt, 2012). First proposed
by Marlatt and Gordon (1985), relapse prevention (RP) is a CBT-based intervention
designed to help clients avoid relapse by replacing previously learned maladaptive
behavior patterns with positive coping skills. For instance, if the client has learned
to cope with life stressors through tobacco use, the therapist would help the client
identify this pattern and replace this learned behavior with other more effective
strategies for dealing with stress. Clients are prepared for an eventual lapse to smoking
and are taught to view this lapse as a learning experience rather than as a failure,
thereby reducing the likelihood of spiraling into a full-blown relapse. Typically, a
relapse prevention plan is constructed by a client and therapist in a collaborative
effort near the end of treatment. Ultimately, the goal of RP is to enhance the client’s
self-control of their addictive behavior, teach them to identify high-risk situations for
relapse, and provide alternative strategies that minimize the likelihood of relapse (Hsu
& Marlatt, 2012).
Effectiveness of Cognitive Behavioral Therapy Interventions

for Tobacco Dependence
General Cognitive Behavioral Approaches

Two recent meta-analyses have examined the effectiveness of individual behavioral
counseling (which included CBT-based interventions) provided by smoking cessation
counselors on smoking quit rates. In 2008, Lancaster and Stead (2005) updated
their Cochrane Review which compared length of smoking cessation at 6 months
following individual behavioral counseling with a trained smoking counselor versus
no treatment, brief advice, or self-help materials. The authors used a broad definition
for counseling as an intervention involving a face-to-face encounter between a client
and a smoking cessation counselor lasting more than 10 minutes, without a focus on
any specific type of behavioral counseling. Studies involving counseling provided by
other health care workers (e.g., physicians) were not included. From the 22 controlled
trials comparing individual counseling to a minimal behavioral intervention, it was
determined that counseling resulted in a significant improvement in smoking cessation

at a ≥ 6-month follow-up (relative risk [RR] 1.39; 95% confidence interval [CI]: 1.24
to 1.57).
Mottillo et al. (2009) recently conducted a meta-analysis which separately examined
the efficacy of several behavioral interventions (i.e., individual counseling, minimal
clinical intervention from a health care worker, group counseling, and telephone
counseling) from 50 randomized controlled trials (RCTs). Of the trials included, 23
employed intensive individual counseling defined as at least one face-to-face encounter
of ≥ 15 minutes between a client and a smoking cessation counselor who was not
involved in routine clinical care. The method of delivery, the number of sessions, the
duration of sessions, the treatment span, and the treatment population comprising
the 23 trials varied. All smoking outcomes were biochemically verified at 6 and/or 12
months posttreatment. Compared with control groups, the pooled results of RCTs
focused on individual behavioral counseling sessions suggested large increases in rates
of smoking abstinence (odds ratio [OR] 1.49; 95% credible interval [Crl]: 1.08 to
2.07) at follow-up. The authors conclude that each type of behavioral intervention
examined (i.e., individual interventions, group interventions, and telephone counsel-
ing) were all associated with increased odds of smoking cessation; however, there was
insufficient evidence to recommend minimal clinical intervention provided by health
care workers.
A number of studies have investigated the effectiveness of purely cognitive,
behavioral, or combined CBT interventions for tobacco dependence. Much of the
available evidence supports the use of CBT-based interventions as effective stand-
alone treatments for increasing smoking quit rates (Vidrine et al., 2006). Several
recent analyses also indicate that CBT may be more effective than other counsel-
ing approaches for achieving tobacco abstinence. For instance, one meta-analysis of
adolescent smoking cessation research found that the most successful programs were
those that included cognitive behavioral principles as a core component (McDon-
ald, Colwell, Backinger, Husten, & Maule, 2003). Similarly, in their meta-analysis
of smoking interventions for teens, Sussman, Sun, and Dent (2006) found that
programs based on cognitive behavioral principles, motivational enhancement (i.e.,
techniques designed to reduce ambivalence toward changing smoking behavior), and
social-influence theory (i.e., techniques designed to challenge social influences which
help to maintain smoking) were especially likely to enhance quit rates.
A key focus of recent studies of CBT-based smoking interventions has been the
use of extended cognitive behavioral therapy (E-CBT) for promoting long-term
tobacco abstinence. For instance, Hall, Humfleet, Reus, Muñoz, and Cullen (2004)
randomly assigned smokers to one of four conditions: E-CBT plus nortriptyline,
E-CBT plus placebo, brief CBT plus nortriptyline, or brief CBT plus placebo. Those
assigned to brief CBT took part in five group counseling sessions whereas the E-
CBT groups received an additional nine monthly sessions. At a 52-week follow-up,
participants in both E-CBT conditions reported significantly higher rates of absti-
nence (i.e., 56% and 57%, respectively) than those in the brief CBT conditions
(21% and 32%, respectively). Hendricks, Delucchi, and Hall (2010) recently exam-
ined potential mediators of E-CBT for smoking cessation among a sample of older
smokers (≥ 50 years of age). Their analyses revealed that E-CBT was successful
in increasing participants’ levels of abstinence self-efficacy (i.e., how successful they

expect to be at quitting) and that self-efficacy accounted for 61–83% of the vari-
ance of treatment condition on abstinence by the 64-week follow-up. This increased
self-efficacy is proposed to serve a protective function against smoking relapse follow-
ing cessation (Bandura, 1977). These research findings indicate that the long-term
focus of E-CBT substantially increases odds of quitting compared to various con-
trol conditions and can play an important role in promoting maintained tobacco
abstinence.
Mindfulness/Urge Surfing
Recent years have seen an increase in the number of studies employing extensions
of CBT for the treatment of numerous psychological disorders (Witkiewitz, Steck-
ler, Gavrishova, Jensen, & Wilder, 2012). Mindfulness in particular has become an
increasingly researched CBT-based intervention for substance use (Zgierska et al.,
2009) and has recently been adapted for smoking. Vidrine et al. (2009) exam-
ined associations between baseline degree of mindfulness and demographic variables,
smoking history, dependence, withdrawal severity, and agency among 158 smokers.
It was found that smokers reporting higher baseline levels of mindfulness were less
nicotine dependent, had lower withdrawal severity, and were more likely to believe
they had the ability to quit smoking. The authors suggest that mindfulness-based
interventions may have the potential to impact smoking cessation and prevent relapse
by enhancing smokers’ emotional and behavioral regulation. Indeed, several stud-
ies indicate that mindfulness techniques can successfully increase rates of continued
abstinence when taught to smokers. For example, Davis, Fleming, Bonus, and Baker
(2007) conducted a small pilot study in which 18 smokers were enrolled in a
mindfulness-based intervention over a 6-week period. Of the 18 participants enrolled,
10 were able to remain tobacco abstinent for the duration of the program. Bowen and
Marlatt (2009) investigated the effectiveness of Marlatt’s mindfulness-based “urge
surfing” technique in a sample of 123 undergraduate smokers. Smokers received
either a mindfulness-based intervention or a no-instruction control while partici-
pating in a cue-exposure paradigm. Compared to control, urge surfing participants
did not significantly differ on subjective measures of smoking urges, but did report
smoking significantly fewer cigarettes at a 7-day follow-up. A recent RCT directly
compared a mindfulness-based intervention with the American Lung Association’s
freedom from smoking (FFS) program (a manual-based and online self-help smoking
cessation program) in a group of 88 treatment-seeking smokers (Brewer et al., 2011).
Clients assigned to the mindfulness condition displayed a greater overall reduction
in smoking during treatment and were significantly more likely to have remained
abstinent at the end of treatment (36% vs. 15%) and at a 17-week follow-up (31%
vs. 6%). Finally, Westbrook et al. (2011) recently examined the extent to which
mindfulness-based techniques could influence neural markers of cue-induced craving
in 47 treatment-seeking smokers. Prior to testing, participants were taught to view
smoking and neutral images either with mindful attention or passively. Compared
to passively viewing smoking images, mindful attention resulted in lower subjective
craving to smoke. In addition, mindful attention was associated with reduced neural
activity in the subgenual anterior cingulate cortex (sgACC), a region of the brain asso-
ciated with craving. This suggests that mindfulness may exert its therapeutic effects on
smoking cessation through reduced activity in brain areas associated with craving. The
sum total of this research suggests that mindfulness-based interventions represent a
promising new approach for increasing smoking cessation rates and reducing craving
following tobacco abstinence.
Relapse Prevention
Marlatt and Gordon’s (1985) RP model is the most extensively researched CBT-
based intervention for smoking cessation. However, evidence from studies examining
the effectiveness of RP for maintaining tobacco abstinence is mixed (Vidrine et al.,
2006). A number of recently published meta-analyses have examined the extent
to which RP programs are successful in preventing relapse to smoking. Hajek,
Stead, West, Jarvis, and Lancaster (2009) meta-analyzed the available evidence on
RP models for smoking in a recent Cochrane Review. For the purposes of their
analyses, they included any behavioral intervention specifically intended to pre-
vent relapse delivered in any format (e.g., group meetings, face-to-face counseling,
written materials). Separate subanalyses were then conducted for studies which
included smokers from the general population who chose to quit on their own
and trials which focused on special populations who were required to quit (i.e.,
pregnant and postpartum ex-smokers, hospital inpatients, and military recruits). The
pooled results of five studies which included smokers from the general popula-
tion who were able to quit unaided (that is, with no formal treatment) indicated
that RP interventions did not significantly decrease relapse to smoking (RR 1.08;
95% CI: 0.98–1.19). The results from five studies which included smokers from
the general population who received formal treatment suggest no benefit for RP
programs in decreasing relapse (RR 1.00; 95% CI: 0.87–1.15). Similarly, results
for pregnant smokers, postpartum ex-smokers, hospital inpatients, and military
recruits indicated no direct benefit of RP programs in preventing relapse. Only
one trial which paired extended RP treatment with varenicline was found to
reduce relapse significantly (RR 1.18; 95% CI: 1.03–1.36). Despite the consis-
tent negative findings, the authors cautioned that most of the experimental designs
included in the review had limited power to detect meaningful differences between
interventions.
Agboola, McNeil, Coleman, and Leonardi Bee (2010) conducted a similar review
and meta-analysis of the literature on RP and smoking cessation. The authors used a
similar strategy to that employed in the Hajek et al. (2009) Cochrane Review; however,
the newer meta-analysis imposed stricter criteria for the comparison of final outcomes.
Specifically, the Hajek et al. review pooled the data at the final follow-up only, whereas
Agboola et al. combined data at similar follow-up time-points only (i.e., short term
[1–3 months post randomization], medium term [6–9 months], and long term
[12–18 months]). Contrary to the findings of Hajek et al., it was found that RP-based
self-help interventions were successful in helping unaided quitters achieve long-term
abstinence (OR 1.52; 95% CI: 1.15–2.01). An increase in short-term abstinence only
was found for aided abstainers who took part in group treatment (OR 2.55; 95% CI:
1.58–4.11), but no other medium- or long-term effects of RP were noted.
Finally, Song, Huttunen-Lenz, and Holland (2009) recently conducted a meta-
analysis of psychoeducational interventions for smoking relapse. Their analysis
included a total of 49 trials, 41 of which were partly or wholly based on CBT
approaches of teaching coping skills for RP. It was found that coping skills train-
ing did not increase rates of abstinence for community quitters who were currently
abstinent for less than one week; however, training did help to prevent relapse for
those who stopped smoking for at least one week at baseline (OR 1.52; 95% CI:
1.20–1.93). No significant effects were found for special population groups such as
pregnant or postpartum women, hospitalized patients, forced quitters, those with
mental illness, or drug abusers. These findings indicate that coping skills training
can enhance RP among community smokers who are motivated to quit. Overall, the
literature for RP in smoking cessation is mixed; however, recent evidence indicates
that RP programs may be effective at preventing relapse for at least certain subgroups
of smokers.
Cognitive Behavioral Therapy for Smoking Cessation

in Special Populations
The accumulated body of evidence on behavioral interventions indicates that many
of the interventions that are successful for treating smokers in the general population
are also readily applicable for treatment of special populations (Fiore et al., 2008;
Vidrine et al., 2006). A recent meta-analysis compared the effectiveness of behavioral
interventions for smoking cessation to control conditions in six disadvantaged groups:
the homeless, prisoners, indigenous populations, at-risk youth, individuals with low
socioeconomic status, and individuals with a mental illness (Bryant, Bonevski, Paul,
McElduff, & Attia, 2011). Behavioral interventions were grouped in this analysis and
included some based on motivational enhancement principles, while others focused
on several forms of behavioral counseling. Positive results were found for increased
short-term abstinence (3 months or less) among low-income female smokers (RR
1.68; 95% CI: 1.21–2.33) and long-term abstinence (6 months or longer) among
individuals with a mental illness (RR 1.35; 95% CI: 1.01–1.81), following treatment
with a behavioral intervention. Webb, de Ybarra, Baker, Reis, and Carey (2010)
recently investigated the efficacy of group-based CBT for tobacco dependence in a
sample of African American smokers. Participants were randomly assigned to either
group CBT or a group general health education condition. In both cases, participants
underwent six counseling sessions and received 8 weeks of transdermal nicotine
patches. Seven-day tobacco abstinence was measured at 2-week (end of counseling),
3-month, and 6-month follow-ups. Rates of abstinence were significantly greater in
the CBT group at 2 weeks (51% vs. 27%), 3 months (34% vs. 20%), and 6 months
(31% vs. 14%).
Considerable attention in the literature has been paid to the use of CBT
for the treatment of tobacco dependence among smokers with a history of
depression. Gierisch, Bastian, Calhoun, McDuffie, and Williams (2012) reviewed
and meta-analyzed the evidence for smoking interventions among depressed

smokers. The interventions included antidepressants, nicotine replacement therapy
(NRT), brief smoking cessation counseling, behavioral counseling, and behavioral
mood management. CBT-based smoking cessation programs were the most
common behavioral counseling intervention. Behavioral mood management
included any interventions designed to influence negative mood and improve
depressive symptoms beyond just smoking cessation counseling, based on the theory
that depressed mood might maintain smoking behavior. Due to an insufficient
number of studies for the meta-analysis, direct comparisons for behavioral-
based interventions were limited to behavioral mood management plus cotreatments
(i.e., NRT or antidepressant) versus cotreatments only. It was found that behavioral
mood management plus cotreatments significantly increased ≤6-month tobacco
abstinence rates (RR 1.41; 95% CI: 1.01–1.96) beyond cotreatments only. These
results suggest that behavioral mood management interventions may influence
smoking relapse in depressed smokers by improving negative mood and thus reducing
a smoking maintenance factor in this special population.
Pairing Cognitive Behavioral Therapy with Pharmacotherapy

for Smoking Cessation
It has been suggested that pairing CBT with pharmacotherapy in a multimodal

approach may significantly improve smoking abstinence rates over medication or
CBT alone (Niaura, 2008). For instance, the U.S. Public Health Service Practice
Guideline recommends that both medication and CBT be provided to smokers
when circumstances are deemed feasible and appropriate (Fiore et al., 2008). Sev-
eral recent trials have compared the effectiveness of CBT alone, medication for
smoking cessation alone, and CBT paired with medication. Recent attention in
the tobacco literature has been paid toward pairing CBT interventions with NRT.
Garc ı́a-Vera (2004) examined the effectiveness of eight sessions of CBT combined
with NRT on smoking behavior in 142 treatment-seeking smokers. Abstinence
rates were examined posttreatment and at a 5-year follow-up. It was found that
the combined therapy resulted in a past 12-month continuous abstinence rate of
33.1% at the 5-year interval. Direct comparisons with either CBT or NRT alone
were not available as the goal of the study was to evaluate the clinical efficacy of
an established smoking cessation program which utilized combined CBT and NRT
only. However, evidence provided from other clinical trials suggests that combined
CBT and NRT may be more efficacious than CBT alone. For instance, Pollak
et al. (2007) examined the efficacy of adding NRT (with a choice of patch, gum,
or lozenge) to CBT in a sample of pregnant women and found that clients who
received both therapies achieved significantly higher abstinence rates at 7 weeks
(24% vs. 8%) and 38 weeks gestation (18% vs. 7%) than those receiving only CBT.
No difference, however, was found at 3 months postpartum (20% vs. 14%). Lastly,
Hall et al. (2009) assigned 402 older smokers (≥ 50 years of age) to four con-
ditions: standard treatment (12 weeks of bupropion, 10 weeks of NRT, and five
group counseling sessions), extended NRT (40 weeks), E-CBT (11 sessions over
40 weeks), and E-CBT plus NRT (11 sessions over 40 weeks with nicotine gum).
Contrary to initial predictions, a nonsignificant trend (p = .06) was found, with
the E-CBT condition reporting higher abstinence rates than the E-CBT plus NRT
condition at most follow-ups (24 weeks: 58% vs. 59%; 52 weeks: 55% vs. 48%; 64
weeks: 55% vs. 51%; 104 weeks: 55% vs. 45%; OR 1.18; 95% CI: 0.99–1.40). The
researchers speculated that the inclusion of NRT with E-CBT may have served to
distract attention away from the skills learned through CBT, with participants then
attributing their continued abstinence to their use of NRT. This is not a unique
finding per se, as a similar pattern has also emerged with combined CBT and
pharmacotherapy for other psychological disorders. For instance, in their review of
treatments for anxiety, Westra and Stewart (1998) reported that combining high
potency benzodiazepines with CBT for the management of anxiety actually leads to
reductions in the long-term benefits of CBT rather than serving as a complement to
psychotherapy.
Significant research focus has also been given to prescription medications available
for smoking cessation such as bupropion and the benefits of combining these
treatments with CBT. A number of recent studies have explored combining CBT
with bupropion for smoking cessation. Schmitz, Stotts, Mooney, DeLaune, and
Moeller (2007) compared individual pharmacotherapy (bupropion vs. placebo),
group psychotherapy (CBT vs. supportive therapy [ST]), and combined options on
tobacco abstinence rates in a sample of women who smoke. A significant interaction
effect was found whereby abstinence rates were higher in the CBT plus bupropion
condition than in the ST plus bupropion condition at end of treatment (44% vs. 18%),
3-month (24% vs. 1%), 6-month (30% vs. 8%), 9-month (23% vs. 5%), and 12-month
(17% vs. 2%) follow-ups. However, the authors suggest that these results should
be interpreted with caution as paired CBT and bupropion was not clearly superior
to placebo plus CBT (end of treatment: ∼14%; 3-month: ∼19%; 6-month: ∼23%;
9-month: ∼13%; and 12-month: ∼12%) nor placebo plus ST (end of treatment:
∼41%; 3-month: ∼40%; 6-month: ∼39%; 9-month: ∼30%; and 12-month: ∼31%).
Levine et al. (2010) also randomly assigned weight-concerned women smokers to
pharmacotherapy (bupropion vs. placebo), group psychotherapy (CBT vs. ST), and
combined options. In this trial, CBT plus bupropion (34%) resulted in significantly
higher 6-month abstinence rates than ST plus bupropion (21%), or CBT plus placebo
(11.5%). However, no significant difference in abstinence rates was found between
CBT plus bupropion and ST plus bupropion at a 12-month follow-up. Lastly, Rovina
et al. (2009) randomly assigned 205 smokers to one of four conditions: bupropion
with brief counseling, bupropion with nonspecific psychological support in groups
(NSGS), bupropion with group CBT, and group CBT only. At a 12-month follow-
up, it was found that abstinence rates were highest in the bupropion with group
CBT condition (34.3%), followed by the bupropion with brief counseling (29.6%),
the bupropion with NSGS (28.1%), and CBT only (19.4%) conditions, respectively.
While results of these studies are mixed, the pairing of CBT with bupropion does
appear to have promise as a more effective treatment of tobacco dependence than
either option alone.
Conclusion and Recommendations for Future Research
Tobacco dependence continues to cause substantial harm to millions of individuals

worldwide. Traditionally, first-line treatment options for smoking have been primarily
pharmacologically based; however, a growing body of literature has emphasized the
importance of cognitive and behavioral approaches to treat tobacco dependence (Fiore
et al., 2008). The collective evidence from meta-analyses and other recent research
studies presented in this chapter indicates that CBT-based interventions are effective
in increasing smoking quit rates and sustained abstinence in the general population,
in special populations, and in individuals with comorbid psychological disorders such
as depression. Recent research also supports the efficacy of mindfulness-based urge
surfing techniques as a promising CBT-based intervention newly tailored to smoking
cessation. In addition, there is some (albeit not always consistent) empirical support
for the role of relapse prevention programs in helping abstinent smokers avoid
problems with relapse. Lastly, a growing body of recently published research supports
the utility of multimodal interventions in which pharmacotherapy is combined with
CBT as a promising approach for increasing rates of tobacco abstinence.
Despite increased focus in the tobacco literature on applying CBT-based techniques
to smoking cessation, there remain several important research questions that have
yet to be adequately addressed. For example, relatively few studies have provided
a direct comparison of different forms of CBT for smoking cessation. There exists
a plethora of CBT-based interventions which differ according to length, intensity,
and delivery format, yet few trials have specifically compared the effectiveness of
these different options for treating tobacco dependence. It has also been suggested
that in order to implement CBT more successfully for substance use disorders, a
client’s potential ambivalence toward changing his or her behavior must first be
acknowledged prior to administering psychotherapy (O’Connor & Stewart, 2010).
Specifically, employing motivational interviewing (MI; Miller & Rollnick, 1991) to
reduce a client’s ambivalence prior to a CBT intervention may show promise for
further enhancing abstinence rates. Using MI techniques, the therapist and client
work in a collaborative fashion to reduce the client’s ambivalence toward change by
first raising awareness of problems associated with the behavior, then setting goals,
and then outlining strategies for change (Witkiewitz et al., 2012). Two recent meta-
analyses suggest that MI for smoking cessation can successfully increase abstinence
rates in adolescent and adult smokers (Heckman, Egleston, & Hofmann, 2010;
Hettema & Hendricks, 2010). However, to date, only a select few studies (e.g., Baker
et al., 2006; Rigotti et al., 2006; Wilson, Fitzsimons, Bradbury, & Elborn, 2008) have
investigated the potential for MI to serve as a prelude to CBT-based interventions for
smoking cessation. Finally, the literature on combining CBT with pharmacotherapy,
while promising, is still in its infancy. More research is needed to delineate the exact
effects, whether beneficial or detrimental, of combining NRT with CBT on long-
term abstinence. In addition, increased focus is required on the potential benefits of
combining newer forms of pharmacotherapy for smoking cessation such as varenicline
with CBT interventions to enhance the odds of successful quitting.
References
Agboola, S., McNeill, A., Coleman, T., & Leonardi Bee, J. (2010). A systematic review
of the effectiveness of smoking relapse prevention interventions for abstinent smokers.
Addiction, 105, 1362–1380. doi:10.1111/j.1360-0443.2010.02996.x
Baker, A., Richmond, R., Haile, M., Lewin, T. J., Carr, V. J., Taylor, R. L., … Wilhelm,
K. (2006). A randomized controlled trial of a smoking cessation intervention among
people with a psychotic disorder. American Journal of Psychiatry, 163, 1934–1942.
doi:10.1176/appi.ajp.163.11.1934
Bandura, A. (1977). Social learning theory. Englewood Cliffs, NJ: Prentice-Hall.
Benowitz, N. L. (2008). Neurobiology of nicotine addiction: Implications for smoking
cessation treatment. American Journal of Medicine, 121, S3–S10.
Botteri, E., Iodice, S., Bagnardi, V., Raimondi, S., Lowenfels, A. B., & Maisonneuve, P.
(2008). Smoking and colorectal cancer: A meta-analysis. Journal of the American Medical
Association, 300, 2765–2778. doi:10.1001/jama.2008.839
Bowen, S., Chawla, N., & Marlatt, G.A. (2011). Mindfulness-based relapse prevention for
addictive behaviors: A clinician’s guide. New York, NY: Guilford Press.
Bowen, S., & Marlatt, A. (2009). Surfing the urge: Brief mindfulness-based interven-
tion for college student smokers. Psychology of Addictive Behaviors, 23, 666–671.
doi:10.1037/a0017127
Brandon, T. H., Juliano, L. M., & Copeland, A. C. (1999). Expectancies for tobacco smoking.
In I. Kirsch (Ed.), How expectancies shape experience (pp. 263–299).Washington, DC:
Brewer, J. A., Mallik, S., Babuscio, T. A., Nich, C., Johnson, H. E., Deleone, C. M., …
Rounsaville, B. J. (2011). Mindfulness training for smoking cessation: Results from a
randomized controlled trial. Drug and Alcohol Dependence, 119, 72–80. doi:10.1016/
j.drugalcdep.2011.05.027
Bryant, J., Bonevski, B., Paul, C., McElduff, P., & Attia, J. (2011). A systematic review
and meta-analysis of the effectiveness of behavioural smoking cessation interventions
in selected disadvantaged groups. Addiction, 106, 1568–1585. doi:10.1111/j.1360-
0443.2011.03467.x
17–31. doi:10.1016/j.cpr.2005.07.003
Carter, B. L., & Tiffany, S. T. (1999). Meta-analysis of cue-reactivity in addiction research.
Addiction, 94, 327–340. doi:10.1046/j.1360-0443.1999.9433273.x
Centers for Disease Control and Prevention. (2002). Annual smoking-attributable mortality,
years of potential life lost, and economic costs: United States, 1995–1999. Morbidity and
Mortality Weekly Report, 51. Washington, DC: U.S. Government Printing Office.
Centers for Disease Control and Prevention. (2011). Quitting smoking among adults: United
States, 2001–2010. Morbidity and Mortality Weekly Report, 60, 1513–1516.
Davis, J. M., Fleming, M. F., Bonus, K. A., & Baker, T. B. (2007). A pilot study on mindfulness
based stress reduction for smokers. BMC Complementary and Alternative Medicine, 7 , 2.
doi:10.1186/1472-6882-7-2
Doll, R., Peto, R., Boreham, J., & Sutherland, I. (2004). Mortality in relation to smoking: 50
years’ observations on male British doctors. British Medical Journal, 328, 1519–1528.
doi:10.1136/bmj.38142.554479.AE
Epstein, J. A., Griffin, K. W., & Botvin, G. J. (2000). A model of smoking among inner-city
adolescents: The role of personal competence and perceived social benefits of smoking.
Preventive Medicine, 31, 107–114. doi:10.1006/pmed.2000.0674
Ferguson, S. G., & Shiffman, S. (2009). The relevance and treatment of cue-induced cravings
in tobacco dependence. Journal of Substance Abuse Treatment, 36, 235–243.
Fiore, M. C., Jaen, C. R., Baker, T. B., Bailey, W. C., Benowitz, N. L., Curry, S. J., …
Wewers, M. E. (2008). Treating tobacco use and dependence: 2008 update. Clinical
practice guidelines. Rockville, MD: U.S. Department of Health and Human Services,
Public Health Service.
Forey, B. A., Thornton, A. J., & Lee, P. E. (2011). Systematic review with meta-analysis of the
epidemiological evidence relating smoking to COPD, chronic bronchitis, and emphysema.
BMC Pulmonary Medicine, 11, 1471–2466.
Gandini, S., Botteri, E., Iodice, S., Boniol, M., Lownfels, A. B., Maisonneuve, P., & Boyle, P.
(2008). Tobacco smoking and cancer: A meta-analysis. International Journal of Cancer,
122, 155–164. doi:10.1002/ijc.23033
Garc ı́a-Vera, M. (2004). Clinical utility of the combination of cognitive-behavioral tech-
niques with nicotine patches as a smoking-cessation treatment: Five-year results of
the “Ex-Moker” program. Journal of Substance Abuse Treatment, 27 , 325–333.
doi:10.1016/j.jsat.2004.09.001
Gierisch, J. M., Bastian, L. A., Calhoun, P. S., McDuffie, J. R., & Williams, J. W. (2012).
Smoking cessation interventions for patients with depression: A systematic review and
meta-analysis. Journal of General Internal Medicine, 27 , 351–360. doi:10.1007/s11606-
011-1915-2
Glock, S., Unz, D., & Kovacs, C. (2012). Beyond fear appeals: Contradicting positive smoking
outcome expectancies to influence smokers’ implicit attitudes, perception, and behavior.
Addictive Behaviors, 37 , 548–551. doi:10.1016/j.addbeh.2011.11.032
Hajek, P., Stead, L. E., West, R., Jarvis, M., & Lancaster, T. (2009). Relapse prevention inter-
ventions for smoking cessation. Cochrane Database of Systematic Reviews, 1, CD003999.
doi:10.1002/14651858.CD003999.pub3
Hall, S. M., Humfleet, G. L., Muñoz, R. F., Reus, V. I., Robbins, J. A., & Prochaska, J.
J. (2009). Extended treatment of older cigarette smokers. Addiction, 104, 1043–1052.
doi:10.1111/j.1360-0443.2009.02548.x
Hall, S. M., Humfleet, G. L., Reus, V. I., Muñoz, R. F., & Cullen, J. (2004). Extended
nortriptyline and psychological treatment for cigarette smoking. American Journal of
Hammersley, R. (1992). Cue exposure and learning theory. Addictive Behaviors, 17 , 297–300.
doi:10.1016/0306-4603(92)90035-T
Heckman, C. J., Egleston, B. L., & Hofmann, M. T. (2010). Efficacy of motivational inter-
viewing for smoking cessation: A systematic review and meta-analysis. Tobacco Control,
19, 410–416. doi:10.1136/tc.2009.033175
Hendricks, P. S., & Brandon, T. H. (2005). Smoking expectancy associates among college
smokers. Addictive Behaviors, 30, 235–245. doi:10.1016/j.addbeh.2004.05.006
Hendricks, P. S., Delucchi, K. L., & Hall, S. M. (2010). Mechanisms of change in extended
cognitive behavioral treatment for tobacco dependence. Drug and Alcohol Dependence,
109, 114–119. doi:10.1016/j.drugalcdep.2009.12.021
Hendricks, P. S., Wood, S. B., & Hall, S. M. (2009). Smokers’ expectancies for abstinence:
Preliminary results from focus groups. Psychology of Addictive Behaviors, 23, 380–385.
doi:10.1037/a0015697
Hettema, J. E., & Hendricks, P. S. (2010). Motivational interviewing for smoking cessation:
A meta-analytic review. Journal of Consulting and Clinical Psychology, 78, 868–884.
doi:10.1037/a0021498
Hsu, S. H., & Marlatt, A. G. (2012). Addiction syndrome: Relapse and relapse prevention.
In H. J. Shaffer, D. A. LaPlante, & S. E. Nelson (Eds), The APA addiction syndrome
handbook: Vol. 2. Recovery, prevention, and other issues (pp. 105–132), Washington, DC:
Hymowitz, N. (2011). Smoking and cancer: A review of public health and clinical implications.
Journal of the National Medical Association, 103, 695–700.
Jha, P., Chaloupka, F. J., Moore, J., Gajalakshmi, V., Gupta, P. C., Peck, R., … Zatonski, W.
(2006). Tobacco addiction. In D. T. Jamison, J. G. Breman, A. R. Measham, G. Alleyne,
M. Claeson, D. B. Evans, … P. Musgrove (Eds.), Disease control priorities in developing
countries (pp. 869–885). Washington, DC: World Bank.
preliminary results. Revision, 7 , 71–72.
Lancaster, T., & Stead, L. F. (2005). Individual behavioural counselling for smoking cessa-
tion. Cochrane Database of Systematic Reviews, 2, CD001292. doi:10.1002/14651858.
CD001292.pub2
Levine, M. D., Perkins, K. A., Kalarchian, M. A., Cheng, Y., Houck, P. R., Slane, J. D.,
& Marcus, M. D. (2010). Bupropion and cognitive behavioral therapy for weight-
concerned women smokers. Archives of Internal Medicine, 170, 543–550. doi:10.1001/
archinternmed.2010.33
Lightwood, J., Collins, D., Lapsley, H., & Novotny, T. (2000). Estimating the costs of
tobacco use. In P. Jha & E. Chaloupka (Eds.), Tobacco control in developing countries (pp.
63–103). Oxford, England: Oxford University Press.
Marlatt, G. A., & Gordon, J. R. (1985). Relapse prevention: Maintenance strategies in the
McDonald, P., Colwell, B., Backinger, C. L., Husten, C., & Maule, C. O. (2003). Better
practices for youth tobacco cessation: Evidence of review panel. American Journal of
Health Behavior, 27 (Suppl. 2), S144–S158. doi:10.5993/AJHB.27.1.s2.5
Meichenbaum, D. (1977). Cognitive behavioral modification: An integrative approach.
New York, NY: Plenum Press.
Mottillo, S., Filion, K. B., Belisle, P., Joseph, L., Gervais, A., O’Loughlin, J., … Eisenberg, M.
J. (2009). Behavioural interventions for smoking cessation: A meta-analysis of randomized
controlled trials. European Heart Journal, 30, 718–730. doi:10.1093/eurheartj/ehn552
Niaura, R. (2008). Nonpharmacologic therapy for smoking cessation: Characteristics
and efficacy of current approaches. American Journal of Medicine, 121, S11–S19.
doi:10.1016/j.amjmed.2008.01.021
O’Connor, R. M., & Stewart, S. H. (2010). Substance use disorders. In D. McKay, J. S.
Abramowitz, & S. Taylor (Eds.), Cognitive-behavioral therapy for refractory cases: Turning
failure into success (pp. 211–229). Washington, DC: American Psychological Association.
Perkins, K. A., Conklin, C. A., & Levine, M. D. (2007). Cognitive behavioral therapy for
smoking cessation: A practical guidebook to the most effective treatments. New York, NY:
Routledge.
Pipe, A. L., Papadakis, S., & Reid, R. D. (2010). The role of smoking cessation in the
prevention of coronary artery disease. Current Atherosclerosis Reports, 12, 145–150.
doi:10.1007/s11883-010-0105-8
Pollak, K. I., Oncken, C. A., Lipkus, I. M., Lyna, P., Swamy, G. K., Pletsch, P.
K., … Myers, E. R. (2007). Nicotine replacement and behavioral therapy for smok-
ing cessation in pregnancy. American Journal of Preventive Medicine, 33, 297–305.
doi:10.1016/j.amepre.2007.05.006
Rigotti, N. A., Park, E. R., Regan, S., Chang, Y., Perry, K., Loudin, B., & Quinn, V. (2006).
Efficacy of telephone counseling for pregnant smokers: A randomized controlled trial.
Obstetrics and Gynecology, 108, 83–92. doi:10.1097/01.AOG.0000218100.05601.f8
Rovina, N., Nikoloutsou, I., Katsani, G., Dima, F., Fransis, K., Roussos, C., & Gratziou,
C. (2009). Effectiveness of pharmacotherapy and behavioral interventions for smoking
cessation in actual clinical practice. Therapeutic Advances in Respiratory Disease, 3,
279–287. doi:10.1177/1753465809350653
Schmitz, J. M., Stotts, A. L., Mooney, M. E., DeLaune, K. A., & Moeller, F. (2007). Bupropion
and cognitive-behavioral therapy for smoking cessation in women. Nicotine and Tobacco
Research, 9, 699–709. doi:10.1080/14622200701365335
Shah, R. S., & Cole, J. W. (2010). Smoking and stroke: The more you smoke the more you
stroke. Expert Review of Cardiovascular Therapy, 8, 917–932. doi:10.1586/erc.10.56
Song, F., Huttunen-Lenz, M., & Holland, R. (2009). Effectiveness of complex psycho-
educational interventions for smoking relapse prevention: An exploratory meta-analysis.
Journal of Public Health, 32, 350–359. doi:10.1093/pubmed/fdp109
Sussman, S., Sun, P., & Dent, C. W. (2006). A meta-analysis of teen cigarette smoking
cessation. Health Psychology, 25, 549–557. doi:10.1037/0278-6133.25.5.549
Tiffany, S. T. (1990). A cognitive model of drug urges and drug-use behavior: Role of automatic
and nonautomatic processes. Psychological Review, 97 , 147–168. doi:10.1037/0033-
295X.97.2.147
Vidrine, J., Businelle, M. S., Cinciripini, P., Li, Y., Marcus, M. T., Waters, A. J., … Wetter,
D. W. (2009). Associations of mindfulness with nicotine dependence, withdrawal, and
agency. Substance Abuse, 30, 318–327. doi:10.1080/08897070903252973
Vidrine, J., Cofta-Woerpel, L., Daza, P., Wright, K. L., & Wetter, D. W. (2006). Smoking
cessation. 2: Behavioral treatments. Behavioral Medicine, 32, 99–109. doi:10.3200/
BMED.32.3.99-109
Waters, A. J., Shiffman, S., Bradley, B. P., & Mogg, K. (2003). Attentional shifts to smoking
cues in smokers. Addiction, 98, 1409–1417. doi:10.1046/j.1360-0443.2003.00465.x
Webb, M. S., de Ybarra, D., Baker, E. A., Reis, I. M., & Carey, M. P. (2010). Cognitive-
behavioral therapy to promote smoking cessation among African American smokers:
A randomized clinical trial. Journal of Consulting and Clinical Psychology, 78, 24–33.
doi:10.1037/a0017669
Westbrook, C., Creswell, J. D., Tabibnia, G., Julson, E., Kober, H., & Tindle, H. A.
(2011). Mindful attention reduces neural and self-reported cue-induced craving in
smokers. Social Cognitive and Affective Neuroscience Advance, SCAN (2011), 1–12.
doi:10.1093/scan/nsr076
Westra, H. A., & Stewart, S. H. (1998). Cognitive behavioural therapy and pharmacother-
apy: Complementary or contradictory approaches to the treatment of anxiety? Clinical
Psychology Review, 18, 307–340. doi:10.1016/S0272-7358(97)00084-6
Wilson, J. S., Fitzsimons, D., Bradbury, I., & Elborn, J. (2008). Does additional support by
nurses enhance the effect of a brief smoking cessation intervention in people with moderate
to severe chronic obstructive pulmonary disease? A randomised controlled trial. Interna-
tional Journal of Nursing Studies, 45, 508–517. doi:10.1016/j.ijnurstu.2006.10.001
Witkiewitz, K., Steckler, G., Gavrishova, A., Jensen, B., & Wilder, M. (2012). Psychotherapies
for addiction: Empirically supported interventions for the addiction syndrome. In H. J.
Shaffer, D. A. LaPlante, & S. E. Nelson (Eds.), The APA addiction syndrome handbook:
Vol. 2. Recovery, prevention, and other issues (pp. 87–103). Washington, DC: American
World Health Organization. (2011). WHO report on the global tobacco epidemic, 2011: Warning
about the dangers of tobacco. Geneva, Switzerland: Author.
Zgierska, A., Rabago, D., Chawla, N., Kushner, K., Koehler, R., & Marlatt, G. A. (2009).
Mindfulness meditation for substance abuse disorders: A systematic review. Substance
Abuse, 30, 266–294. doi:10.1080/08897070903250019
55
Alcohol Problems
Nailah O. Harrell
Paola Pedrelli
Carl W. Lejuez and Laura MacPherson

Introduction
Alcohol misuse is an international problem, affecting most populations across age,

gender, and cultural bounds. Due to the pervasiveness of alcohol consumption,
alcohol use disorders (AUDs) represent one of the most comprehensively studied psy-
chological phenomena resulting in well-formulated, empirically supported cognitive
behavioral interventions for this constellation of behaviors. In addition, individuals
who seek treatment for other psychological disorders often experience problems with
alcohol use. This chapter aims to provide a basic overview of what constitutes diag-
nostic and problem levels of alcohol use, including common comorbid conditions
associated with AUDs, established cognitive behavioral therapy (CBT) interventions
for AUDs, and integrated treatments for co-occurring psychological conditions, as
well as a review of medications that are supported in their combination with psycho-
social interventions. Finally, we present considerations for ways that CBT interven-
tions for AUDs have increased in their reach to broader populations of individuals
facing problems with alcohol through integration with technological advances such
as Web-based modalities.
Nature of the Problem

Alcohol is the most commonly used addictive substance in the United States (National
Council on Alcoholism and Drug Dependence, 2011). The Centers for Disease Con-
trol outline moderate drinking as no more than one drink per day for women

DOI: 10.1002/9781118528563.wbcbt55
and two drinks per day for men. Alcohol use that exceeds these recommendations
is considered excessive and increases risk for alcohol abuse and dependence, as
well as organ-related pathology, among adults in the United States (Li, Hewitt,
& Grant, 2007). Health consequences resulting from excessive alcohol use include
neuropsychiatric, cardiovascular, cancer, and psychological pathology. Moreover,
alcohol misuse is a causal factor in more than 60 major diseases and injuries result-
ing in approximately 2.5 million deaths each year (World Health Organization,
2011).
Even moderate alcohol use increases risks for negative health consequences
(Bagnardi, Blangiardo, La Vecchia, & Corrao, 2001). Recommended alcohol use
guidelines provide necessary public health information and are essential for aiding
in health professionals’ screenings. As evidenced by the DSM-IV criteria, exceeding
daily or weekly recommendations alone is not indicative of an alcohol problem.
Specifically, a variety of negative social, interpersonal, and legal consequences are
associated with excessive drinking behaviors. A definition of problem drinking covers
a range of drinkers from those who experience a few consequences and drink
beyond recommended levels to those defined as alcohol dependent (Cunning-
ham, Kypri, & McCambridge, 2011). For diagnostic purposes, alcohol problems
are characterized by the psychological, behavioral, and physiological impact and
not solely by the amount of alcohol consumed. As such, these are classified as
AUDs.
Diagnostic Considerations
We approach this discussion of AUDs awaiting revisions to the psychiatric diagnostic
standards. The expected publication date for the fifth revision of the Diagnostic
and Statistical Manual of Mental Disorders (DSM) is May of 2013 and the 11th
revision of the ICD-11 (International Classification of Diseases) is in 2015. Both
are gold standards in the evaluation of AUDs, broadly defined as maladaptive pat-
terns of alcohol use leading to clinically significant impairment or stress. Clinically
significant impairment is evaluated through symptoms endorsed as well as reported
events. AUDs have a heterogeneous presentation; thus, categorization of an alco-
hol problem does not rely solely on an individual’s endorsement of distress or
impairment.
Differences in the ICD and DSM classifications of AUDs have resulted in minor
to significant differences in case identification (First, 2009). The revisions to both
texts represent a collaborative effort by the World Health Organization (WHO) and
the American Psychiatric Association (APA) with the goal of reducing differences
across diagnostic structures. Uniformity in diagnostic criteria supports the reliability
of case identification and the development of internationally utilized evidenced-based
interventions (First, 2009). Although the current diagnostic format will soon be
replaced with the revisions to the DSM and the ICD, review of the current systems
is essential to provide context for the new diagnostic format as well as for the extant
literature surrounding behavioral interventions for AUDs.
Alcohol Problems 1317
Alcohol Use Disorders: Present
The DSM-IV-TR is structured as a bi-axial categorization of AUDs. Alcohol abuse and

alcohol dependence represent hierarchical diagnoses where an alcohol abuse diag-
nosis is considered less severe than that of alcohol dependence. Alcohol abuse
criteria focus on disruptive social behaviors and interpersonal difficulties secondary
to maladaptive alcohol use. The drinking pattern usually compromises attendance to
daily obligations. The diagnostic threshold for alcohol abuse is met when at least
one of four criteria related to interpersonal, legal, work, or continued use despite
problems is present within a 12-month period. While the behavior may not be
recognized as problematic by the drinker, the impact of the individual’s drinking
may strain interpersonal relationships. These drinking patterns may also result in
reckless actions with impact on themselves or on others. The current structure allows
a diagnosis of alcohol abuse after an alcohol-related arrest for crimes such as driving
under the influence (DUI) or domestic abuse. In these situations, the client may not
agree that his or her alcohol use is problematic or has played a role in the arrest;
however, such a diagnosis may be given. The corresponding ICD-10 diagnosis of
harmful use is regarded as a more broad definition than its DSM-IV counterpart (First,
2009). Harmful use refers to alcohol consumption that results in consequences to
physical and mental health requiring a clear relationship between the two. Clinicians
have since argued for the importance of social consequences within this criterion. The
drinking behavior must be present as a pattern persisting for at least one month or
occurring repeatedly over the last 12 months.
Both the ICD-10 and the DSM-IV describe alcohol dependence as the more severe
condition, associated with major physiological consequences and life impairment
(Schuckit, 2009). The criteria for dependence are consistent across both texts
in addressing the negative social and interpersonal outcomes while referencing
psychological and physiological dependence. Similar to alcohol abuse and harmful use
diagnoses, alcohol consumption continues despite negative consequences denoting
diminished control. Tolerance and withdrawal symptoms reflect physiological
dependence. The single deviation is the presence of the craving item in the ICD-10
criteria only. The duration of the symptoms necessary for diagnosis also differs in each
text. Consistent with the harmful use parameters, the ICD-10 requires three or more
criteria to be met for one month or repeated occurrences over a 12-month period.
The DSM-IV requires three or more criteria to be met during a 12-month period.
Analyses of the current ICD and DSM diagnostic standards indicate that depen-
dence criteria are reliable across demographics. The validity for the abuse and harmful
use diagnoses are far less reliable as separate diagnoses and possess low concordance
(Hasin et al., 2003). In addition, the bi-axial system creates the assumption that a
diagnosis of alcohol abuse is a precursor to dependence but considerable empirical
literature indicates this is not the case.
Perhaps the most consequential critique of the current DSM is the void between the
criteria for alcohol abuse and alcohol dependence resulting in “diagnostic orphans,”
referring to individuals who do not meet diagnostic criteria for an AUD but meet
one to two criteria for dependence (McBride, Adamson, Bunting, & McCann, 2009;
Pollock & Martin, 1999). For example, an individual may meet criteria for tolerance
and for the persistent desire or unsuccessful attempts to cut down, which are an
insufficient number of criteria to meet for dependence and meet no criteria for
abuse. In addition, the current diagnostic system lacks a severity qualifier which has
implications in diagnostic nuance and clinical recommendations.
Alcohol Use Disorders: Future
The coordinated revisions to the AUD diagnostic structure in the DSM and ICD shift
from the bi-axial format. One diagnostic code is assigned for AUD with specifiers
for severity and physiological dependence. The change in framework is responsive to
critiques of both texts and provides a consistent international standard. The revised
diagnosis necessitates at least two of the 10 criteria in a 12-month period. The criteria
are comprised of all prior DSM abuse and dependence criteria, with the exception of
the alcohol abuse item pertaining to recurrent substance-related legal problems (e.g.,
arrests for DUI). The craving item formerly found only in the ICD-10 dependence
criteria is also included. A severity index categorizes two to three criteria to a
“moderate” AUD and four or more to a “severe” AUD. Physiological dependence is
evaluated as either present or absent, but is not required for diagnostic confirmation.
Other Problem Drinking Behaviors
Our discussion of alcohol problems would be incomplete without addressing

problematic alcohol use behaviors outside the diagnostic spectrum. These patterns of
alcohol use may be precursors to AUDs and present a pivotal opportunity for inter-
vention. However, problematic patterns of use may also be associated with immediate
consequences warranting intervention in their own right. The National Institute of
Table 55.1 Categories of Problematic Alcohol Use
Drinking category Blood alcohol level Time period Quantity (no. of standard
(BAC) (frequency) drinks*)
Risky 0.05 — —
Binge (male) 0.08 2 hours >5
Binge (female) — 2 hours >4
Heavy (male) — 1 week >14
Heavy (female) — 1 week >7
Hazardous (male) — 1 week >21 (or 7 drinks, 3 times per week)
Hazardous (female) — 1 week >14 (or 5 drinks, 3 times per week)
Note. *Standard drink = 12 oz. beer, 5 oz. table wine, 1.5 oz. (80 proof) spirits, 8–9 oz. malt liquor.
Adapted from National Institutes of Alcohol Abuse and Alcoholism (2004).
Alcohol Abuse and Alcoholism recognizes several excessive drinking behaviors. Classi-
fications are made by the quantity and frequency of consumption or the blood/alcohol
level reached in a drinking episode. We outline these categories in Table 55.1.
Much of the current research on problem alcohol use has focused on binge
drinking particularly in underaged and college-aged populations. Binge drinking has
been identified as a typical pattern at these developmental periods due, in part, to
the emphasis on social settings which often contextualize normal youth drinking. A
survey of college-aged drinkers found a drinking event with many people intoxicated
and having school friends present predicted binge drinking five or more drinks on
that occasion (Clapp & Shillington, 2001; Courtney & Polich, 2009). Binge drinking
as a pattern of alcohol consumption is associated with alcohol poisoning, uninten-
tional injuries, suicide, hypertension, pancreatitis, sexually transmitted diseases, and
meningitis (Courtney & Polich, 2009). While binge drinking is identified as a sepa-
rate category of drinking behavior, individuals with AUDs can also engage in binge
patterns of use.
While a clear link between binge drinking and diagnostic-level AUDs has yet to be
elucidated, there is evidence that binge drinking increases the risk for alcohol abuse
and alcohol dependence. One study of college students who were frequent heavy
episodic drinkers (defined as five or four drinks respectively for men and women on
three or more occasions in the past 2 weeks) had 19 times greater odds of meeting
criteria for alcohol dependence and 13 times greater odds of being classified with
alcohol abuse compared with non-heavy episodic drinkers (Courtney & Polich, 2009;
Knight et al., 2002).
Comorbidity of Mood and Anxiety Disorders
AUDs frequently co-occur with a number of Axis I disorders. For brevity and because
of the frequency with which these concurrent disorders are presented, we will focus
here on mood and anxiety disorders. The relationships between anxiety, mood, and
AUDs are complex, especially as they pertain to causality. Comorbidity frequently
exacerbates symptoms of both disorders. Data from the National Epidemiologic
Survey on Alcohol and Related Conditions (NESARC), a population-representative
sample assessed for psychiatric disorders, indicated that the prevalence of independent
mood and anxiety disorders within 12 months for any AUD was 18.85% and 17.05%
respectively (Grant et al., 2004). It is noted that mood disorders were composed of
major depression, dysthymia, mania, and hypomania, and anxiety disorders included
panic disorder, social phobia, specific phobia, and generalized anxiety disorder. The
survey also found that 17.3% of respondents with an independent mood or anxiety
disorder also had an AUD. Taken together, the comorbidity of AUDs with anxiety
and mood disorders is significant, with clear implications for treatments targeted
toward intervening on both sets of symptomatology.
Despite the established literature on the comorbidity of AUDs with anxiety and
depressive disorders, commonly held logic has recommended the treatment of these
disorders in isolation, with the AUD given priority. However, long-held views that
patients with co-occurring depression and alcohol dependence must achieve absti-
nence from alcohol before treatment of depression can begin (Pettinati & Dundon,
2011) are being challenged. This is aided by a shift in treatment delivery from
primarily inpatient to outpatient, and a growing recognition that interrelationships
between symptoms of both disorders are appropriate for simultaneous targeting
with integrated interventions. Later in this chapter we highlight some examples of
integrated CBT-based interventions for comorbid AUDs with other Axis I conditions.
Comorbidity within Substance Use Disorders
Alcohol dependence is frequently part of a larger cluster of poly-drug use behaviors

and dependence. National epidemiological studies indicate alcohol dependence is
associated with increased drug use disorders and drug dependence based on DSM-IV
diagnostic criteria (odds ratios 9.0 and 18.7, respectively; Compton, Thomas, Stinson,
& Grant, 2007). An integrated treatment for alcohol and substance use disorders can
require a collaborative pharmacologic and behavioral treatment in order to adequately
address the complexities of physiological and psychological addiction. A number of
cognitive behavioral interventions that we review in this chapter (including relapse
prevention, coping skills training, and cue exposure) have overlapping applicability
in the treatment of alcohol and other substance dependence. In both inpatient
and outpatient settings the dual treatment of these disorders can support positive
treatment outcomes.
Overview of Cognitive Behavioral Therapy

for Alcohol Use Disorders
Cognitive behavioral therapy (CBT) for AUDs refers to several approaches developed
in the context of frameworks provided primarily by two models: the social learning
theory (SLT) model (Bandura, 1969, 1997) and the relapse prevention (RP) model
(Marlatt & Gordon, 1985). We will first illustrate the theoretical bases of these
two models, and then we will describe several treatment approaches for AUDs that
fall in the CBT interventions framework, and finally illustrate findings from relevant
meta-analyses summarizing evidence for these approaches.
Social Learning Theory

The SLT model (Bandura, 1969, 1997) has exerted a major influence on the
development of CBT-based approaches for AUDs. The SLT model postulates that
alcohol use is often initiated at a young age via socialization and continues in the
context of the processes of operant conditioning, being maintained by environmental
contingencies, as well as cognitive factors. SLT illustrates that both positive and
negative reinforcement play an important role in the initiation and maintenance of
alcohol use behavior. Behavior maintained by seeking of feelings of euphoria often
associated with alcohol consumption are well characterized by positive reinforcement,

and engagement in alcohol use to reduce aversive stimuli such as negative mood
states is consistent with negative reinforcement. As the consumption of alcohol is
repeatedly reinforced through these processes, individuals increasingly engage in this
behavior as a primary coping strategy to manage aversive experiences, which may
lead to the development of an AUD. Thus, individuals may be motivated to drink
in the context of experiencing positive feelings as well as a focus on the short-term
reduction of stress or negative affect associated with alcohol consumption. The SLT
model also emphasizes the importance of cognitive factors in alcohol consumption
influenced by the individual outcome expectations of its effects and by an individual’s
own self-efficacy expectations. Outcome expectancies associated with alcohol use are
simply the expected consequences that a person holds for engaging in alcohol use.
Additionally, Bandura (1997) posited that an individual’s self-efficacy to abstain will
affect whether this person will drink or not in a specific context.
Finally, alcohol-related cues that can be internal, such as emotional states, as well
as environmental, such as any myriad of places, people, and objects that have been
associated with alcohol consumption, may influence drinking behavior via classical
conditioning. Alcohol-related cues may also make the effects of alcohol more salient,
increasing cravings and the desire to drink in individuals with AUDs. Furthermore,
the presence of environmental cues related to alcohol may engender reactions such
as arousal and increased attention to alcohol that may impair the individual’s ability
to use coping skills and avoid drinking. Individuals may also have the expectation
of low self-efficacy around alcohol-related cues that will influence drinking outcome.
As such, CBT interventions for AUDs that are based on SLT focus on improving
coping skills, addressing self-efficacy, targeting expectancies for the effects of alcohol
use, and managing cravings and triggers associated with alcohol-related cues.
Relapse Prevention Model

Marlatt and Gordon’s (1985) RP model posits that maintenance of addiction is
due to both the presence of a physiological vulnerability and the existence of several
maladaptive behavioral patterns. The RP model in particular focuses on how alcohol
use patterns unfold subsequent to efforts to initiate abstinence after protracted periods
of use. The major contribution of the RP model to the addictions field consists in the
novel conceptualization of lapses and relapses not as treatment failures but as a part of
the process of recovery from an AUD and as an opportunity to learn skills to deal with
high-risk situations (Hendershot, Witkiewitz, George, & Marlatt, 2011). In the RP
model, lapses and relapses are characterized by a return to various levels of previous
alcohol use behaviors consistent with patterns of use exhibited prior to abstinence.
Similar to the SLT model, the RP model postulates an association between lack of
skills and maintenance of AUDs. While traditional models conceptualized lapses as
resulting from endogenous factors such as cravings and withdrawal symptoms, the
RP model introduces the importance of considering external factors and high-risk
contexts that increase the vulnerability to engage in alcohol use. High-risk situations
have been described as including internal emotional states, as well as environmental
cues and physiological states. Moreover, the RP model illustrates the significance of
cognitive factors derived from SLT, such as self-efficacy and outcome expectancies,
on relapse. Thus, RP treatment programs combine behavioral skills training with
cognitive interventions, with the goal of preventing and limiting relapse episodes.
RP was developed to provide individuals with coping strategies to prevent a
“slip” or a “lapse” from becoming a full-blown relapse. As such, RP includes an
assessment of risk factors for relapse including triggers or situations followed by
the application of cognitive and behavioral techniques to address them. Moreover,
RP programs determine overt and covert antecedents of relapse and strategies to
address them. Strategies included in RP are skills training, cognitive restructuring,
and lifestyle balance. For example, RP focuses on increasing coping skills and self-
efficacy, and on challenging individuals’ expectation of positive outcome associated
with alcohol use. These techniques address immediate precursors of relapse as well
as positive outcome expectancies associated with alcohol use. Given that RP provides
a set of skills for maintaining sobriety, it is best administered after the individuals
have stopped alcohol use and thus have some period of abstinence. Although the
term relapse prevention initially indicated a specific treatment program (Marlatt &
Gordon, 1985), RP strategies have been progressively incorporated into a variety of
approaches for AUDs and this term has evolved to describe any psychosocial treatment
including the teaching of coping skills and cognitive behavioral strategies to prevent
relapse. Recently, a reformulated cognitive behavioral model of relapse was introduced
from Marlatt’s group to clarify and extend the original model (Hendershot et al.,
2011). The revised model places more emphasis on describing relapse as a dynamic
process where distal and stable factors interact with transient factors to determine the
likelihood of relapse (Hendershot et al., 2011).
Cognitive Behavioral Therapy-Based Treatment Approaches
Numerous CBT-based approaches to treating AUDs have been developed on the

basis of principles outlined by the SLT and RP models. Approaches included in
the CBT family are implemented both alone and in combination with one another.
Descriptions of the most prominent approaches are outlined in the rest of this section.
Functional Analysis
Although not specific to any one CBT intervention described below, functional
analysis (FA) is a basic assessment and monitoring approach, grounded in basic
reinforcement theory, of a specific behavior that frequently is integrated with CBT-
based treatments for AUDs. FA provides ideographic information regarding the
environmental contexts maintaining a behavior that allow for the identification of
situations and applications of skills that may be most relevant to a specific individual. At
its most fundamental level, FA involves a focus on the antecedents of a behavior (A),
the behavior itself (B), such as alcohol use, and the resultant positive and negative
consequences of that behavior (C). A clinician reviews the function of a specific
behavior with the client, identifying the associated antecedents and consequences that
were relevant for that behavior when it occurred in a given situation. In line with
the SLT and RP models described earlier, more comprehensive FA models suggest
that antecedents may include environmental factors as well as thoughts and feelings,
and consequences can include both positive and negative outcomes of engagement
in a specific behavior. Integrating FA into the following CBT approaches allows for
tailoring the appropriate skills and strategies to the factors that are maintaining an
AUD for a client. A brief example of FA is discussed in the section “Example of a
Cognitive Behavioral Therapy-Based Intervention.”
Coping and Social Skills Training

The coping and social skills training (CSST) approach is based on the SLT prin-
ciple that alcohol use may occur in the absence of skills to cope with distressing,
uncomfortable, or unknown situations, and hence individuals may consume alcohol
as a coping strategy. Monti et al. (1982) extended this model and described as key
components of CSST the provision of interpersonal skills to enhance relationships,
of cognitive-emotional coping skills to regulate affect, and of skills to cope with
daily stressors, high-risk situations, and substance use cues. Thus, CSST focuses on
providing skills alternative to consuming alcohol.
Cue Exposure
The cue exposure model is based on the associative principle that people, places,
and events consistently preceding alcohol use become associated with the positive
outcomes of consumption and thus alcohol use becomes a conditioned response to
the presence of these cues (Drummond and Glautier, 1994a, 1994b; Gossop et al.,
2002). The association between alcohol cues and cravings can be explained by both
classical conditioning and SLT. Thus, the cue exposure model posits that repeated
exposure to the cues (e.g., sight of alcohol) in association with resisting the craving
for alcohol eventually leads to extinction of conditioned responses. Moreover, cue
exposure approaches may also include coping skills training. Given the variety of
situations where one may have consumed alcohol, cue exposure may include the use
of imagery in which the patient imagines the situations where he or she has previously
consumed alcohol (Havermans, Mulkens, Nederkoorn, & Jansen, 2007; Rohsenow
et al., 2001) and, more recently, computer-simulated environments, through virtual
reality, intended to allow for exposure to a vast array of cues simultaneously (Lee,
Kwon, Choi, & Yang, 2007). Cue exposure therapy may last from six to 12 sessions,
is often conducted in a laboratory setting, and is frequently carried out in conjunction
with other skills training.
Behavioral Couples Therapy

Behavioral couples therapy (BCT) includes both the problem drinker and his or her
partner or spouse. BCT postulates that substance abuse and relationship functioning
are related in that they both have a deteriorating effect on each other (Epstein &
McGrady, 1998; O’Farrell, 1989). Thus, BCT encompasses two main components:
alcohol-focused interventions, including strategies to establish and maintain
abstinence, and relationship-focused interventions including strategies to improve the

nature of the relationship. BCT teaches spouses techniques to reinforce abstinence,
and to reduce behaviors that may trigger alcohol use as well as behaviors that protect
partners from consequences associated with their drinking. For example, the couple is
helped to identify activities that are rewarding and that do not involve alcohol. BCT
may also include a “recovery contract” consisting of the couple engaging in daily
rituals that reward abstinence. BCT is similar to other couple therapy models in that it
includes techniques to improve the relationship. Several studies have been conducted
to evaluate BCT. Powers, Vedel, and Emmelkamp (2008) evaluated 12 randomized
controlled trial studies examining the effect of BCT in which they observed at
posttreatment a medium effect size (Cohen’s d = 0.54) in favor of BCT relative to
individual-based treatment with regard to relationship satisfaction. At follow-up, BCT
was better than individual-based treatment on relationship satisfaction (d = 0.57),
as well as reducing frequency of use (d = 0.36) and consequences of use (d = 0.52).
Behavioral Self-Control Training

Behavioral self-control training (BSCT) was developed in the context of the harm
reduction model as it teaches strategies to reduce alcohol consumption to a low-
risk level rather than complete abstinence. This approach is widespread in Australia,
Norway, the United Kingdom, and Switzerland, but it is less common in some
countries such as the United States and Canada where the abstinence model has
more support (Ambrogne, 2002; Gastfriend, Garbutt, Pettinati, & Forman, 2007).
BSCT involves several strategies including self-monitoring, setting drinking limits,
controlling rates of drinking, identifying problem drinking situations, and self-reward
for limited drinking. Walters (2000) illustrated in a meta-analysis of 17 randomized
controlled trials that BSCT was better than no treatment in reducing alcohol use and
problematic drinking (Cohen’s d = 0.94).
Example of a Cognitive Behavioral

Therapy-Based Intervention
CBT-based treatment programs are typically delivered with a similar format and
include components deriving from the models briefly described above. Herein we
illustrate the protocol used in the MATCH (Matching Alcoholism Treatments to
Clients Heterogeneity; Project MATCH Research Group, 1993) study that integrates
CSST and RP techniques as an example of a CBT-based intervention for AUDs
(Kadden et al., 1992). The MATCH study was a large multisite study comparing the
effectiveness of different psychosocial treatments including CBT for AUD.
The CBT-based protocol used in the MATCH study initially provides an illustration
of the CBT model of how alcohol dependence develops, that is followed by an
examination of high-risk situations in which a patient is more likely to drink. To this
end patients are asked to complete a self-monitoring form, guided by the principles of
FA described above, on which they record triggers, thoughts, feelings, behaviors, and
positive and negative consequences they experience associated with these behaviors.
As noted, this FA of alcohol use behaviors is instrumental to targeting CBT-based

interventions to the needs of a particular patient. Cravings or relapses are often
associated with environmental cues such as being exposed to alcohol, to people with
whom patients used to consume alcohol, or to other people consuming alcohol.
Situations patients associate with alcohol consumption such as bars, parties, family
events, concerts, and sports events may also be triggering. Finally, internal triggers
may consist of aversive emotions such as anger, sadness, or anxiety experienced by
patients. Upon identifying high-risk situations, sessions focus on reviewing strategies
and skills to cope with triggers and the functional role of alcohol use in their
lives.
One important strategy related to exposure therapy is for patients to avoid or mini-
mize exposure to cues that may increase relapse, in particular during the early recovery
stage, by developing a new social network, and by identifying alternative activities
to alcohol behaviors. Thus, the completion of an FA that is a behavioral assessment
of antecedents of alcohol consumption, the pattern of the alcohol consumption, the
consequences of alcohol consumption, and reinforcement of drinking is performed
and informs treatment.
In addition to an illustration of triggers, CBT-based treatment programs include
a description of what constitute cravings, how to recognize them, and how to cope
with them. Some examples of strategies to cope with cravings include increasing
involvement in distracting activities, discussing cravings and urges with supportive
friends, or engaging in “urge surfing,” which involves recognizing that one is having
a craving but allowing oneself to sit with the experience while it dissipates, rather than
to act on it. Challenging and changing specific thoughts that may increase the risk
for relapse is also critical. Individuals with AUDs may engage in maladaptive thinking
that alcohol consumption would improve their mood, even though in reality it will
not, with a focus on positive memories associated with consuming alcohol. In line
with the concept of alcohol expectancies derived from SLT, individuals may have
existing cognitions of alcohol use as an aid to relax, escape, socialize, and engage in
romantic relationships which may undermine motivation for sobriety. Patients may
have distortions in their thinking which contribute to overestimating the positive effect
of alcohol and underestimating the negative consequences associated with alcohol use.
CBT-based programs include an examination of patients’ thoughts about alcohol use
that may trigger relapse and a review of negative consequences of drinking and positive
consequences of sobriety. In this context, patients’ expectations of positive outcomes
associated with alcohol may be reviewed and challenged. During this exercise patients’
motivation to stay sober may become more salient and thus it is critical to monitor
this in relation to the implementation of new skills for managing sobriety.
CBT-based treatment programs for AUDs also include teaching interpersonal and
communication skills with the use of role plays and behavioral rehearsal. Specific skills
may include listening and conversation skills, nonverbal communication, and conflict
resolution skills. Interpersonal conflicts often trigger relapse; hence, learning effective
communication strategies may reduce the risk for situations associated with negative
emotions with which patients may cope by consuming alcohol. In the context of
teaching communication skills, drinking refusal skills are also reviewed. Often patients
with AUDs do not have effective coping strategies to manage the offer of alcohol due
to barriers in explaining their refusal (Epstein, Zhou, Bang, & Botvin, 2007; Scheier,
Botvin, Diaz, & Griffin, 1999). Reviewing scenarios where patients may be offered
alcohol and strategies to refuse it may reduce the likelihood of a relapse. Additional
skills also reviewed include problem solving and anticipating emergency situations
associated with relapse.
The outpatient treatment format provides an ideal opportunity to examine problems
encountered by patients in the real world and to practice the generalizability of skills
reviewed in session to the patients’ reality. During sessions instances of difficulties
from the patients’ lives can be used to illustrate and practice new skills. Situations and
triggers that may have caused cravings or relapses can be examined and strategies to
cope with them can be discussed.
Review of the Empirical Literature on Cognitive Behavioral

Therapy for Alcohol Use Disorders
Although a number of reviews and meta-analyses have been conducted on CBT for
AUDs, several challenges present when comparing them. First, given that CBT for
AUDs includes a family of approaches, some reviews have focused only on some
CBT approaches and not on others. Moreover, some meta-analyses examined CBT
treatment for AUDs together with CBT for other substance use disorders, making it
difficult to discern the specific effect of alcohol-focused CBT. Here we present the
most relevant systematic reviews.
Irvin et al. (1996) conducted a meta-analysis of RP treatment for AUDs as well as
for smoking and for other substances. They evaluated 26 published and unpublished
studies on RP and observed a medium effect size for treatment using RP for alcohol
use (r = .27). The effect of CBT treatment for AUDs was also examined, together
with other interventions for AUDs, by the Mesa Grande project, a widely referenced
meta-analysis of treatment for AUDs (Miller & Wilbourne, 2002). The Mesa Grande
meta-analysis reviewed a total of 361 studies, and 46 different treatment modalities
were ranked on the basis of the amount of support from clinical trials weighted
on the basis of their methodological quality. Results indicated that several CBT
approaches such as social skills training, behavioral contracting, and behavioral marital
therapy had the strongest evidence. In particular, social skills training was second
in the amount of evidence supporting its effectiveness for treatment-seeking clinical
populations.
More recently, Magill and Ray (2009) conducted a meta-analytic review of ran-
domized controlled trials of CBT treatments for alcohol problems as well as for
illicit drug use. This meta-analysis did not differentiate among CBT approaches and
collapsed in this category general cognitive behavioral, relapse prevention, and coping
skills training approaches. The authors examined 53 studies, of which 23 had alcohol
use behaviors as the treatment focus. Magill and Ray (2009) observed that CBT
approaches for substance use had a small but significant treatment effect (Hedge’s
g = 0.15; Hedges, 1994) and that the effect of CBT approaches was greater in
studies with a no-treatment comparison condition (g = 0.79). The meta-analysis
also indicated small pooled effect sizes (g = 0.07) for CBT approaches for AUDs
specifically. The difference in effect sizes between Irvin et al.’s (1996) and Magill and
Ray’s (2009) meta-analyses may be due to the fact that in the latter, a number of
different CBT approaches for AUDs were included, whereas the former focused only
on RP approaches for AUDs. To our knowledge, a systematic review of the benefit of
RP versus other CBT approaches for AUDs has not been conducted.
In sum, making a clear determination of the relative effectiveness of various forms of
CBT for AUDs is difficult. However, despite these challenges, there is strong evidence
suggesting that CBT approaches including social skills training and RP components
are effective for AUDs, although the overall clinical magnitude of the effect of CBT
for AUDs remains unclear.
Treatment with Comorbid Disorders
As noted earlier, while historically it has been standard practice to treat co-occurring
disorders sequentially, it has become more common to use combined approaches
for patients with dual diagnoses. However, findings on the superiority of combined
treatment are still mixed and vary across disorders co-occurring with AUDs. The
numerous combined treatment formats available in the community for individuals
with dual diagnoses often correspond to different permutations of CBT, empirically
supported treatment for a specific Axis-I disorder, and standard alcohol treatment and
pharmacotherapy. Some examples of combined psychosocial interventions follow as
an illustration.
Some treatment protocols for patient with co-occurring disorders focus on adding
an empirically supported CBT treatment for a specific disorder to a standard treatment.
A protocol adding an empirically supported CBT treatment for panic disorders to
standard treatment was examined relative to standard alcohol treatment by Bowen,
D’Arcy, Keegan, and Senthilselvan (2000). They observed no additional effect of
adding CBT at 3 months posttreatment on abstinence rates (52% of patients in alcohol
treatment vs. 56.5% of patients who also received CBT for panic). The treatment
protocol consisted of six sessions (12 hours) of group-based panic management
protocol that had been found effective for patients with panic disorders (Craske,
Brown, & Barlow, 1991).
There is also support for an integrated treatment in individuals with dual PTSD
and AUDs. Back, Brady, Sonne, and Verduin (2006) conducted an assessment of
symptom improvement in participants of a randomized, placebo-controlled trial on
the use of sertraline in the treatment of comorbid PTSD and alcohol dependence. The
initial study (Brady et al., 2000) utilized a combined behavioral and pharmacologic
12-week intervention of a weekly manualized CBT for alcohol dependence and a
simultaneous course of either sertraline or placebo. Results were classified as alcohol
treatment responder, PTSD responder only, global responder, or nonresponder.
At the conclusion of 12 weeks of outpatient treatment nearly 50% of participants
evidenced substantial improvement in both PTSD and alcohol-related outcomes
(Back et al., 2006). The results provide support for the simultaneous treatment of
anxiety and AUDs.
However, some have also advocated for using an empirically supported treatment
for only one of the co-occurring disorders. In the area of PTSD, Hein, Cohen, Litt,
Miele, and Capstick (2004) compared the effectiveness of “seeking safety,” a CBT-
based treatment looking at PTSD in the context of alcohol use, with relapse prevention
and with community care for women with PTSD and substance use disorders. Results
showed that patients in the seeking safety group and relapse prevention group did
better than the women in the third group at the first follow-up. However, patients in
the relapse prevention group sustained improved substance use outcome at 9-month
follow-up, whereas seeking safety patients did not differ from the community care
group.
With regard to treatment for patients with AUDs and depressive symptoms, the
examination of the effectiveness of CBT as an adjunct to standard treatments for
AUDs has yielded mixed results. R. A. Brown, Evans, Miller, Burgess, and Mueller
(1997) observed that 47% of patients receiving an eight-session CBT for Depression
(CBT-D) protocol were abstinent from alcohol compared to 13% of patients in a
relaxation training control (RTC) condition. However, the same group conducted
a similar randomized controlled study with the aim to replicate earlier findings but
did not observe the same results (R. A. Brown et al., 2011). Specifically, at the
6-month follow-up patients in both groups reported consuming approximately four
drinks per drinking day while at baseline they reported consuming approximately 12
in the RTC condition and 14 in the CBT condition. Thus, patients in the CBT-D
condition and patients in the RTC condition did not differ with regard to their
alcohol use after treatment. In this protocol standard CBT-D corresponded to the
Coping with Depression Course (R. A. Brown & Lewinsohn, 1984) and included
standard CBT for depression strategies such as training in daily mood monitoring,
where patients are asked to track their mood daily, increasing the number of pleasant
activities patients engaged in to improve their mood, and cognitive restructuring,
where cognitive distortions are identified and disputed to lead to healthier and more
helpful thoughts.
S. A. Brown et al. (2006) also developed an integrated protocol for MDD and
substance use disorders that combined two empirically validated interventions: a CBT
manual for depression developed by Muñoz and Ying (2002) and the CBT-based
program from Project MATCH. The Internet cognitive behavioral therapy (ICBT)
protocol included a cognitive restructuring module that aimed to identify and change
distorted thoughts associated with depressive symptoms as well as with high-risk
situations. ICBT also focused on identifying and scheduling pleasant activities that
would improve negative mood and preclude substance use. A final module focused
on people learning communication and assertiveness skills to improve mood as well
as increase self-efficacy in refusing substances. They examined the effectiveness of
ICBT relative to a Twelve-Step Facilitation program and observed that while both
approaches were associated with improvement in depressive symptoms as well as in
substance use outcomes at the end of treatment, patients in ICBT appeared to have a
better and more stable long-term outcome (S. A. Brown et al., 2006).
With regard to protocols combining different empirically supported treatments
for AUDs for patients with other co-occurring disorders, Baker et al. (2010) have
developed a manual that integrates CBT with motivational interviewing (MI), an
intervention that has also been found effective for AUDs (Lundahl & Burke, 2009).
The protocol consists of a 10-week intervention that includes one session of MI and
nine weekly CBT sessions focused on treating both depression and AUDs. In the MI
session, patients receive feedback about their alcohol use and, in collaboration with
the patient, the counselor develops a plan for behavior change with regard to both
depression and alcohol use. Starting from session 2, patients begin monitoring mood
as well as cravings, start scheduling activities, and learn mindful walking. The following
session focuses on cognitive restructuring, coping with impulses, and problem-solving
strategies. The latter sessions review refusal skills, and skills from Marlatt’s RP program
(Marlatt & Gordon, 1985). The program includes also a review of how alcohol and
depression affect each other. Baker et al. (2010) examined the effectiveness of this
integrated program relative to treatments focusing only on alcohol or on depression
and observed that the integrated treatment was associated with better mood and
alcohol use outcome.
In summary, it appears that for some comorbid diagnoses associated with AUDs,
adding CBT may have some immediate benefits over standard care, but it is unclear
whether patients may sustain improvement over time.
Medications Approved for the Treatment of

Alcohol Use Disorders
In consideration of CBT-based interventions for AUDs, it is also crucial to review

approved medications for AUDs given that combined therapies (i.e., behavioral
therapies with medications) have been found to be most effective.
To date, the Food and Drug Administration (FDA) has approved three medica-
tions for the specific treatment of alcohol dependence: disulfiram, naltrexone, and
acamprosate. Behavioral interventions are a standard recommendation with both
naltrexone and acamprosate (Williams, 2005). AUD symptoms have also been found
responsive to other medications used as “off label” treatment depending on clinical
presentation.
Disulfiram, an aversive agent, is the oldest and best-researched of the three
medications. The medication responds only after alcohol has been consumed by
blocking the metabolism of alcohol, and thus is used as a deterrent to alcohol
consumption. The result is an accumulation of acetaldehyde which incites a cluster of
unpleasant symptoms including shortness of breath, nausea, vomiting, palpitations,
and headache. Disulfiram is administered in oral form, making compliance a significant
challenge. An unmotivated patient is unlikely to adhere to a continuous regimen. This
compromises the utility of this medication, particularly in outpatient treatment. More
severe reactions to alcohol–disulfiram interactions can be potentially life-threatening.
As such, the American Academy of Family Physicians does not recommend the use
of disulfiram in the primary care setting (Williams, 2005). In more than 40 years,
efficacy for disulfiram in the treatment of AUDs has been weak. Several reviews of the
efficacy of disulfiram indicate a lack of evidence overall but show that the medication
had greater efficacy when given under supervision (Berglund, Thelander, & Jonsson,
2004; De Sousa, De Sousa, & Kapoor, 2007). In an outpatient capacity, it is advised
for those who have demonstrated periods of abstinence. The overall clinical utility of
this drug has been outlined for limited time periods, such as when trying to assess for
the existence of comorbid psychiatric disorders independent of alcohol dependence
(Heilig & Egli, 2006).
Another medication approved for the treatment of AUDs is naltrexone, a selective
opioid antagonist which reduces the reinforcing effects of alcohol. Naltrexone blocks
opioid receptors leading to less alcohol-induced pleasure, high, and intoxication and,
ultimately, less craving and relapse (Anton et al., 2008). Naltrexone is available in
both oral and injectable form. While it has been shown to decrease the frequency
of drinking and quantity of alcohol consumed during short-term treatment, there
is far less support for its long-term benefit in continued abstinence. For example, a
12-month double-blind, placebo-controlled study compared 627 primarily alcohol
dependent men randomized to one of three treatment conditions: 12 months of
naltrexone, 3 months of naltrexone plus 9 months of placebo, and 12 months of
placebo only. At week 52 there was no significant difference among the three groups
on percentage of drinking days and on the number of drinks on a drinking day
(Krystal, Cramer, Krol, Kirk, & Rosenheck, 2001). A number of research studies
have evaluated the combination of naltrexone with medications that increase these
benefits. We will discuss this further in the last paragraph of this section.
Acamprosate is the most recently approved medication for the treatment of AUDs.
The exact mechanism of action for acamprosate remains unknown although it is
believed to work as a γ -Aminobutyric acid (GABA) and functional glutamate agonist.
Reviews indicate that it reduces short- and long-term (more than 6 months) relapse
rates when combined with psychosocial treatment (Mohan, Shankar, Raut, & Gyawali,
2010). In a recent review of 24 randomized controlled trials, acamprosate reduced
the risk of any drinking after detoxification to 86% of the risk a patient would have
under placebo and increased the number of abstinent days by about three additional
days a month (Rosner et al., 2010).
Some encouraging results have been found in the combination of naltrexone and
acamprosate. Naltrexone reduces the quantity of ingested alcohol by decreasing the
reward effect, while acamprosate increases the likelihood that current abstainers will
remain abstinent (Mohan et al., 2010). Thus there is some evidence suggesting that
a combined use of the two medications encourages short- and long-term abstinence
outcomes.
Non-FDA Approved Medications
A variety of other medications have shown promise in decreasing drinking behaviors in

alcohol dependent patients. Preliminary research has focused on anticonvulsants and
serotonergic agents prescribed independently or as additive pharmacologic treatments
(Mohan et al., 2010).
Previously anticonvulsant drugs were limited to use during detoxification to treat
alcohol withdrawal seizures. However, extending regimens of anticonvulsant drugs,
such as topiramate, gabapentin, and zonisamide, into the postdetoxification phase
has shown promise (Anton et al., 2011). The most widely researched of these,
topiramate, is believed to inhibit the mesocorticolimbic dopamine release and thus

reduce alcohol craving. In a recent randomized controlled trial, a 14-week trial of
topiramate combined with a brief behavioral compliance enhancement treatment
was significantly more efficacious than placebo in reducing the percentage of heavy
drinking days (a mean of 81.91%–43.81% for topiramate vs. 81.97%–51.76% for
placebo) in an outpatient alcohol dependent sample (Johnson et al., 2007). In
addition, topiramate is safe for use with individuals who are actively drinking.
Recent research has also investigated the efficacy of gabapentin for prolonged
alcohol withdrawal. The cluster of alcohol withdrawal symptoms includes sleep
disturbances, irritability, inattentiveness, anxiety, as well as mood dysregulation which
persists for some individuals. These symptoms may be associated with increased alcohol
craving and contribute an additional risk factor for relapse. In a randomized controlled
clinical trial comparing three groups of naltrexone alone, naltrexone–gabapentin, and
placebo, the naltrexone–gabapentin combination was found effective on a number of
drinking and craving outcomes for 6 weeks. Specifically, the naltrexone–gabapentin
group exhibited a longer time to relapse than the naltrexone-only group (p = .04).
However, after 10 weeks, effects were no longer significant (Anton et al., 2011). This
supports at least the short-term effect of gabapentin on aiding abstinence.
Serotonergic agents are medications acting on serotonin receptors in the brain.
Although usually associated with the treatment of depression, these medications
have also been used in the treatment of co-occurring alcohol and mood disor-
ders. Serotonergic agents include SSRIs and serotonin antagonists. Fluoxetine has
been shown to decrease the number of drinks, drinking days, and heavy drinking days
overall in a psychiatric population with major depression (Williams, 2005). However,
alcohol-using patients without comorbid depression have shown no clear response.
There is also some support for citalopram as helpful in reducing the number of drinks
and increasing the number of days abstinent in nondepressed, early stage drinkers
(Mohan et al., 2010). Ondansetron, a 5-HT3 receptor antagonist, has been used as
an additive medication for naltrexone. The combination is effective on reward-type
craving and self-reported drinking behaviors in early-onset alcohol dependent individ-
uals (Heilig & Egli, 2006). Ondansetron has also been shown to reduce self-reported
drinking when combined with weekly cognitive behavioral therapy.
New Directions: Integrating Technology
As an increasing segment of the population has access to the Internet not only
through computers but also through mobile and tablet devices, a burgeoning focus
of alcohol research has been on the role these technologies may have in prevention,
screening, and treatment for AUDs. In a review of technology-assisted therapies for
drug and alcohol abuse and smoking, Newman, Szkodny, Llera, and Przeworski
(2011) categorized computer-assisted screening and therapeutic interventions, rang-
ing from self-administered to therapist-administered, and classified them by differing
amounts of online versus face-to-face therapist contact. Screening tools were gener-
ally self-administered and focused on alcohol abuse and prevention. These screening
tools often utilized a Web-based format to provide personalized feedback about
drinking behavior. In contrast, computerized treatments were facilitated by clinical

professionals. Thus, computerized treatment content can be utilized to reinforce
concepts introduced by a clinical professional.
Promising research has emerged on computerized CBT as an adjunctive treat-
ment for substance dependent populations including current alcohol dependence. A
randomized controlled trial of a six-module multimedia computer-assisted training
program for cognitive behavioral therapy (CBT4CBT) was conducted in an intensive
outpatient substance treatment setting (Carroll et al., 2008). Participants were ran-
domized to either 8 weeks of standardized treatment (weekly individual and group
sessions) of general drug sessions or 8 weeks of standardized treatment with biweekly
CBT4CBT. The six modules focused on introducing CBT, coping with craving,
refusal skills, problem solving, recognizing and challenging cognitions, and decision-
making skills. At the conclusion of the treatment, the CBT4CBT group submitted
fewer drug positive urine specimens and tended to have longer periods of abstinence
than the standard treatment group (Carroll et al., 2008). A 6-month follow-up of
the CBT4CBT group found that they reported a significantly longer duration of
continuous abstinence from all drugs during the follow-up period. Moreover, those
assigned to CBT4CBT were significantly more likely to submit a drug-negative urine
specimen at the 1-, 3-, and 6-month follow-ups. While the difference between the
3- and 6-month follow-up rates were not statistically significant, the 1-month follow-
up rates for drug-negative urine specimens were higher in CBT4CBT (76%) versus
standardized treatment (48%; p = .05) (Carroll et al., 2009).
The development of computer-administered prevention, screening, and treatment
tools has potential impact in the expansion of alcohol services. For example, treatment
access varies greatly across rural and urban settings. Rural areas have less substance
abuse and mental health treatment services compared to urban settings, and the
physical proximity of the services also plays a role in the willingness to pursue treatment
(Hutchison & Blakely, 2003). Stigma has also been shown to negatively impact
willingness to initiate treatment. Specifically, individuals with AUDs who perceive
high stigma in the community are less likely to utilize standard face-to-face alcohol
treatment services (Keyes et al., 2010). Internet and computer-based services allow
a degree of anonymity, thus providing an option for those concerned with seeking
more public services. In this way, intervention approaches for AUDs that capitalize
on available technologies may help to increase the reach of behavioral therapies to
individuals who might historically not have sought out help via conventional treatment
modalities.
Conclusion
Alcohol problems range from risky episodic drinking behaviors to diagnostic levels of
dependence and affect a large population of individuals. This spectrum of problematic
alcohol use behaviors can also include a myriad of associated diagnoses and behavioral
deficits that exacerbate treatment for the comorbid problems. In considering the most
appropriate interventions for an AUD, formulating a treatment approach requires
appropriate assessment of the function of alcohol use for that individual as well as
consideration of these concomitant factors in determining the relevant behavioral

intervention and appropriate pharmacologic supports. CBT-based treatments for
AUDs are well established with solid supporting evidence. Research continues to
expand the standardized CBT-based interventions for alcohol problems.
References
Ambrogne, J. A. (2002). Reduced-risk drinking as a treatment goal: What clinicians need
to know. Journal of Substance Abuse Treatment, 22, 45–53. doi:10.1016/S0740-
5472(01)00210-0
Anton, R. F., Myrick, H., Wright, T. M., Latham, P. K., Baros, A. M., Waid, L. R.,
& Randall, P. K. (2011). Gabapentin combined with naltrexone for the treatment
of alcohol dependence. American Journal of Psychiatry, 168, 709–717. doi:10.1176/
appi.ajp.2011.10101436
Anton, R. F., Oroszi, G., O’Malley, S., Couper, D., Swift, R., Pettinati, H., & Goldman, D.
(2008). An evaluation of μ-opioid receptor (OPRM1) as a predictor of naltrexone response
in the treatment of alcohol dependence: Results from the Combined Pharmacotherapies
and Behavioral Interventions for Alcohol Dependence (COMBINE) study. Archives of
Back, S. E., Brady, K. T., Sonne, S. C., & Verduin, M. L. (2006). Symptom improvement
in co-occurring PTSD and alcohol dependence. Journal of Nervous and Mental Disease,
194, 690–696.
Bagnardi, V., Blangiardo, J., La Vecchia, C., & Corrao, G. (2001). Alcohol consumption and
the risk of cancer: A meta-analysis. Alcohol Research & Health, 25, 236–270.
Baker, A. L., Kavanagh, D. J., Kay-Lambkin, F. J., Hunt, S. A., Lewin, T. J., Carr, V. J.,
& Connolly, J. (2010). Randomized controlled trial of cognitive-behavioural therapy
for coexisting depression and alcohol problems: Short-term outcome. Addiction, 105,
87–99. doi:10.1111/j.1360-0443.2009.02757.x
Bandura, A. (1969). Principles of behavior modification. New York, NY: Holt, Rinehart &
Winston.
Bandura, A. (1997). Self-efficacy: The exercise of control. New York, NY: W. H. Freeman.
Berglund, M., Thelander, S., & Jonsson, E. (2004). Treating alcohol and drug abuse: An
evidence based review. Darmstadt, Germany: Wiley-VCH.
Bowen, R. C., D’Arcy, C., Keegan, D., & Senthilselvan, A. (2000). A controlled trial of
cognitive behavioral treatment of panic in alcoholic inpatients with comorbid panic
disorder. Addictive Behaviors, 25, 593–597.
Brady, K. T., Pearlstein, T., Asnis, G. M., Baker, D., Rothbaum, B., Sikes, C. R., &
Farfel, G. M. (2000). Efficacy and safety of sertraline treatment of posttraumatic stress
disorder: A randomized controlled trial. Journal of the American Medical Association, 283,
1837–1844.
Brown, R. A., Evans, D. M., Miller, I. W., Burgess, E. S., & Mueller, T. I. (1997). Cognitive-
behavioral treatment for depression in alcoholism. Journal of Consulting and Clinical
Psychology, 65, 715–726. doi:10.1037/0022-006X.65.5.715
Brown, R. A., & Lewinsohn, P. M. (1984). A psychoeducational approach to the treatment of
depression: Comparison of group, individual, and minimal contact procedures. Journal of
Brown, R. A., Ramsey, S. E., Kahler, C. W., Palm, K. M., Monti, P. M., Abrams, D., …
Miller, I. W. (2011). A randomized controlled trial of cognitive-behavioral treatment
for depression versus relaxation training for alcohol-dependent individuals with elevated
depressive symptoms. Journal of Studies on Alcohol and Drugs, 72, 286–296.
Brown, S. A., Glasner-Edwards, S. V., Tate, S. R., McQuaid, J. R., Chalekian, J., &
Granholm, E. (2006). Integrated cognitive behavioral therapy versus twelve-step facil-
itation therapy for substance-dependent adults with depressive disorders. Journal of
Psychoactive Drugs, 38, 449–460.
Carroll, K. M., Ball, S. A., Martino, S., Nich, C., Babuscio, T. A., Nuro, K. F., & Rounsaville,
B. J. (2008). Computer-assisted delivery of cognitive-behavioral therapy for addiction:
A randomized trial of CBT4CBT. American Journal of Psychiatry, 165, 881–888.
doi:10.1176/appi.ajp.2008.07111835
Carroll, K. M., Ball, S. A., Martino, S., Nich, C., Babuscio, T. A., & Rounsaville, B. J. (2009).
Enduring effects of a computer-assisted training program for cognitive behavioral therapy:
A 6-month follow-up of CBT4CBT. Drug and Alcohol Dependence, 100, 178–181.
Clapp, J. D., & Shillington, A. M. (2001). Environmental predictors of heavy episodic drinking.
American Journal of Drug and Alcohol Abuse, 27 , 301–313.
Compton, W. M., Thomas, Y. F., Stinson, F. S., & Grant, B. F. (2007). Prevalence, correlates,
disability, and comorbidity of DSM-IV drug abuse and dependence in the United States:
Results from the National Epidemiologic Survey on Alcohol and Related Conditions.
Courtney, K. E., & Polich, J. (2009). Binge drinking in young adults: Data, definitions, and
determinants. Psychological Bulletin, 135, 142–156. doi:10.1037/a0014414
Craske, M. G., Brown, T. A., & Barlow, D. H. (1991). Behavioral treatment of panic
disorder: A two-year follow-up. Behavior Therapy, 22, 289–304. doi:10.1016/S0005-
7894(05)80367-3
Cunningham, J. A., Kypri, K., & McCambridge, J. (2011). The use of emerging technologies
in alcohol treatment. Alcohol Research and Health, 33, 320–326.
De Sousa, A. A., De Sousa, J., & Kapoor, H. (2007). An open randomized trial comparing
disulfiram and topiramate in the treatment of alcohol dependence. Journal of Substance
Abuse Treatment, 34, 460–463. doi:10.1016/j.jsat.2007.05.012
Drummond, D. C., & Glautier, S. (1994a). A conditioning approach to the analysis and
treatment of drinking problems. British Medical Bulletin, 50, 186–199.
Drummond, D. C., & Glautier, S. (1994b). A controlled trial of cue exposure treatment
in alcohol dependence. Journal of Consulting and Clinical Psychology, 62, 809–817.
doi:10.1037/0022-006X.62.4.809
Epstein, E. E., & McGrady, B. S. (1998). Behavioral couples treatment of alcohol and drug
use disorders: Current status and innovations. Clinical Psychology Review, 18, 689–711.
doi:10.1016/S0272-7358(98)00025-7
Epstein, J. A., Zhou, X. K., Bang, H., & Botvin, G. J. (2007). Do competence skills moderate
the impact of social influences to drink and perceived social benefits of drinking on alcohol
use among inner-city adolescents? Prevention Science, 8, 65–73.
First, M. B. (2009). Harmonisation of ICD-11 and DSM-V: Opportunities and challenges.
British Journal of Psychiatry, 195, 382–390. doi:10.1192/bjp.bp.108.060822
Gastfriend, D., Garbutt, J. C., Pettinati, H. M., & Forman, R. F. (2007). Reduction in
heavy drinking as a treatment outcome in alcohol dependence. Journal of Substance Abuse
Treatment, 33, 71–80. doi:10.1016/j.jsat.2006.09.008
Gossop, M., Keaney, F., Stewart D., Marshall E. J., & Strang, J. (2002). A Short Alcohol
Withdrawal Scale (SAWS): Development and psychometric properties. Addiction Biology,
7 , 37–43. doi:10.1080/135562101200100571
Grant, B. F., Stinson, F. S., Dawson, D. A., Chou, S. P., Dufour, M. C., Compton, W.,
… Kaplan, K. (2004). Prevalence and co-occurrence of substance use disorders and
independent mood and anxiety disorders: Results from the National Epidemiologic
Survey on Alcohol and Related Conditions. Archives of General Psychiatry, 61, 807–816.
Hasin, D. S., Schuckit, M. A., Martin, C. S., Grant, B. F., Bucholz, K. K., & Helzer, J.
E. (2003). The validity of DSM-IV alcohol dependence: What do we know and what
do we need to know? Alcoholism: Clinical and Experimental Research, 27 , 244–252.
doi:10.1097/01.ALC.0000060878.61384.ED
Havermans, R. C., Mulkens, S., Nederkoorn, C., & Jansen, A. (2007). The efficacy of cue
exposure with response prevention in extinguishing drug and alcohol cue reactivity.
Behavioral Interventions, 22, 121–135. doi:10.1002/bin.219
Hedges, L.V. (1994). Statistical considerations. In H. M. Cooper & L. V. Hedges (Eds.), The
handbook of research synthesis (pp. 29–38). New York, NY: Sage.
Heilig, M., & Egli, M. (2006). Pharmacological treatment of alcohol dependence: Tar-
get symptoms and target mechanisms. Pharmacology & Therapeutics, 111, 855–876.
doi:10.1016/j.pharmthera.2006.02.001
Hein, D. A., Cohen, L. R., Litt, L. C., Miele, G. M., & Capstick, C. (2004). Promising
treatments for women with comorbid PTSD and substance use disorders. American
Hendershot, C. S., Witkiewitz, K., George, W., & Marlatt, G.A. (2011). Relapse prevention
for addictive behaviors. Substance Abuse Treatment, Prevention, and Policy, 6, 17–33.
Hutchison, L., & Blakely, C. (2003). Substance abuse—trends in rural areas: A literature review.
In Rural Healthy People 2010: A companion document to Healthy People 2010 (Vol. 2;
Chapter 9). Retrieved from http://srph.tamhsc.edu/centers/rhp2010/Volume2.pdf
Irvin, J. E., Bowers, C. A., Dunn, M. E., & Wong, M. C. (1996). Efficacy of relapse
prevention: A meta-analytic review. Journal of Consulting and Clinical Psychology, 67 ,
563–570. doi:10.1037/0022-006X.67.4.563
Johnson, B. A., Rosenthal, N., Capece, J. A., Wiegand, F., Mao, L., Beyers, K., …
Swift, R. M. (2007). Topiramate for treating alcohol dependence: A randomized
doi:10.1001/jama.298.14.1641
Kadden, R., Carroll, K. M., Donovan, D., Cooney, N., Monti, P., Abrams, D., … Hester, R.
(1992). Cognitive-behavioral coping skills therapy manual: A clinical research guide
for therapists treating individuals with alcohol abuse and dependence. Retrieved from
http://pubs.niaaa.nih.gov/publications/MATCHSeries3/index.htm
Keyes, K. M., Hatzenbuehler, M. L., McLaughlin, K. A., Link, B., Olfson, M., Grant, B. F.,
& Hasin, D. (2010). Stigma and treatment for alcohol disorders in the United States.
American Journal of Epidemiology, 172, 1364–1372. doi:10.1093/aje/kwq304
Knight, J. R., Wechsler, H., Kuo, M., Seibring, M., Weitzman, E. R., & Schukit, M. A. (2002).
Alcohol abuse and dependence among U.S. college students. Journal of Studies on Alcohol
and Drugs, 63, 263–270.
Krystal, J. H., Cramer, J. A., Krol, W. F., Kirk, G. F., & Rosenheck, R. A. (2001). Naltrexone in
the treatment of alcohol dependence. New England Journal of Medicine, 345, 1734–1739.
Lee, J. H., Kwon, J., Choi, J., & Yang, B. (2007). Cue-exposure therapy to decrease
alcohol craving in virtual environment. Cyberpsychology & Behavior, 10, 617–623.
doi:10.1089/cpb.2007.9978
Li, T., Hewitt, B. G., & Grant, B. F. (2007). The alcohol dependence syndrome, 30 years later:
a commentary. Addiction, 102, 1522–1530. doi: 10.1111/j.1360-0443.2007.01911.x
Lundahl, B., & Burke, B. L. (2009). The effectiveness and applicability of motivational inter-
viewing: A practice-friendly review of four meta-analyses. Journal of Clinical Psychology,
65, 1232–1245.
Magill, M., & Ray, L. A. (2009). Cognitive behavioral treatment with adult alcohol and illicit
drug users: A meta-analysis. Journal of Studies on Alcohol and Drugs, 70, 516–527.
Marlatt, G. A., & Gordon, J. R. (1985). Relapse prevention: Maintenance strategies in the
McBride, O., Adamson, G., Bunting, B. P., & McCann, S. (2009). Characteristics of
DSM-IV alcohol diagnostic orphans: Drinking patterns, physical illness, and negative
life events. Drug and Alcohol Dependence, 99, 272–279. doi:10.1016/j.drugalcdep.
2008.09.008
Miller, W. R., & Wilbourne, P. L. (2002). Mesa grande: A methodological analysis of clinical
treatments for alcohol use disorders. Addiction, 97 , 265–277.
Mohan, L., Shankar, P. R., Raut, P., & Gyawali, S. (2010). Pharmacotherapy of alcohol
dependence. Journal of Clinical and Diagnostic Research, 4, 2947–2955.
Monti, P. M., Corriveau, D. P., Curran, & J. P. (1982). Social skills training for psychiatric
patients: Treatment and outcome. In J. P. Curran & P. M. Monti (Eds.), Social skills
training: A practical handbook for assessment and treatment (pp. 185–223). New York,
NY: Guilford Press.
Muñoz, R. F., & Ying, Y. W. (Eds.). (2002). The prevention of depression: Research practice.
Baltimore, MD: Johns Hopkins University Press.
National Council on Alcoholism and Drug Dependence. (2011). Alcohol and drug
information [Press release]. Retrieved from http://www.ncadd.org/index.php/for-the-
media/alcohol-a-drug-information
National Institutes of Alcohol Abuse and Alcoholism. (2004). NIAA Council approves def-
inition of binge drinking. NIAAA Newsletter, 3, 3. Retrieved from http://pubs.niaaa.
nih.gov/publications/Newsletter/winter2004/Newsletter_Number3.pdf
Newman, M. G., Szkodny, L. E., Llera, S. J., & Przeworski, A. (2011). A review of technology-
assisted self-help and minimal contact therapies for drug and alcohol abuse and smoking
addiction: Is human contact necessary for therapeutic efficacy? Clinical Psychology Review,
31, 178–186. doi:10.1016/j.cpr.2010.10.002
O’Farrell, T. J. (1989). Marital and family therapy in alcoholism treatment. Journal of Substance
Abuse Treatment, 6, 23–9. doi:10.1016/0740-5472(89)90016-0
Pettinati, H. M., & Dundon, W. D. (2011). Comorbid depression and alcohol dependence.
Psychiatric Times, 28, 49–55.
Pollock, N., & Martin, C. S. (1999). Diagnostic orphans: Adolescents with alcohol symptoms
who do not qualify for DSM-IV abuse or dependence diagnoses. American Journal of
Powers, M. B., Vedel, E., & Emmelkamp, P. M. (2008). Behavioral couples therapy (BCT) for
alcohol and drug use disorders: A meta-analysis. Clinical Psychology Review, 28, 952–962.
doi:10.1016/j.cpr.2008.02.002
Project MATCH Research Group. (1993). Project MATCH: Rationale and methods for a
multisite clinical trial matching alcoholism patients to treatment. Alcoholism: Clinical and
Experimental Research, 17 , 1130–1145.
Rohsenow, D. J., Monti, P. M., Rubonis, A. V., Gulliver, S. B., Colby, S. M., Binkoff, J. A., &
Abrams, D. B. (2001). Cue exposure with coping skills training and communication skills
training for alcohol dependence: 6- and 12-month outcomes. Addiction, 96, 1161–1174.
doi:10.1046/j.1360-0443.2001.96811619.x
Rosner, S., Hackl-Herrwerth, A., Leucht, S., Lehert, P., Vecchi, S., & Soyka, M. (2010).
Acamprosate for alcohol dependence. Cochrane Database of Systematic Reviews, 9.
doi:10.1002/14651858.CD004332.pub2
Scheier, L. M., Botvin, G. J., Diaz, T., & Griffin, K. W. (1999). Social skills, competence, and
drug refusal efficacy as predictors of adolescent alcohol use. Journal of Drug Education, 29,
253–280.
Schuckit, M. A. (2009). Alcohol-use disorders. Lancet, 373, 492–501. doi:10.1016/
S0140-6736(09)60009-X
Walters, G. D. (2000). Behavioral self-control training for problem drinkers: A meta-analysis
of randomized controlled studies. Behavior Therapy, 31, 135–149. doi:10.1016/S0005-
7894(00)80008-8
Williams, S. (2005). Medications for treating alcohol dependence. American Family Physician,
72, 1775–1780.
World Health Organization. (2011). Global status report on alcohol and health. Geneva,
Switzerland: Author.
56
Illegal Drug Use
Brian D. Kiluk and Kathleen M. Carroll
Yale School of Medicine
Overview
Cognitive behavioral treatments are among the most well-defined and rigorously
studied psychotherapeutic interventions for substance use disorders. While this chapter
focuses primarily on cognitive behavioral therapy (CBT) for illegal drug use, it should
be noted that CBT shares several features with other empirically supported behavioral
approaches. First, it is applicable across a broad range of substance use disorders.
That is, well-controlled trials have supported its efficacy across cocaine, marijuana,
stimulant, and opioid dependent populations. Second, CBT was developed from
well-founded theoretical traditions with established theories and principles of human
behavior. Third, it is highly flexible and can be implemented in a wide range of clinical
modalities and settings. Moreover, it is compatible with a variety of pharmacotherapies
and, in many cases, can foster compliance and enhance the effects of pharmacotherapies
for specific drugs of abuse including methadone, naltrexone, and disulfiram. Finally,
CBT is highly focused and relatively brief/short-term, emphasizing rapid, targeted
change in substance use and related problems. In this manner, it is very compatible
in a health care environment that is increasingly influenced by managed care, best
clinical practice models, and professional accountability (Carroll, 2011a, 2011b).
At the most simple level, CBT for illegal drug use attempts to help individual
patients recognize, avoid, and cope; that is, recognize the situations in which they
are most likely to use drugs, avoid those situations when possible or appropriate, and
cope more effectively with a range of problems and problematic behaviors associated
with substance use. CBT has two critical components and defining features. The
first is a thorough functional analysis of the role illicit drugs play in the individual’s
life. For each instance of substance use the patient experiences during treatment, the
therapist and patient will identify the patient’s thoughts, feelings, and circumstances

DOI: 10.1002/9781118528563.wbcbt56
before the substance use, as well as the patient’s thoughts, feelings, and circumstances
after the substance use. Early in treatment, the functional analysis plays a critical role
in helping the patient and therapist assess the determinants, or high-risk situations,
that are likely to lead to substance use, as well as in shedding light on some of the
reasons the individual may be using drugs. The second critical component of CBT is
skills training. In CBT, this consists of a highly individualized training program that
helps substance users change old habits associated with their drug use and learn or
relearn more adaptive skills and habits (Carroll, 2011b).
This chapter explores each of these components in more detail, describing specific
techniques and strategies, as well as providing a review of the empirical support for
CBT. It also covers several areas that require special consideration when implementing
CBT for drug use, such as therapist training and competence, and the impact of
impaired cognitive functioning associated with chronic drug use. The chapter ends
with an overview of new developments in the treatment of drug use disorders.
However, first, because an effective treatment begins with a strong theoretical basis,
we will provide a brief overview of the theory underlying CBT for substance use
disorders.
Theoretical Basis
Cognitive behavioral treatments have their roots in classical behavioral theory and the
pioneering work of Pavlov, Watson, Skinner, and Bandura (see reviews by Craske,
2010; Rotgers, 2012). Pavlov’s work on classical conditioning demonstrated that
a previously neutral stimulus could elicit a conditioned response after being paired
repeatedly with an unconditioned stimulus. Furthermore, repeated exposure to the
conditioned stimulus without the unconditioned stimulus would eventually lead to
extinction of the conditioned response. These classical conditioning concepts play an
important role in CBT, and particularly in interventions directed at reducing some
forms of craving for drugs. For instance, the therapist attempts to help the patient
understand and recognize conditioned craving, identify his or her own idiosyncratic
array of conditioned cues for craving, avoid exposure to those cues, and cope effectively
with craving when it does occur without using drugs so that conditioned craving is
reduced and eliminated over time.
Skinner’s work on operant conditioning demonstrated that behaviors that are
positively reinforced are likely to be exhibited more frequently. Behavior therapies
assume that drug use and related behaviors are learned through their association
with the positively reinforcing properties of the drugs themselves as well as their
secondary association with other environmental stimuli. CBT attempts to disrupt
this learned association between drug-related cues or stimuli and drug craving or
use by understanding and changing these behavior patterns. Operant conditioning
concepts are used in several ways in CBT for illegal drug use. First, through a detailed
examination of the antecedents and consequences of drug use, the therapist attempts
to develop an understanding of the reasons the patient may be more likely to use in
a given situation and to understand the role that drugs play in his or her life. This
“functional analysis” of substance use is thus used to identify the high-risk situations
Illegal Drug Use 1341
in which the patient is likely to use drugs and thus to provide the basis for learning
more effective coping behaviors in those situations. Second, the therapist attempts
to help the patient develop meaningful alternate reinforcers to drug use; that is,
other activities and involvements (relationships, work, hobbies) that serve as viable
alternatives to drug use and help the patient remain abstinent. Finally, a detailed
examination of the consequences, both long- and short-term, of his or her drug use,
is used as a strategy to build or reinforce the patient’s resolve to reduce or eliminate
his or her drug use.
CBT conceives substance use disorders as complex, multidetermined problems,
with a number of influences playing a role in the development or perpetuation of
the disorder. These may include family history and genetic factors; the presence of
comorbid psychopathology; personality traits such as sensation seeking or impulsivity;
and a host of environmental factors, including drug availability and lack of counter-
vailing influences and rewards. Though CBT for illegal drug use primarily emphasizes
the reinforcing properties of drugs as central to the acquisition and maintenance of
substance abuse and dependence, these etiological influences are seen as heightening
risk or vulnerability to the development of substance use problems. For example,
some individuals may find drugs unusually highly rewarding secondary to genetic
vulnerability, comorbid depression, a high need for sensation seeking, and model-
ing of family and friends who use substances or environments devoid of alternative
reinforcers.
Cognitive behavioral treatments also reflect the pioneering work of Ellis and Beck
that emphasizes the importance of the person’s thoughts and feelings as determinants
of behavior. CBT evolved in part from dissatisfaction with the extreme positions of
radical behaviorism (e.g., emphasis on overt behaviors) and classical psychoanalysis
(emphasis on unconscious conflicts or representations). CBT emphasizes how the
individual perceives and interprets life events as important determinants of behavior
(Meichenbaum, 1995). A person’s conscious thoughts, feelings, and expectancies
mediate an individual’s response to the environment. CBT for illegal drug use seeks
to help patients become aware of maladaptive cognitions and change them (Carroll,
2011a, 2011b).
Just as CBT for illegal drug use assumes that many individuals essentially “learn”
to become drug users over time, through complex interplays of modeling, classical
conditioning, or operant conditioning, each of these principles is invoked in CBT to
help the patient stop using drugs. For example, modeling is used to help the patient
learn new behaviors (e.g., how to refuse an offer of drugs, how to break off or limit
a relationship with a drug-using associate) by having the patient participate in role
plays with the therapist during the treatment. That is, the patient learns to respond in
new, unfamiliar ways first by watching the therapist model those new strategies and
then by practicing those strategies within the supportive context of the therapy hour
(Carroll, 2011b).
Learning serves as an important metaphor for the treatment process throughout.
CBT therapists tell patients that a goal of the treatment is to help them “unlearn”
old, ineffective behaviors and “learn” new ones. Patients, particularly those who
are demoralized by their failure to change their substance use, or for whom the
consequences of addiction have been severe, are frequently surprised to think about
substance use as a type of skill, as something they have learned to do over time:
In effect they have learned a complex set of skills that enabled them to acquire the
money needed to buy drugs and alcohol (which often led to another set of licit or
illicit skills), avoid detection, and so on. Patients who can reframe their self-appraisals
in terms of being “skilled” in this way can often see that they also have the capacity to
learn a new set of skills—this time, though, skills that will help them remain abstinent
(Carroll, 1998).
Defining Features of Cognitive Behavioral Therapy

for Illegal Drug Use
Specific techniques vary widely with the type of cognitive behavioral treatment used,
and there are a variety of manuals, protocols, and training programs available which
describe the techniques associated with each approach (Carroll, 1998; Kadden et al.,
1992; Marlatt & Donovan, 2005; Parrish, 2009; Sobell & Sobell, 2011). The two
key defining features of CBT for illegal drug use are (a) functional analysis of drug
use, that is, understanding drug use with respect to its antecedents and consequences,
and (b) skills training. CBT includes a range of skills to foster or maintain abstinence.
These typically include strategies for:
• understanding the patterns that maintain drug use and developing strategies
for changing these patterns (this often involves self-monitoring of thoughts and
behaviors that take place before, during, and after high-risk situations or episodes
of drug use);
• fostering the resolution to stop substance use through exploring positive and
negative consequences of continued use (also known as the decisional balance
technique);
• understanding craving, craving cues, and the development of skills for coping
with craving when it occurs (these include a variety of affect regulation strategies:
distraction, talking through a craving, “urge surfing” and so on);
• recognizing and challenging the cognitions that accompany and maintain patterns
of substance use;
• increasing awareness of the consequences of even small decisions (e.g., which
route to take home from work), and the identification of “seemingly irrelevant”
decisions which can culminate in high-risk situations;
• developing problem-solving skills, and practicing application of those skills to
substance-related and more general problems (e.g., managing the various social
and legal problems associated with illegal drug use);
• planning for emergencies and unexpected problems and situations that can lead
to high-risk situations; and
• developing skills for assertively refusing offers of drugs, as well as reducing exposure
to drugs and drug-related cues.
These basic skills are useful in their application to helping patients control and stop
illegal drug use, but it is essential that therapists also point out how these same skills
can be applied to a range of other problems. For example, a functional analysis can
be used to understand the determinants of a wide range of behavior patterns, skills
used to cope with craving can easily be applied to other aspects of affect control, the
principles used in the sessions on seemingly irrelevant decisions can easily be adapted
to understanding a wide range of behavior chains, and drug refusal skills can easily
be transferred to more effective and assertive responding in a number of situations. It
is essential that when therapists teach coping skills, they emphasize and demonstrate
that the skills can be applied immediately to control substance use, but also can be
used as general strategies that can be useful across a wide range of situations and
problems the patient may encounter in the future.
CBT for illegal drug use is typically highly structured. That is, it is generally
brief (12–24 weeks) and organized closely around well-specified treatment goals.
An articulated agenda exists for each session and the clinical discussion remains
focused around issues directly related to substance use. Progress toward treatment
goals is monitored closely and frequently, with frequent monitoring of drug use
through urine toxicology screens, and the therapist takes an active stance throughout
treatment. In broad spectrum cognitive behavioral approaches, sessions often are
organized roughly in thirds (the 20/20/20 rule), with the first third of the session
devoted to the assessment of the patient’s substance use, general functioning in
the past week, and report of current concerns and problems; the second third
is more didactic and devoted to skills training and practice; and the final third
allows time for therapist and patient to plan for the week ahead and discuss how
new skills will be implemented. The therapeutic relationship is seen as principally
collaborative. Thus, the role of the therapist is one of consultant, educator, and
guide who can lead the patient through a functional analysis of his or her substance
use, aid in identifying and prioritizing target behaviors, and consult in selecting and
implementing strategies to foster the desired behavior changes (Carroll, 1998, 2011a,
2011b).
An overview of topics and session goals in a standard CBT for illegal drug use
(adapted from Carroll, 1998) is provided in Table 56.1. Typically, the early sessions
focus on gathering history, building a therapeutic relationship, introducing the CBT
model, and teaching some of the more fundamental skills to achieve abstinence (e.g.,
functional analysis for identifying triggers, coping with craving, building motivation).
As the patient progresses, later sessions build on these basic skills by addressing more
complex topics, such as problem solving and case management. Additionally, an
aspect of CBT for illegal drug use that is often not present in CBT for nonsubstance
psychiatric disorders is a focus on reducing HIV-risk behaviors. This is an important
topic, regardless of whether the patient is an injection drug user, because many
drug users engage in unsafe sexual practices that increase their risk of HIV and other
sexually transmitted diseases (Scheinmann et al., 2007; Woody et al., 1999).
While structured and didactic, CBT for illegal drug use is also a highly individ-
ualized and flexible treatment. Rather than viewing CBT treatment as cookbook
“psychoeducation,” the therapist carefully matches the content, timing, and nature
of presentation of the material to the individual patient. The therapist attempts to
provide skills training that is highly tailored to the individual’s strengths, weaknesses,
and current level of functioning. For instance, the therapist does not belabor topics
Table 56.1 Session Overview of Cognitive Behavioral Therapy for Illegal Drug Use
Topic Session goals
Introduction to treatment • Establish relationship with patient.

and CBT • Assess substance use and other problems.
• Provide rationale for treatment.
• Establish structure of remaining sessions.
• Initiate skills training.
Coping with craving • Understand patient’s experience of craving.
• Describe craving as a normal, time-limited experience.
• Help patient identify craving cues and triggers.
• Introduce and practice craving and urge-control techniques.
Shoring up motivation and • Revisit and clarify treatment goals.
commitment to stop • Acknowledge and address ambivalence.
• Learn to identify and cope with thoughts about drug use.
Refusal skills/assertiveness • Assess drug availability and steps needed to reduce it.
• Explore strategies for breaking contacts with drug suppliers.
• Learn and practice drug refusal skills.
• Review the difference between passive, aggressive, and
assertive responding.
Seemingly irrelevant • Understand seemingly irrelevant decisions and their
decisions relationships to high-risk situations.
• Identify examples of seemingly irrelevant decisions.
• Practice safe decision making.
All-purpose coping plan • Anticipate future high-risk situations.
• Develop a personal, generic coping plan.
Problem solving • Introduce and review basic steps of problem solving.
• Practice problem-solving skills in session.
Case management • Review and apply problem-solving skills to psychosocial
problems that present a barrier to treatment.
• Develop a concrete plan for addressing psychosocial
problems.
• Monitor and support patient’s efforts to carry out the plan.
HIV risk reduction • Assess patient’s risk for HIV infection and build motivation
to change risky behaviors.
• Set behavior change goals.
• Problem solve barriers to risk reduction.
• Distribute specific risk-reduction guidelines.
such as breaking ties with drug suppliers with a patient who is highly motivated and
has been abstinent for several weeks. Similarly, the therapist does not race through
material in an attempt to “cover” all of it in a few weeks; for some patients, it may take
several weeks to master a basic skill (Carroll, 1998, 2011a, 2011b). Along these lines,
therapists should also be careful to use language that is compatible with the patient’s
level of understanding, making frequent attempts to check with patients to be sure
they understand a concept and are comfortable with a specific skill. For example,
while some can readily understand the concept of conditioned craving, others may
require further explanation through use of concrete examples and more familiar
language. Therefore, therapists should always be aware of patients’ comprehension of
the material, and should feel free to repeat session material as many times and in as
many different ways as needed.
Importance of Extra-Session Practice (Homework) in

Cognitive Behavioral Therapy for Drug Use Disorders
In CBT, therapists encourage patients to practice new skills, as such practice is a

central, essential, component of treatment. The degree to which the treatment is a
“skills training” versus merely a “skills exposure” approach has to do with the degree
to which there is opportunity to practice and implement coping skills, making extra-
session practice and homework all the more important. It is critical that patients have
the opportunity to “try out” new skills within the supportive context of treatment.
Through first-hand experience, patients can learn what new approaches work or do
not work for them, where they have difficulty or problems, and so on. There are many
opportunities for practice within CBT, both within sessions and outside of them.
Within each session, there are opportunities for patients to rehearse and review ideas,
raise concerns, and get feedback from the therapist.
The converging evidence suggesting that CBT is a particularly durable approach has
led to increased focus on unique or distinctive aspects of CBT that might account for
its durability. Encouraging clients to implement and practice skills outside of sessions
via homework assignments is one possible mechanism for this effect. Homework
encourages practice of skills outside of sessions and possibly generalization of skills
to other problems, and emphasis on extra-session practice assignments is a unique
feature of CBT, and particularly important in CBT for illegal drug use. Moreover,
investigators evaluating CBT in nonsubstance psychiatric disorders have noted the
importance of homework in CBT’s effectiveness (Cowan et al., 2007; Edelman &
Chambless, 1995; Freeman, 2007; Westra, Dozois, & Marcus, 2007).
The relationships between homework compliance, skills acquisition, and outcome
in CBT have received very little attention in the substance abuse literature. In one
of our more recent trials (Carroll, Nich, & Ball, 2005), we evaluated homework
completion in detail, collecting data on the specific type of homework assigned
and how well it was done (e.g., fully, partially, no attempt made) at every ses-
sion. We found strong relationships between homework compliance and outcome.
Compared with the participants assigned to CBT who did not do homework or
who did it only rarely, the participants who did homework consistently stayed in
treatment significantly longer, and had more consecutive days of cocaine abstinence
(a strong predictor of long-term outcome) and fewer cocaine-positive urines during
treatment. Similar effects were found for the subset of participants who completed
treatment in this study, suggesting that the effects of homework compliance on
better substance use outcomes were not completely accounted for by differential
retention. In addition, we found strong relationships between homework compli-
ance and acquisition of coping skills, as well as between homework completion and
participants’ ratings of their confidence in avoiding use in a variety of high-risk
situations. Participants who completed homework had significant increases over time
in their self-reported confidence in handling a variety of high-risk situations, while
scores for the subgroup that did not do homework did not change over time (Carroll
et al., 2005).
Several other studies have highlighted the importance of homework completion in
CBT for drug use. Gonzalez, Schmitz, and DeLaune (2006) examined the effect of
homework compliance on treatment outcome from two randomized trials of CBT
combined with pharmacotherapy for cocaine dependence. They determined that
homework compliance predicted less cocaine use during treatment for those higher
on a readiness to change measure, and it was also associated with better retention
in treatment. Farabee, Rawson, and McCann (2002) evaluated the extent to which
cocaine users reported engaging in a series of specific drug avoidance activities (e.g.,
avoiding drug-using friends and places where cocaine would be available, exercising,
using thought-stopping) after CBT versus alternate treatments (e.g., contingency
management [CM] and a control condition). They found that, by the end of
treatment, participants assigned to CBT reported more frequent engagement in drug-
avoidance activities than participants in the comparison treatments. Furthermore,
the frequency of drug avoidance activities was strongly related to better cocaine use
outcomes over the one-year follow-up. Taken together, these studies suggest that
CBT interventions that foster the patient’s engagement in active behavior change may
play a key role in CBT’s comparative durability (Carroll, 2011a, 2011b).
Empirical Support
CBT has been shown to be effective across a wide range of substance use dis-
orders, including marijuana dependence (Babor, 2004; Copeland, Swift, Roffman,
& Stephens, 2001), cocaine dependence (Carroll et al., 2004; Carroll, Nich, Ball,
McCance-Katz, & Rounsaville, 1998; Rawson et al., 2002), methamphetamine
dependence (Lee & Rawson, 2008), and polysubstance dependence (Pollack et al.,
2002). A recent meta-analysis of 53 controlled trials of CBT for alcohol or illicit drug
use disorders reported a small but statistically significant overall effect size (g = 0.15,
p < .005), with statistical transformations indicating that 58% of patients receiving
CBT fared better than patients in the comparison condition (Magill & Ray, 2009).
CBT for illegal drug use has also been shown to be compatible with a number
of other treatment approaches, including pharmacotherapy (Schmitz et al., 2002;
Schmitz, Stotts, Rhoades, & Grabowski, 2001) and traditional counseling approaches
(Morgenstern, Morgan, McCrady, Keller, & Carroll, 2001) and thus can be imple-
mented in a wide range of settings. These findings are consistent with evidence
supporting the effectiveness of CBT across a number of other psychiatric disorders as
well, including depression, anxiety disorders, and eating disorders.
Our group at Yale has been involved in a programmatic series of studies on the
effectiveness of CBT for illegal drug use, alone and in combination with pharma-
cotherapy, for more than 20 years. As our understanding of CBT has deepened over
time, this series of studies has been marked by progressively larger effect sizes for
CBT over the comparison or control conditions. For example, in our first random-
ized trial, we conducted a direct comparison of CBT with another active therapy,
interpersonal psychotherapy (IPT), adapted for cocaine users. In that trial, CBT
was not found to have a main effect over IPT, but was found to be significantly
more effective among the more severely dependent cocaine abusers, with 54% of
those receiving CBT achieving abstinence compared to only 9% for IPT (Carroll,
Rounsaville, & Gawin, 1991), suggesting that the higher levels of structure and
emphasis on skills may have been particularly helpful for the more severely impaired
cocaine users.
This finding that CBT was more effective based on the severity of cocaine depen-
dence was also replicated in our next study (Carroll, Rounsaville, Gordon, et al.,
1994). This study examined the combination of psychotherapy and pharmacotherapy
by comparing desipramine versus placebo, and CBT versus supportive clinical man-
agement, which is a supportive psychotherapy control condition. This was the first
study to find that after the treatments were terminated, those that had been assigned
to CBT continued to reduce the frequency of their cocaine use throughout the one-
year follow-up (i.e., the “sleeper effect”) (Carroll, Rounsaville, Nich, et al., 1994).
Evidence of continued improvement associated with CBT in turn led to increasing
interest in mechanisms that might underlie this effect, with skills training and behav-
ioral practice through homework assignments as prime candidates, as described in
more detail in later sections of this chapter.
Thus, in our next study, which was the first to report a significant main effect
for CBT over supportive clinical management and which replicated the “sleeper
effect” for CBT over a one-year follow-up (Carroll, Nich, Ball, et al., 2000), we
evaluated the acquisition of coping skills in CBT and their relationship to outcome
in this population. The main treatment findings indicated that 58% of those receiving
a combination of CBT and disulfiram achieved at least 3 consecutive weeks of
abstinence from cocaine, compared to 30% of those receiving clinical management
plus disulfiram (Carroll et al., 1998). Also in this study, evaluation of a role-
play task for assessing patient coping skills demonstrated the following: (a) coping
skills increase significantly after CBT, (b) patients demonstrated increases in coping
skills that were parallel to those taught in the treatment they had been assigned
(i.e., differential acquisition of specific behavioral and cognitive coping strategies
in CBT with respect to alternate behavioral therapies), and finally, (c) greater
acquisition of CBT-specific behavioral and cognitive coping skills was associated with
significantly less cocaine use over the one-year follow-up (Carroll, Nich, Ball, et al.,
2000).
In one of our most recently completed trials of CBT for illegal drug use (Carroll
et al., 2004), 121 cocaine-dependent individuals were randomized to one of four
conditions: disulfiram (250 mg/day) plus CBT, disulfiram plus IPT, placebo plus
CBT, or placebo plus IPT. Across outcome measures and for the full intention-
to-treat sample (as well as across all subsamples including treatment initiators and
treatment completers), patients assigned to CBT reduced their cocaine use signifi-
cantly more than those assigned to IPT, and patients assigned to disulfiram reduced
their cocaine use significantly more than those assigned to placebo. Effects of CBT
plus placebo were comparable to those of the CBT–disulfiram combination. This
was our first trial to identify a significant main effect for CBT over another active
behavioral therapy (IPT). Furthermore, although retention was a significant predictor
of better drug use outcomes, the CBT by time effect remained statistically significant
after controlling for retention. Thus, this series of trials has demonstrated increas-
ingly strong effects for CBT over time and our follow-up studies have consistently
indicated high durability of CBT compared to other approaches (Carroll, 2011a,
2011b).
Cognitive Behavioral Therapy Combined with

Motivational Enhancement
Although the durability of CBT for illegal drug use has been well documented, one
of the relative weaknesses has been its mixed effect on early retention in treatment,
and the limited focus on patient motivation and engagement. One way to address
this has been to combine CBT with motivational enhancement therapy (MET;
Miller, Zweben, DiClemente, & Rychtarik, 1992), which is an empirically supported
treatment that targets patient motivation and has been conceptualized as an adjunctive
or preparatory treatment, particularly for more severe drug users (Miller, Yahne, &
Tonigan, 2003). The idea is that strategies used in MET, which is the manualized
version of motivational interviewing (MI; Miller & Rollnick, 2002), would be more
appropriate for addressing patient ambivalence and/or resistance to changing their
drug use that is often encountered early in treatment. While CBT for illegal drug use
does cover the topic of building patient motivation, there was a perception that more
concerted efforts were needed to handle the various motivational issues that arise
with substance-using populations. Therefore, several studies have investigated the
combination of MET and CBT for various drugs of abuse, including amphetamines
(Baker et al., 2005), cocaine (McKee et al., 2007; Rohsenow et al., 2004), marijuana
(Babor, 2004; Dennis et al., 2004), and methamphetamines (Bux & Irwin, 2006).
Although the findings have been mixed with respect to effect on drug use outcomes,
there is some evidence to suggest that adding motivational enhancement to the early
stages of CBT for illegal drug use can be effective at increasing motivation and
improving retention in treatment.
Cognitive Behavioral Therapy Combined with

Another attempt to address the weaker effects of CBT on engaging patients early in
treatment involves combining it with an approach that has strong empirical support for
improving early treatment adherence. Contingency management (CM), where par-
ticipants receive incentives (i.e., vouchers redeemable for goods and services, chances
to draw prizes from a bowl) contingent on demonstrating acquisition of treatment
goals (e.g., submitting drug-free urine specimens, attending treatment sessions) has
been an exciting development in the treatment of drug dependence, particularly in
achieving rapid behavior change (Lussier, Heil, Mongeon, Badger, & Higgins, 2006;
Petry et al., 2006; Prendergast, Podus, Finney, Greenwell, & Roll, 2006). Given that
CM has strong immediate effects but those effects tend to weaken after the contin-
gencies are terminated, while CBT tends to have more modest effects initially but is
comparatively durable, several investigators have evaluated various combinations of
CBT and CM, reasoning that the relative strengths and weaknesses of these may be
offset by combining them. For example, Rawson et al. (2002) compared group CBT,
voucher CM, and a CM/CBT combination in conjunction with standard methadone
maintenance treatment for cocaine-using methadone maintenance patients. During
the acute phase of treatment, the two groups featuring CM had significantly bet-
ter cocaine use outcomes, with 63% of those assigned to CM and 57% assigned to
CM/CBT achieving at least 3 consecutive weeks of abstinence from cocaine compared
to 40% of those assigned to CBT. However, during the follow-up period, a CBT
“sleeper” effect emerged again, where the group assigned to CBT essentially caught
up to the other groups by the 52-week follow-up (i.e., 60% of those assigned to CBT
provided a negative urine sample at this time point, compared to 53% in the CM
group, and 40% in the CBT/CM group). Epstein et al. (2003) conducted a similar
study, again in the context of intensive methadone maintenance, where participants
were offered CM, group CBT, or a combination, in addition to standard individual
counseling. Results were largely parallel to the Rawson study, in that the investigators
reported large initial effects for CM, with a drop-off after the termination of the
contingencies; however, the best one-year outcomes were present for the CM plus
CBT combination.
These effects have also been replicated in treatment studies for other illegal drugs. A
study conducted among a large sample (N = 171) of stimulant-dependent individuals
treated as outpatients produced similar results (Rawson et al., 2006), with CM being
associated with better retention and substance use outcomes during treatment (i.e.,
60% assigned to CM and 69% assigned to CM plus CBT achieved at least 3 consecutive
weeks of abstinence compared to 35% receiving CBT only), but outcomes for all three
groups were comparable at one year. For marijuana-dependent individuals, Budney,
Moore, Rocha, and Higgins (2006) found abstinence-based vouchers (i.e., CM)
were more effective at producing abstinence during the treatment period than CBT
(i.e., 50% of those assigned to CM and 40% assigned to CM plus CBT achieved at
least 6 consecutive weeks of abstinence compared to 17% assigned to CBT only),
whereas the combination of CM and CBT had the greatest effect on abstinence
through a follow-up period (i.e., 37% provided a negative urine sample at 12-month
follow-up compared to 27% assigned to CBT and 17% assigned to CM). Kadden,
Litt, Kabela-Cormier, and Petry (2007) conducted a larger study with 240 marijuana-
dependent participants, and again found that participants in the CM-only condition
had the highest rates of abstinence during the treatment period, but the combination
of CM plus CBT (which included motivational enhancement therapy) produced
the highest rates of abstinence at later follow-up periods. Additionally, our research
group conducted a similar study with marijuana-dependent young adults referred to
treatment by the criminal justice system (Carroll et al., 2006), and found virtually
identical findings to those listed above. Taken together, there is promising evidence
that CM procedures are effective for achieving initial drug abstinence, whereas the
addition of CBT may demonstrate its effect on abstinence following the completion
of treatment.
Areas Requiring Special Consideration
Training and Competence in Cognitive Behavioral Therapy

The strong evidence base for CBT and the increased emphasis on incorporating
empirically supported therapies into clinical practice has also led to greater focus on
training and dissemination. Although standard methods used to train clinicians to
use CBT in clinical efficacy trials have generally been associated with high levels of
treatment fidelity and comparatively small levels of variation in treatment delivery,
these methods (intensive didactic workshop training plus structured feedback on
supervised training cases) had not been empirically evaluated, nor are they commonly
used to train clinicians to use novel approaches (Weissman et al., 2006).
Thus, we initiated a series of studies systematically evaluating different training
strategies for clinicians wishing to learn empirically supported therapies such as
CBT by randomizing clinicians working full-time in substance abuse treatment
facilities to different training conditions. In our initial study of CBT training methods
(Sholomskas et al., 2005), 78 clinicians were assigned to one of three training
conditions: (a) review of the National Institute on Drug Abuse (NIDA) CBT
manual only (Carroll, 1998), (b) access to a Web-based training site (which included
additional frequently asked questions, role plays, and practice exercises) plus the
manual, or (c) a 3-day didactic seminar plus up to three sessions of supervision from
a CBT expert trainer based on actual session tapes submitted by the participants
(i.e., seminar plus supervision). Outcomes focused on clinician behavior and included
(a) between-group comparisons of the clinicians’ ability to demonstrate key CBT
techniques based on structured role plays administered before and after training,
and (b) scores on a CBT knowledge quiz. The videotaped role plays were scored
by independent raters, blind to the participants’ training condition as well as time
(e.g., pre- versus posttraining), on an adherence/competence ratings of specific CBT
techniques from the Yale Adherence and Competence Scale (YACS) (Carroll, Nich,
Sifry, et al., 2000).
Although all groups demonstrated improved adherence and competence scores
over time, the only training condition that reached levels of skill consistent with those
required of clinicians participating in our CBT efficacy trials was the seminar plus
supervision condition, with intermediate ratings for the Web condition. The mean
effect size for the seminar plus supervision versus manual-only condition comparisons
was consistent with a large effect (0.69), while the average effect size for the Web
versus manual-only condition contrasts was consistent with a medium size effect
(0.30). In addition, the seminar plus supervision condition was associated with
significantly more clinicians reaching criterion levels for adequate fidelity than those
assigned to the manual-only condition (54% vs. 15%).
These findings underscore that merely making manuals available to clinicians
has little enduring effect on clinicians’ ability to implement complex treatments
such as CBT. This has important implications for current efforts to disseminate
new treatments. Our findings suggest that face-to-face training followed by direct
supervision and credentialing may be essential for effective technology transfer, and
raise questions regarding whether practitioners should feel competent (from an ethical
perspective) to administer an empirically supported treatment on the basis of reading
a manual alone. Finally, the findings suggest that standard strategies used to train
clinicians in clinical trials can be effective for community based-clinicians and may be
pursued as a strategy for future dissemination trials and bridging the gap between
research and practice (Sholomskas et al., 2005).
Impaired Cognitive Functioning

Patients’ cognitive functioning is another area that may require special attention.
CBT is considered a cognitively demanding treatment, in that patients are asked to
learn a range of new concepts and skills, including monitoring and remembering
cognitions and inner states, implementing new skills while in stressful situations,
and so on. However, these demands may be particularly difficult for some patients
given the cognitive deficits associated with chronic drug use (Goldstein & Volkow,
2002; Vik, Cellucci, Jarchow, & Hedt, 2004). Although the evidence directly
linking cognitive function with treatment outcome is relatively weak, emerging data
suggest that substance users with higher levels of cognitive and neuropsychological
impairment have poorer treatment retention in CBT than those who are less impaired
(Aharonovich et al., 2006; Aharonovich, Nunes, & Hasin, 2003). Additionally,
cognitive impairment has been shown to have an effect on therapeutic mechanisms of
change, such as self-efficacy (Bates, Pawlak, Tonigan, & Buckman, 2006) and coping
skills acquisition (Kiluk, Nich, & Carroll, 2011). This suggests that clinicians should
monitor the cognitive skills of their patients, and in cases of memory, attention, or
impulse control problems, to adapt the implementation of CBT accordingly, with
slower progression through concepts, frequent repetition of material and checking
back with the patient to assess understanding, and providing more structure on
extra-session assignments.
New Developments in Cognitive Behavioral Therapy

for Drug Use
The last decade has been characterized by exponential growth in the development
of technology-based interventions for psychiatric disorders, and in particular the
creation of computer-delivered versions of CBT. Given the structure and didactic
nature of CBT, it appears to be one of the empirically supported treatments that
is more easily transferrable into a computerized format, which offers the benefits of
standardized delivery and broader access. In conjunction with our considerable efforts
toward disseminating empirically supported treatments to community substance abuse
clinics, we developed a computer-assisted version of CBT for substance use disorders,
called CBT4CBT (computer based training for cognitive behavioral therapy). The
content of CBT4CBT is based closely on our NIDA CBT manual, but is delivered in
seven sessions, or modules, and makes extensive use of the multimedia capabilities of
computers to convey CBT principles and illustrate implementation of new cognitive
and behavioral strategies (Carroll et al., 2008). That is, key CBT concepts are taught
through short movies, or vignettes, which feature engaging characters in realistic

settings confronting a number of challenging situations as well as a number of
interactive games and exercises to teach CBT strategies. In a clinical trial where
CBT4CBT was delivered in addition to standard outpatient treatment, exposure to
the program was associated with significantly fewer drug-positive urine specimens
submitted and longer durations of abstinence during treatment (Carroll et al., 2008).
In addition, data from a 6-month follow-up indicated the durability of these effects
in that the “sleeper effect” of CBT appeared to extend to its computer-based version
(Carroll et al., 2009). Finally, participants’ level of neuropsychological functioning
did not appear to be associated with outcome in the CBT4CBT program (Carroll
et al., 2011), perhaps because little or no reading of text is required, and users can
control the speed of presentation of material, can repeat material as often as they wish,
and can select the types of exercises and issues they would like to address, thereby
reducing the “cognitive load” of CBT. Although CBT4CBT and other computer-
assisted programs have great potential to make empirically supported therapies more
widely available and to broaden the base of substance abuse treatment, and some of
the early data on their effectiveness is very encouraging, substantially more testing and
evaluation is needed before they can be widely distributed (Kiluk, Sugarman, et al.,
2011).
Another recent development has been a greater understanding of how CBT works
to reduce patients’ rates of substance use (i.e., the mechanisms of action). As described
earlier, coping skills training is one of the defining features of CBT for substance
use disorders; however, statistical demonstration that the acquisition of coping skills
serves to mediate the effect of CBT has been elusive (Morgenstern & Longabaugh,
2000). There is evidence to suggest that CBT does improve patients’ coping skills
(Carroll, Nich, Frankforter, & Bisighini, 1999), and an improvement in coping
skills is associated with better treatment outcomes (Carroll, Nich, Ball, et al., 2000;
Litt, Kadden, Cooney, & Kabela, 2003), but these relationships had never been
demonstrated in a model supporting mediation. However, in one of our recently
completed trials examining CBT4CBT, the quality of skills rather than the sheer
number of skills acquired by patients was found to mediate CBT’s effects on reducing
drug use (Kiluk, Nich, Babuscio, & Carroll, 2010). This is not only significant for
being the first study to demonstrate coping skills as a mediator, but also because of
the finding that the quality of skills acquired may be more important than the quantity
of skills for reducing substance use. This indicates a need for greater focus on the
therapist methods for teaching coping skills, and further highlights the benefits of
multimedia skills training offered by computerized interventions, such as CBT4CBT.
Lastly, given the association between impaired cognitive function and poor out-
comes in CBT for substance use disorders, there have been recent attempts at
incorporating interventions aimed at improving cognitive function. Although the
evidence is mixed, there is some indication that computer-assisted cognitive rehabil-
itation (CACR) designed to enhance cognitive skills may be effective at improving
treatment retention and outcomes among substance users (Grohman, Fals-Stewart, &
Donnelly, 2006). CACR has strong support for improving various aspects of cognitive
function among patients diagnosed with schizophrenia (Medalia & Choi, 2009), yet
more research is needed to determine if this approach can be effective at improving
the cognitive function of chronic drug users, and if it could be useful as a primer
for a cognitively demanding treatment, such as CBT. Another recently developed
method for targeting the cognitive function of drug users is through pharmacologic
intervention. For instance, galantamine, a reversible and competitive inhibitor of
acetylcholinesterase used clinically for the treatment of Alzheimer’s dementia, has
shown some promising evidence as a potential cognitive enhancer among drug users,
particularly at improving sustained attention (Sofuoglu & Carroll, 2011; Sofuoglu,
Waters, Poling, & Carroll, 2011). Although this line of research is still in its infancy,
pharmacologic interventions could become a useful method for enhancing cognitive
function among drug users, which in turn may reduce the early treatment dropout in
CBT associated with cognitive deficits.
Summary
CBT for illegal drug use is an empirically supported behavioral approach that has
strong theoretical and empirical support in a variety of substance-abusing popula-
tions, and can be combined and integrated effectively with a range of other empirically
supported behavioral therapies (e.g., motivational enhancement, contingency man-
agement) as well as pharmacotherapies. CBT also appears to be particularly durable,
an important feature among treatments for illegal drug use, which is characterized by
frequent patterns of relapse. CBT for illegal drug use is relatively brief, and is highly
structured, but also requires therapist flexibility in order to individualize treatment
strategies/techniques to match patient characteristics. Attempts to disseminate this
empirically supported treatment have produced a range of practical resources (e.g.,
books, videotapes, manuals, training resources and programs) for implementing them
effectively in clinical practice, and data from recent trials evaluating computer-assisted
versions of CBT have been promising. Thus, due to its comparatively strong evidence
base, flexibility, broad applicability across a range of patient types and settings, and
durability, CBT for illegal drug use should be a component of all substance abuse
clinicians’ repertoire.
Acknowledgements
Support was provided by NIDA grants P50 DA09241, U10 DA13038, R37 DA15969
and K05-DA00457.
References
Aharonovich, E., Hasin, D. S., Brooks, A. C., Liu, X., Bisaga, A., & Nunes, E. V. (2006).
Cognitive deficits predict low treatment retention in cocaine dependent patients. Drug
and Alcohol Dependence, 81, 313–322. doi:10.1016/j.drugalcdep.2005.08.003
Aharonovich, E., Nunes, E. V., & Hasin, D. (2003). Cognitive impairment, retention and
abstinence among cocaine abusers in cognitive-behavioral treatment. Drug and Alcohol
Dependence, 71, 207–211. doi:10.1016/S0376-8716(03)00092-9
Babor, T. F. (2004). Brief treatments for cannabis dependence: Findings from a ran-
domized multisite trial. Journal of Consulting and Clinical Psychology, 72, 455–466.
doi:10.1037/0022-006X.72.3.455
Baker, A., Lee, N. K., Claire, M., Lewin, T. J., Grant, T., Pohlman, S., … Carr, V. J. (2005).
Brief cognitive behavioural interventions for regular amphetamine users: A step in the
right direction. Addiction, 100, 367–378. doi:0.1111/j.1360-0443.2005.01002.x
Bates, M. E., Pawlak, A. P., Tonigan, J. S., & Buckman, J. F. (2006). Cognitive impairment
influences drinking outcome by altering therapeutic mechanisms of change. Psychology of
Addictive Behavior, 20, 241–253. doi:10.1037/0893-164X.20.3.241
Budney, A. J., Moore, B. A., Rocha, H. L., & Higgins, S. T. (2006). Clinical trial of abstinence-
based vouchers and cognitive-behavioral therapy for cannabis dependence. Journal of
Bux, D. A., Jr., & Irwin, T. W. (2006). Combining motivational interviewing and
cognitive-behavioral skills training for the treatment of crystal methamphetamine
abuse/dependence. Journal of Gay & Lesbian Psychotherapy, 10, 143–152. doi:10.1300/
J236v10n03_13
Carroll, K. M. (1998). A cognitive-behavioral approach: Treating cocaine addiction. Rockville,
MD: NIDA.
Carroll, K. M. (2011a). Cognitive-behavioral therapies. In M. Galanter & H. D. Kleber (Eds.),
Psychotherapy for the treatment of substance abuse (pp. 175–192). Arlington, VA: American
Psychiatric Publishing.
Carroll, K. M. (2011b). Cognitive behavioral therapy. In P. Ruiz & E. C. Strain (Eds.),
Lowinsohn & Ruiz’s substance abuse: A comprehensive textbook (5th ed., pp. 593–602).
Philadelphia, PA: Lippincott Williams & Wilkins.
Carroll, K. M., Ball, S. A., Martino, S., Nich, C., Babuscio, T., Gordon, M. A., … Roun-
saville, B. J. (2008). Computer-assisted cognitive-behavioral therapy for addiction. A
randomized clinical trial of CBT4CBT. American Journal of Psychiatry, 165, 881–888.
doi:10.1176/appi.ajp.2008.07111835
Carroll, K. M., Ball, S. A., Martino, S., Nich, C., Babuscio, T. A., & Rounsaville, B. J.
(2009). Enduring effects of a computer-assisted training program for cognitive-behavioral
therapy: A six-month follow-up of CBT4CBT. Drug and Alcohol Dependence, 100,
178–181. doi:10.1016/j.drugalcdep.2008.09.015
Carroll, K. M., Easton, C. J., Nich, C., Hunkele, K. A., Neavins, T. M., Sinha, R., …
Rounsaville, B. J. (2006). The use of contingency management and motivational/skills-
building therapy to treat young adults with marijuana dependence. Journal of Consulting
and Clinical Psychology, 74, 955–966. doi:10.1037/0022-006X.74.5.955
Carroll, K. M., Fenton, L. R., Ball, S. A., Nich, C., Frankforter, T. L., Shi, J., … Rounsaville,
B. J. (2004). Efficacy of disulfiram and cognitive-behavioral therapy in cocaine-dependent
outpatients: A randomized placebo controlled trial. Archives of General Psychiatry, 64,
264–272. doi:10.1001/archpsyc.61.3.264
Carroll, K. M., Kiluk, B. D., Nich, C., Babuscio, T. A., Brewer, J., Potenza, M., … Lejuez,
C. W. (2011). Cognitive function and treatment response in a randomized clinical trial
of computer-based training for cognitive behavioral therapy (CBT4CBT). Substance Use
and Misuse, 46, 23–34. doi:10.3109/10826084.2011.521069
Carroll, K. M., Nich, C., & Ball, S. A. (2005). Practice makes progress: Homework assignments
and outcome in the treatment of cocaine dependence. Journal of Consulting and Clinical
Psychology, 73, 749–755. doi:10.1037/0022-006X.73.4.749
Carroll, K. M., Nich, C., Ball, S. A., McCance-Katz, E. F., Frankforter, T. F., & Rounsaville,
B. J. (2000). One year follow-up of disulfiram and psychotherapy for cocaine-alcohol
abusers: Sustained effects of treatment. Addiction, 95, 1335–1349. doi:10.1046/j.1360-

0443.2000.95913355.x
Carroll, K. M., Nich, C., Ball, S. A., McCance-Katz, E., & Rounsaville, B. J. (1998). Treatment
of cocaine and alcohol dependence with psychotherapy and disulfiram. Addiction, 93,
713–728. doi:10.1046/j.1360-0443.1998.9357137.x
Carroll, K. M., Nich, C., Frankforter, T. L., & Bisighini, R. M. (1999). Do patients change in
the way we intend? Treatment-specific skill acquisition in cocaine-dependent patients using
the Cocaine Risk Response Test. Psychological Assessment, 11, 77–85. doi:10.1037/1040-
3590.11.1.77
Carroll, K. M., Nich, C., Sifry, R., Frankforter, T., Nuro, K. F., Ball, S. A., … Rounsaville,
B. J. (2000). A general system for evaluating therapist adherence and competence in
psychotherapy research in the addictions. Drug and Alcohol Dependence, 57 , 225–238.
doi:10.1016/S0376-8716(99)00049-6
Carroll, K. M., Rounsaville, B. J., & Gawin, F. H. (1991). A comparative trial of
psychotherapies for ambulatory cocaine abusers: Relapse prevention and interper-
sonal psychotherapy. American Journal of Drug and Alcohol Abuse, 17 , 229–247.
doi:10.3109/00952999109027549
Carroll, K. M., Rounsaville, B. J., Gordon, L. T., Nich, C., Jatlow, P. M., Bisighini,
R. M., … Gawin, F. H. (1994). Psychotherapy and pharmacotherapy for ambulatory
cocaine abusers. Archives of General Psychiatry, 51, 177–197. doi:10.1001/archpsyc.
1994.03950030013002
Carroll, K. M., Rounsaville, B. J., Nich, C., Gordon, L. T., Wirtz, P. W., & Gawin, F.
H. (1994). One year follow-up of psychotherapy and pharmacotherapy for cocaine
dependence: Delayed emergence of psychotherapy effects. Archives of General Psychiatry,
51, 989–997. doi:10.1001/archpsyc.1994.03950120061010
Copeland, J., Swift, W., Roffman, R., & Stephens, R. (2001). A randomized controlled trial
of brief cognitive behavioral interventions for cannabis use disorder. Journal of Substance
Abuse Treatment, 21, 55–64. doi:10.1016/S0740-5472(01)00179-9
Cowan, M. J., Freedland, K. E., Burg, M. M., Saab, P. G., Youngblood, M. E., Cornell,
C. E., … Czajkowski, S. M. (2007). Predictors of treatment response for depression and
inadequate social support: The ENRICHD randomized clinical trial. Psychotherapy and
Psychosomatics, 77 , 27–37. doi:10.1159/000110057
Craske, M. G. (2010). Cognitive-behavioral therapy. Washington, DC: American Psychological
Association.
Dennis, M., Godley, S. H., Diamond, G., Tims, F. M., Babor, T., Donaldson, J.,
… Funk, R. (2004). The Cannabis Youth Treatment (CYT) study: Main findings
from two randomized trials. Journal of Substance Abuse Treatment, 27 , 197–213.
doi:10.1016/j.jsat.2003.09.005
Edelman, R. E., & Chambless, D. L. (1995). Adherence during sessions and homework in
cognitive-behavioral group treatment of social phobia. Behaviour Research and Therapy,
33, 573–577. doi:10.1016/0005-7967(94)00068-U
Epstein, D. E., Hawkins, W. E., Covi, L., Umbricht, A., & Preston, K. L. (2003). Cogni-
tive behavioral therapy plus contingency management for cocaine use: Findings during
treatment and across 12-month follow-up. Psychology of Addictive Behaviors, 17 , 73–82.
doi:10.1037/0893-164X.17.1.73
Farabee, D., Rawson, R. A., & McCann, M. J. (2002). Adoption of drug avoidance strategies
among patients in contingency management and cognitive-behavioral treatments. Journal
of Substance Abuse Treatment, 23, 343–350. doi:10.1016/S0740-5472(02)00297-0
Freeman, A. (2007). The use of homework in cognitive behavior therapy: Working with
complex anxiety and insomnia. Cognitive and Behavioral Practice, 14, 261–267.
doi:10.1016/j.cbpra.2006.10.005
Goldstein, R., & Volkow, N. D. (2002). Drug addiction and its underlying neurobiological
basis: Neuroimaging evidence for the involvement of the frontal cortex. American Journal
Gonzalez, V. M., Schmitz, J. M., & DeLaune, K. A. (2006). The role of homework in
cognitive-behavioral therapy for cocaine dependence. Journal of Consulting and Clinical
Psychology, 74, 633–637. doi:10.1037/0022-006X.74.3.633
Grohman, K., Fals-Stewart, W., & Donnelly, K. (2006). Improving treatment response of cog-
nitively impaired veterans with neuropsychological rehabilitation. Brain and Cognition,
60, 203–204.
Kadden, R., Carroll, K. M., Donovan, D., Cooney, J. L., Monti, P., Abrams, D., … Hester, R.
(1992). Cognitive-behavioral coping skills therapy manual: A clinical research guide for
therapists treating individuals with alcohol abuse and dependence. Rockville, MD: NIAAA.
Kadden, R. M., Litt, M. D., Kabela-Cormier, E., & Petry, N. M. (2007). Abstinence rates
following behavioral treatments for marijuana dependence. Addictive Behaviors, 32,
1220–1236. doi:10.1016/j.addbeh.2006.08.009
Kiluk, B. D., Nich, C., Babuscio, T., & Carroll, K. M. (2010). Quantity vs. quality: Acquisition
of coping skills following computerized cognitive behavioral therapy for substance use
disorders. Addiction, 105, 2120–2127. doi:10.1111/j.1360-0443.2010.03076.x
Kiluk, B. D., Nich, C., & Carroll, K. M. (2011). Relationship of cognitive function and the
acquisition of coping skills in computer assisted treatment for substance use disorders.
Drug & Alcohol Dependence, 114, 169–176. doi:10.1016/j.drugalcdep.2010.09.019
Kiluk, B. D., Sugarman, D., Nich, C., Gibbons, C. J., Martino, S., Rounsaville, B. J., … Carroll,
K. M. (2011). A methodological analysis of randomized clinical trials of computer-assisted
therapies for psychiatric disorders: Towards improved standards for an emerging field.
Lee, N. K., & Rawson, R. A. (2008). A systematic review of cognitive and behavioural
therapies for methamphetamine dependence. Drug and Alcohol Review, 27 , 309–317.
doi:10.1080/09595230801919494
Litt, M. D., Kadden, R. M., Cooney, N. L., & Kabela, E. (2003). Coping skills and treatment
outcomes in cognitive behavioral and interactional group therapy for alcoholism. Journal
of Consulting and Clinical Psychology, 71, 118–128. doi:10.1037/0022-006X.71.1.118
Lussier, J. P., Heil, S. H., Mongeon, J. A., Badger, G. J., & Higgins, S. T. (2006). A meta-
analysis of voucher-based reinforcement therapy for substance use disorders. Addiction,
101, 192–203. doi:10.1111/j.1360-0443.2006.01311.x
Magill, M., & Ray, L. A. (2009). Cognitive-behavioral treatment with adult alcohol and illicit
drug users: A meta-analysis of randomized controlled trials. Journal of Studies on Alcohol
and Drugs, 70, 516–527.
Marlatt, G. A., & Donovan, D. M. (2005). Relapse prevention: Maintenance strategies in the
treatment of addictive behaviors (2nd ed.). New York, NY: Guilford Press.
McKee, S. A., Carroll, K. M., Sinha, R., Robinson, J. E., Nich, C., Cavallo, D., …
O’Malley, S. (2007). Enhancing brief cognitive-behavioral therapy with motivational
enhancement techniques in cocaine users. Drug and Alcohol Dependence, 91, 97–101.
doi:10.1016/j.drugalcdep.2007.05.006
Medalia, A., & Choi, J. (2009). Cognitive remediation in schizophrenia. Neuropsychology
Review, 19, 353–364. doi:10.1007/s11065-009-9097-y
Meichenbaum, D. H. (1995). Cognitive-behavioral therapy in historical perspective. In

B. M. Bongar & L. E. Beutler (Eds.), Comprehensive textbook of psychotherapy: Theory
and practice (pp. 140–158). New York, NY: Oxford University Press.
Miller, W. R., Yahne, C. E., & Tonigan, J. S. (2003). Motivational interviewing in drug abuse
services: A randomized trial. Journal of Consulting and Clinical Psychology, 71, 754–763.
doi:10.1037/0022-006X.71.4.754
Miller, W. R., Zweben, A., DiClemente, C. C., & Rychtarik, R. G. (1992). Motivational
enhancement therapy manual: A clinical research guide for therapists treating individuals
with alcohol abuse and dependence. Rockville, MD: NIAAA.
Morgenstern, J., & Longabaugh, R. (2000). Cognitive-behavioral treatment for alcohol depen-
dence: A review of the evidence for its hypothesized mechanisms of action. Addiction, 95,
1475–1490. doi:10.1046/j.1360-0443.2000.951014753.x
Morgenstern, J., Morgan, T. J., McCrady, B. S., Keller, D. S., & Carroll, K. M. (2001). Manual-
guided cognitive behavioral therapy training: A promising method for disseminating
empirically supported substance abuse treatments to the practice community. Psychology
of Addictive Behaviors, 15, 83–88. doi:10.1037/0893-164X.15.2.83
Parrish, D. E. (2009). Cognitive behavioral coping skills therapy for adults. In D. W. Springer
& A. Rubin (Eds.), Substance abuse treatment for youth and adults: Clinician’s guide to
evidence-based practice (pp. 259–310). Hoboken, NJ: John Wiley & Sons, Inc.
Petry, N. M., Alessi, S. M., Carroll, K. M., Hanson, T., McKinnon, S., Rounsaville, B. J., …
Sierra, S. (2006). Contingency management treatments: Reinforcing abstinence versus
adherence with goal-related activities. Journal of Consulting and Clinical Psychology, 74,
592–601. doi:10.1037/0022-006X.74.3.592
Pollack, M. H., Penava, S. A., Bolton, E., Worthington, J. J., III, Allen, G. L., Farach, F. J., …
Otto, M. W. (2002). A novel cognitive-behavioral approach for treatment-resistant drug
dependence. Journal of Substance Abuse Treatment, 23, 335–342. doi:10.1016/S0740-
5472(02)00298-2
Prendergast, M., Podus, D., Finney, J. W., Greenwell, L., & Roll, J. M. (2006). Contingency
management for treatment of substance use disorders: A meta-analysis. Addiction, 101,
1546–1560. doi:10.1111/j.1360-0443.2006.01581.x
Rawson, R. A., Huber, A., McCann, M., Shoptaw, S., Farabee, D., Reiber, C., … Ling, W.
during methadone maintenance treatment for cocaine dependence. Archives of General
Psychiatry, 59, 817–824. doi:10.1001/archpsych.59.9.817
Rawson, R. A., McCann, M. J., Flammino, F., Shoptaw, S., Miotto, K., Reiber, C., … Ling, W.
for stimulant-dependent individuals. Addiction, 101, 267–274. doi:10.1111/j.1360-
0443.2006.01312.x
Rohsenow, D. J., Monti, P. M., Martin, R. A., Colby, S. M., Myers, M. G., Gulliver,
S. B., … Abrams, D. B. (2004). Motivational enhancement and coping skills train-
ing for cocaine abusers: Effects on substance use outcomes. Addiction, 99, 862–874.
doi:10.1111/j.1360-0443.2004.00743.x
Rotgers, F. (2012). Cognitive-behavioral theories of substance abuse. In S. T. Walters & F.
Rotgers (Eds.), Treating substance abuse: Theory and technique (3rd ed., pp. 113–137).
Scheinmann, R., Hagan, H., Lelutiu-Weinberger, C., Stern, R., Des Jarlais, D. C., Flom,
P. L., … Strauss, S. (2007). Non-injection drug use and hepatitis C virus: A systematic
review. Drug and Alcohol Dependence, 89, 1–12. doi:10.1016/j.drugalcdep.2006.

11.014
Schmitz, J. M., Averill, P., Sayre, S., McCleary, P., Moeller, F. G., & Swann, A. (2002).
Cognitive-behavioral treatment of bipolar disorder and substance abuse: A preliminary
randomized study. Addictive Disorders & Their Treatment, 1, 17–24.
Schmitz, J. M., Stotts, A. L., Rhoades, H. M., & Grabowski, J. (2001). Naltrexone and relapse
prevention treatment for cocaine-dependent patients. Addictive Behaviors, 26, 167–180.
doi:10.1016/S0306-4603(00)00098-8
Sholomskas, D., Syracuse, G., Ball, S. A., Nuro, K. F., Rounsaville, B. J., & Carroll, K. M.
(2005). We don’t train in vain: A dissemination trial of three strategies for training
clinicians in cognitive behavioral therapy. Journal of Consulting and Clinical Psychology,
73, 106–115. doi:10.1037/0022-006X.73.1.106
Sobell, L. C., & Sobell, M. B. (2011). Group therapy for substance use disorders: A motivational
cognitive-behavioral approach. New York, NY: Guilford Press.
Sofuoglu, M., & Carroll, K. M. (2011). Effects of galantamine on cocaine use in chronic
cocaine users. American Journal on Addictions, 20, 302–303. doi:10.1111/j.1521-
0391.2011.00130.x
Sofuoglu, M., Waters, A. J., Poling, J., & Carroll, K. M. (2011). Galantamine improves sus-
tained attention in chronic cocaine users. Experimental and Clinical Psychopharmacology,
19, 11–19. doi:10.1037/a0022213
Vik, P. W., Cellucci, T., Jarchow, A., & Hedt, J. (2004). Cognitive impairment in
substance abuse. Psychiatric Clinics of North America, 27 , 97–109. doi:10.1016/S0193-
953X(03)00110-2
Weissman, M. M., Verdeli, H., Gameroff, M. J., Bledsoe, S. E., Betts, K., Mufson, L., …
Wickramaratne, P. (2006). National survey of psychotherapy training in psychiatry,
psychology, and social work. Archives of General Psychiatry, 63, 925–934. doi:10.1001/
archpsyc.63.8.925
Woody, G. E., Donnell, D., Seage, G. R., Metzger, D., Marmor, M., Koblin, B. A., …
Judson, F. N. (1999). Non-injection substance use correlates with risky sex among men
having sex with men: Data from HIVNET. Drug and Alcohol Dependence, 53, 197–205.
doi:10.1016/S0376-8716(98)00134-3
57
Gambling
Jon E. Grant
University of Chicago, United States
Brian L. Odlaug
University of Copenhagen, Denmark
Christopher Donahue
University of Minnesota, United States
Gambling is a lucrative industry, with over $34 billion in gross gaming revenue
captured by the commercial casino industry of the United States in 2010 (American
Gaming Association, 2012). Although the majority of individuals who gamble report
no significant financial consequences associated with their gaming, an estimated
0.4–5.3% worldwide have a problematic or pathological form of gambling behavior
(Bakken, Götestam, Gråwe, Wenzel, & Øren, 2009; Cunningham-Williams, Cottler,
Compton, & Spitznagel, 1998; Odlaug & Grant, 2010; Petry & Armentano, 1999;
Shaffer, Hall, & Vander Bilt, 1999; Toce-Gerstein, Gerstein, & Volberg, 2009;
Wardle et al., 2007). According to the Diagnostic and Statistical Manual of Mental
Disorders (5th ed.; DSM-5), gambling disorder or “pathological” gambling (PG)
is defined by a repetitive engagement in gambling behavior resulting in significant
financial, occupational, and/or psychosocial dysfunction (American Psychiatric Asso-
ciation, 2013). For these individuals, a multitude of viable and efficacious therapeutic
interventions have been developed. Understanding the clinical characteristics of these
individuals may aid the clinician and researcher in the advancement of existing and
new treatment approaches for this population.
Clinical Characteristics
PG usually begins in adolescence or early adulthood, with males tending to start at

an earlier age (Ibáñez, Blanco, & Sáiz-Ruiz, 2002; Shaffer et al., 1999). Although
prospective studies are largely lacking, PG appears to follow a trajectory similar

DOI: 10.1002/9781118528563.wbcbt57
to that of substance dependence, with high rates in adolescent and young adult
groups, lower rates in older adults, and periods of abstinence and relapse (Grant,
2008).
Individuals with PG suffer significant impairment in their ability to function socially
and in their occupations. Many individuals report intrusive thoughts and urges
related to gambling that interfere with their ability to concentrate at home and
at work (Grant & Kim, 2001). Work-related problems such as absenteeism, poor
performance, and job loss are common (National Opinion Research Center, 1999).
The inability to control behavior that a person does not want to engage in may lead
to feelings of shame and guilt (Grant & Kim, 2001). PG is also frequently associated
with marital problems and diminished intimacy and trust within the family (Grant
& Kim, 2001). PG is also associated with greater health problems (for example,
cardiac problems, liver disease) and increased use of medical services (Morasco et al.,
2006).
For the Clinician

Gambling symptomology is similar to that seen in substance use disorders, with a
higher male preponderance, symptoms of tolerance and withdrawal, and low rates
of treatment-seeking. The clinician must be aware of the significant psychosocial
problems often associated with PG, including marital, occupational, and financial
issues, and acknowledge these concerns with the client.
Neurocognition
Cognitive distortions are common in PG and are a primary target for cognitive
therapy. A variety of different misperceptions or illusions of control are often
associated with PG, including the “near miss” (the belief that an outcome close to
a win means that a win is imminent), active illusory control (superstitions or lucky
objects will promote winning), passive illusory control (luck is the key factor in
success), and memory biases (remembering wins, forgetting losses) (Clark, 2012;
Myrseth, Brunborg, & Eldem, 2010). These distortions correlate with the gambler’s
tendency to seek immediate reward through risky decision making and have been
physiologically illustrated in several functional brain imaging studies (Balodis et al.,
2012; Chase & Clark, 2010; Potenza et al., 2003).
Neurocognitive assessments testing aspects of executive functioning, including
working memory, response inhibition, attention, visual perception, and cognitive
flexibility, have yielded conflicting results in pathological gamblers (Forbush et al.,
2008; Goudriaan, Oosterlaan, de Beurs, & Van den Brink, 2004). Results of cognitive
testing on inhibitory control, however, suggest dysfunction in the ventromedial
prefrontal cortex, potentially explaining the risky decision-making and loss-chasing
behavior characteristic of PG (Cavedini, Riboldi, Keller, D’Annucci, & Bellodi, 2002;
Clark, 2010; Clark et al., 2008; Odlaug, Chamberlain, Kim, Schreiber, & Grant,
2010).
Gambling 1361
For the Clinician

Clinicians must be aware of the wide array of cognitive distortions often present
in those presenting for PG treatment. Properly identifying and addressing these
distortions early in treatment is of vital importance to the gambler’s engagement in
other aspects of therapy. For example, gamblers often believe that they are “due”
for a win and the therapist must explain that their odds of winning are no more
likely after 50 losses than after one loss. Furthermore, given the high reward-seeking
tendencies and sensation-seeking behaviors in PG, it is important to educate patients
about the potential for addiction transference if they stop or reduce their gambling
behavior. Teaching patients to recognize the signs and symptoms in the development
of other problematic behaviors (such as compulsive shopping, drinking, sex, etc.) is
important for global and sustained life improvement.
Gender Differences
Not all pathological gamblers display the same clinical presentation, and several
studies have found that significant clinical differences exist between male and female
pathological gamblers. Research indicates that men present with a gambling problem
at a 2:1 male-to-female ratio and being male is actually a risk factor for the development
of a gambling problem (Johansson, Grant, Kim, Odlaug, & Götestam, 2009),
although the type of gambling engaged in generally differs between genders (Grant
& Kim, 2001; National Opinion Research Center, 1999; Odlaug, Marsh, Kim, &
Grant, 2011; Potenza et al., 2001). Males have higher rates of strategic gambling
preferences (e.g., poker, blackjack, sports/track betting) while women have higher
rates of nonstrategic gambling (primarily slot machines) (Odlaug et al., 2011; Potenza,
Maciejewski, & Mazure, 2006; Stevens & Young, 2010). Men are also more likely to
be single and living alone, are more likely to have received treatment for substance
abuse in the past, and have more antisocial personality traits compared to females
with PG who are much more likely to seek treatment for a gambling problem, present
with more depressive symptoms, and have poorer self-esteem (Crisp et al., 2004;
Echeburúa, González-Ortega, de Corral, & Polo-López, 2011; Feigelman, Wallisch,
& Lesieur, 1998; Ingle, Marotta, McMillan, & Wisdom, 2008; Ladd & Petry, 2002;
Weinstock et al., 2011).
For the Clinician

Clinicians must be aware of the phenomenon of telescoping—where women start
to gamble later in life but progress to a pathologic state at a faster rate than males
(Tavares et al., 2003). Clinically and from a public health perspective, it may be
advantageous to encourage formal treatment for women presenting with a “gambling
problem” later in life as they may be more likely to develop a pathologic form of
gambling faster than their male counterparts. It is important to note, however, that
PG in both men and women is associated with a variety of mental and physical health
consequences, such as depression, anxiety, and heart and liver problems, that should
not be discounted in a treatment setting (Afifi, Cox, Martens, Sareen, & Enns, 2010;
Bergh & Kühlhorn, 1994; Erickson, Molina, Ladd, Pietrzak, & Petry, 2005; Germain
et al., 2011; Morasco et al., 2006).
Finances
It is not surprising, given that the means of gambling is monetary, that financial
consequences are commonplace among individuals seeking treatment for problem
gambling. Bankruptcy, defaulting on credit cards, mortgage foreclosures, delinquent
bank loans, and medical costs coupled with illegal behaviors to fund gambling
behavior or to repay debt, such as bad checks, embezzlement, and theft, are common
in PG (Blaszczynski & McConaghy, 1989; Grant & Kim, 2001; Grant & Potenza,
2007; Grant, Schreiber, Odlaug, & Kim, 2010; Ledgerwood, Weinstock, Morasco,
& Petry, 2007; Lesieur, 1979; National Opinion Research Center, 1999; Potenza,
Steinberg, McLaughlin, Rounsaville, & O’Malley, 2000).
For the Clinician

Since financial pressures are common in PG (and may actually prompt the individual
to seek treatment), the incorporation of aspects of financial counseling into treatment,
such as budgeting and spending, should be considered. It is important, however, that
the therapist not engage in formal financial counseling with the patient. Encouraging
the patient to develop a weekly or monthly budget, track income/expenses, and
involve a family member or friend in helping them to manage finances are therapeutic
aspects that the therapist should engage in with the patient. Further, given over-
whelming debt, gamblers may erroneously believe that the only way of “digging out
of the hole” is to gamble more. Discussing these thoughts with the patient and having
referrals to available financial counseling resources is of vital importance and should
be addressed with the patient. The importance of addressing the often overwhelming
financial burden associated with PG should not be underestimated.
Comorbidity
Psychiatric comorbidity is the rule, not the exception, in PG (Chou & Afifi, 2011), and
this comorbidity often needs to be addressed either simultaneously or sequentially
when treating PG. PG has been associated with increased rates of co-occurring
substance use disorders (including nicotine dependence), with the highest mean
prevalence for nicotine dependence (60.1%; McGrath & Barrett, 2009) followed by
a substance use disorder (57.5%; Lorains, Cowlishaw, & Thomas, 2011).
Other studies examining the rates of co-occurring psychiatric disorders in
pathological gamblers have reported mood (37.9%), anxiety (37.4%), attention-
deficit/hyperactivity (25%), and impulse control disorders (22.9%) (most commonly
compulsive sexual behavior) (Bakken et al., 2009; Grall-Bronnec et al., 2011; Grant
Gambling 1363
& Kim, 2001; Lorains et al., 2011). Rates of bipolar disorder may be two to three
times higher in pathological gamblers than those without gambling problems (Edens
& Rosenheck, 2011). Generally lacking from these studies, however, is whether the
co-occurring disorder is secondary to the gambling, a trigger for the gambling, or
simply an independent health issue.
Gambling is often associated with significant and chronic physical health conditions
as well (Afifi et al., 2010; Bergh & Kühlhorn, 1994; Erickson et al., 2005; Germain
et al., 2011; Morasco et al., 2006). Higher than average rates of coronary heart disease
(39.8%), arthritis (30.1%), and obesity (32.0%) have been found in individuals with
PG (Desai, Desai, & Potenza, 2007). Consequently, and given the high prevalence
of, and potential for, serious health problems in PG, encouraging the patient to visit
a primary care physician for preventative medical care is important.
For the Clinician

Although co-occurring mental health disorders are common among pathological
gamblers, there is very little evidence to guide treatment approaches for the dually
diagnosed client. Should gambling be treated first or simultaneously with the co-
occurring disorder? Research on individuals in gambling treatment centers has found
that PG is associated with high rates of suicide ideation and attempts (Ledgerwood
& Petry, 2004; Wong, Chan, Conwell, Conner, & Yip, 2010). Clinicians need
to screen for suicidal ideation and if necessary address that before working on
the gambling problem. In the case of co-occurring bipolar disorder, active manic
symptoms may interfere with gambling treatment (e.g., not coming to appointments
or doing the homework, being unable to track discussion during therapy, getting into
legal troubles). Drug and alcohol use may also negatively influence decision making,
often worsen impulsivity, and prevent full compliance with gambling treatment.
Recent research indicates that although alcohol use may decrease during treatment,
risky drinking practices are present in a substantial number (31%) of gamblers
posttreatment, endorsing the need to address drinking practices during treatment
(Rash, Weinstock, & Petry, 2011). Thus, clinicians must assess for mood and
substance use at the initial evaluation as well as during treatment. Mood and
substance use may need to be addressed through other means such as hospitalization,
medication intervention, detoxification, or residential treatment. Likewise, given the
high prevalence of physical ailments in PG, clinicians should encourage the client to
seek medical health care for the screening and treatment of chronic health conditions.
Adolescent Gambling
Prevalence studies show gambling’s popularity among adolescents and young adults.
A recent study of over 15,000 eighth-graders found that 33% of boys and 17%
of girls had gambled in the past 3 months (Chaumeton, Ramowski, & Nystrom,
2011). Like their adult counterparts, most youth who gamble do so responsibly. For
a small number, however, gambling becomes excessive and results in a number of
short- and long-term consequences—early school dropout, neglect of peers, poor
mental and physical health, delinquency, and legal problems (Yip et al., 2011).
Prevalence research indicates that the rate of problem gambling among adolescents
and young adults (3.4–7.4%) is typically greater than that of older adults (Caillon,
Grall-Bronnec, Bouju, Lagadec, & Vénisse, 2012; Derevensky & Gupta, 2000; Shaffer
& Hall, 1996; Splevins, Mireskandari, Clayton, & Blaszczynski, 2010). Research has
found that traits such as sensation-seeking and high levels of disinhibition have been
associated with the prediction of problem gambling in youth (Gupta, Deverensky,
& Ellenbogen, 2006). Adolescent gambling has also been associated with parental
gambling behavior, susceptibility to peer pressure, conduct problems, binge drinking,
and drug use (Chalmers & Willoughby, 2006; Langhinrishsen-Rohling, Rohde,
Seeley, & Rohling, 2004). There is also speculation that electronic forms of gambling,
such as Internet-based gambling, may be particularly problematic for youth (Potenza
et al., 2011).
Co-occurring problems in adolescent gamblers mirror those found in adults. Ado-
lescent problem gamblers have high rates of depression (Gupta et al., 2006), suicidal
ideation (Gupta & Derevensky, 1998), anxiety (Ste-Marie, Gupta, & Dereven-
sky, 2006), substance abuse (Barnes, Welte, Hoffman, & Tidwell, 2011; Gupta &
Derevensky, 1998), and attention-deficit/hyperactivity disorder (Breyer et al., 2009).
Although there is no empirically validated treatment protocol specifically designed
for youth gamblers, a limited number of treatment studies have reported success in
using approaches known to be helpful for adults with PG. One study examining CBT
(17 sessions) in four male adolescent gamblers reported that three of the adolescents
remained abstinent for 3 to 6 months following treatment (Ladouceur, Boisvert,
& Dumont, 1994). Treatment facilities such as the International Center for Youth
Gambling report using an approach similar to that used for adults—functional assess-
ment, assessing motivation to change, goal setting, working on cognitive distortions,
improving coping skills, and building interpersonal relationships.
Because youth are active online and use the Internet for social networking and
recreation, some researchers are examining Internet-based therapy and guided inter-
ventions. Research has demonstrated that online therapeutic support is perceived to
be acceptable and useful by youth (Monaghan & Wood, 2010). Research has also
demonstrated positive effects for Internet-based interventions for adolescents with
nicotine or alcohol problems (Abroms, Windsor, & Simons-Morton, 2008; Walters,
Miller, & Chiauzzi, 2005; Walters, Wright, & Shegog, 2005), but there is little
empirical evidence supporting their use for gambling-related problems in adolescents.
One examination of an Internet-based service offering individual and group chats
with topics focusing on various gambling-related problems found that the adolescents
who visited the site found the information and help to be valuable (Gainsbury, 2011).
For the Clinician

Given evidence of the rise of nontraditional gambling forums such as the Internet,
all forms of gambling, including Internet gambling, must be broached with the
client. Although a substantial proportion of adolescents and young adults report
symptoms consistent with older adult problem gambling, few youth seek treatment.
This may suggest that traditional services are failing to help this vulnerable population
Gambling 1365
and, although no validated treatments exist specifically for adolescents, CBT and
Internet-based therapeutic support have demonstrated promise in youth gambling
treatment. Like adults, adolescent gambling is associated with high rates of psychiatric
comorbidity. The clinician must screen for this and be vigilant of mood and anxiety
changes throughout the course of therapy.
Clinical Assessment: An Overview
The assessment of individuals with probable PG begins with the identification of

other mental health concerns, including addictions, that may be potentially causing
and/or contributing to the gambling (e.g., gambling within context of a manic
episode, excessive gambling only when under the influence of substances). In the
case of comorbid conditions, the clinician will determine the course of treatment,
treating the conditions simultaneously, in parallel, or sequentially (Najavits, 2003).
The pretreatment assessment of the individual with PG includes broad-based and
specific measures of impulse control disorders, as well as mental health measures.
Before beginning any intervention that aims to modify a behavior, the clinician must
undertake a complete evaluation of different variables, such as the extent of the
gambling and the repercussions of the problem for the individual’s life (for example,
financial, social, psychological, and familial implications). Additional objectives to
consider in a pretreatment assessment of PG include an evaluation of the individual’s
readiness for change, an assessment of risk aversion, a measure of the consequences
of gambling, and the individual’s sense of control over the gambling.
Overview of Treatment for Pathological Gambling
Despite the significant personal costs associated with PG, prevalence surveys indicate
that only a small proportion of the individuals who are suffering from gambling
disorders seek formal treatment (Cunningham, 2005; Slutske et al., 2009; Suur-
vali, Hodgins, Toneatto, & Cunningham, 2008, 2011). In fact, Suurvali et al.
(2008) found that less than 6% of problem gamblers actually seek formal treatment.
A desire to handle the problem on their own, lack of knowledge about where to
receive treatment, and shame have been identified as factors contributing to a low
percentage of individuals seeking treatment (Suurvali, Cordingley, Hodgins, & Cun-
ningham, 2009). A comparison of past-year prevalence rates of gambling disorders
with lifetime rates suggests a one-third recovery rate (Hodgins, Wynne, & Makarchuk,
1999; Slutske, 2006). Research suggests that the majority of these individuals have
accomplished their recoveries without accessing formal treatment services (Hodgins,
Stea, & Grant, 2011; Hodgins, Wynne, & Makarchuk, 1999), which is consistent with
what is found for other addictive disorders (Sobell, Cunningham, & Sobell, 1996).
In-depth interviews with recovered gamblers reveal that their recovery strategies are
behavior-focused and similar to the strategies of those who have accessed treatment
(for example, involvement in time-consuming activities that are incompatible with
gambling, avoiding conditioned cues to gamble such as gambling venues) (Hodgins

& el-Guebaly, 2000; Hodgins et al., 2011).
Although the phenomenon of natural recovery from problem gambling occurs
in an estimated 35% of individuals (Nathan, 2003; Slutske, 2006), most problem
gamblers report a chronic course, with symptom severity fluctuating over time (Petry,
2005). The importance of identifying and treating PG is underscored by a study of
those seeking treatment for problem gambling which found that 48% had frequent
suicidal ideation while 12% reported a gambling-related suicide attempt (Ledgerwood
& Petry, 2004). Some form of treatment, therefore, is needed for the majority of
individuals with a gambling problem.
Self-exclusion contracts (Ladouceur, Jacques, Giroux, Ferland, & Leblond, 2000),
where a person reports their gambling problem to the gaming venue, effectively “ban-
ning” themselves from the gaming venue, have been reported as effective in a minority
of participants. Approximately 24–30% of self-excluded participants complied with
their initial agreement and remained abstinent from all forms of gambling over a
period of 1 to 5 years (Ladouceur, Sylvain, & Gosselin, 2007; Nelson, Kleschinsky,
LaBrie, Kaplan, & Shaffer, 2010; Tremblay, Boutin, & Ladouceur, 2008). Those
who participated in complementary treatment or self-help groups had more positive
outcomes (Nelson et al., 2010). No controlled studies, however, have been conducted
using this type of intervention as a formal treatment for problematic gambling.
Current treatment for PG involves a number of different options—inpatient
treatments; intensive outpatient, individual, and group CBT; and pharmacotherapy—
which have all demonstrated benefit in treating gambling disorders (Hodgins et al.,
2011; Pallesen, Mitsem, Kvale, Johnsen, & Molde, 2005). Although there is currently
no agreed-upon standard of care for disordered gambling, the most widely studied
treatment for PG has been some form of CBT (Table 57.1). A meta-analysis identified
22 randomized trials published between 1968 and 2004 (Pallesen et al., 2005). This
meta-analysis revealed that in general, psychological treatments were more effective
than no treatment at both posttreatment (overall effect size = 2.01) and at follow-
up averaging 17 months later (overall effect size = 1.59) (Hodgins et al., 2011).
A more recent meta-analysis that included 25 studies (Gooding & Tarrier, 2009)
found that although there was considerable variability in the outcomes reported,
posttreatment effects were generally positive for different types of therapy (e.g.,
behavioral, cognitive) and mode of therapy (e.g., individual, group, self-directed).
To date, there are no randomized trials of inpatient treatment (Hodgins & Holub,
2007).
Psychotherapy
A variety of psychosocial treatments have been examined in the treatment of PG.

Cognitive strategies have traditionally included cognitive restructuring, psychoeduca-
tion, understanding of gambling urges, and irrational cognition awareness training.
Behavioral approaches focus on developing alternative activities to compete with
reinforcers specific to PG, as well as on the identification of gambling triggers.
Table 57.1 Controlled Psychological Treatment Trials for Pathological Gambling
Reference Study design and Subjects Outcome

duration
Cognitive therapy
Sylvain, Ladouceur, CT + relapse 40 enrolled CT: 36% improved on
& Boisvert, 1997 prevention vs. 14, 22 in treatment five gambling severity
wait-list; groups completed variables vs. 6% on
30 sessions with wait-list control
6-month follow-up
Ladouceur et al., CT + relapse 88 enrolled CT: 32% improved on

2001 prevention vs. 35,59 in treatment four variables vs. 7%
wait-list; 20 sessions groups completed on wait-list
with 12-month
follow-up
Ladouceur et al., GCT + relapse 71 enrolled GCT: 65% no longer

2003 prevention vs. 34,46 in treatment met PG criteria vs.
wait-list; 10 weeks groups completed 20% on wait-list
with 2-year
follow-up
Cognitive behavioral therapy

Echeburúa, Baez, SCERP vs. cognitive 64 enrolled At 12 months,
& Fernández- restructuring vs. 50 completed abstinence or much
Montalvo, combined treatment reduced gambling
1996 vs. wait-list; 6 weeks present in 69% of
with 12-month SCERP group vs.
follow-up 38% of cognitive
restructuring or
combined treatment
groups
Milton, Crino, Individual CBT vs. 47 enrolled 65% of CBT + compl-

Hunt, & Prosser, CBT + inter- 40 assigned to iance interventions
2002 ventions to improve treatment (20 in group completed vs.
treatment CBT, 20 in CBT + 35% of CBT-only
compliance; 8 compliance group
sessions with a interventions)
9-month follow-up 20 completed
(72.5% male)

duration
Melville, Davis, Group CBT, group + Group #1: CBT with mapping
Matzenbacher, & interactive written 20 enrolled, 13 group decreased PG
Clayborne, 2004 assignments treated symptoms compared
(mapping) vs. Group #2: with control group.
wait-list control; 28 enrolled, 19 Exp. #2 added
two 90-minute treated depression and anxiety
sessions each week (84.2% female) comorbidity, which
for 8 weeks decreased compliance;
maintained at
6-month follow-up
Petry et al., 2006 Manualized CBT in 231 enrolled CBT was more effective
individual 181 completed than Gamblers
counseling vs. CBT Anonymous and
workbook vs. individual counseling
Gamblers more effective than
Anonymous referral; workbook; at 12
8 sessions with months, groups did
1-year follow-up not differ in
abstinence rates
Wulfert, Blanchard, CMBT vs. TAU; 9 of 9 completed Significant PG symptom

& Freidenberg, mean of 16 sessions CMBT group improvement was
2006 with 3-, 6-, and 8 of 12 completed maintained at
12-month follow-up TAU group 12-month follow-up
(100% male) for CMBT group
Myrseth, Litlerè, Manualized GCBT vs. 14 enrolled (7 per 85.7% of the treatment
Støylen, & wait-list control; six group) group had significant
Pallesen, 2009 2-hour group (78.6% male) reductions in DSM-IV
meetings with PG criteria; however.
3-month follow-up no differences noted
between GCBT and
wait-list group in
money spent gambling
Table 57.1

duration
Echeburúa, Gómez, Psychoeducation, 44 enrolled CBT group had greater

& Freixa, 2011 stimulus control, 41 completed improvement in
gradual exposure gambling episodes and
and relapse preve- money spent on
ntion; 20 sessions gambling; less robust at
with 3-, 6-, and 6- and 12-month
12-month follow-up follow-up
Cue exposure
McConaghy, Aversion therapy vs. 20 enrolled Improvement in both
Armstrong, imaginal 20 completed treatment groups over
Blaszczynski, & desensitization 12 months
Allcock, 1983
McConaghy, ID vs. IR; 14 sessions 20 enrolled Both ID and IR groups

Armstrong, in a 1-week period 20 completed improved at posttreat-
Blaszczynski, & (inpatient sample) (95% male) ment, but improvement
Allcock, 1988 lessened by 12-month
follow-up
McConaghy, Aversion therapy vs. 120 enrolled Imaginal desensitization

Blaszczynski, & imaginal desensit- 63 available 2 and improved at 1 month
Frankova, 1991 ization vs. in vivo 9 years later and 9 years
desensitization vs.
imaginal relaxation
Grant et al., 2009; Manualized CBT with 68 enrolled Greater gambling severity
Grant, Donahue, IDMI vs. Gamblers 55 completed reduction overall and
Odlaug, & Kim, Anonymous referral; (63.2% female) abstinence rates 1 month
2011 6 sessions with posttreatment were
6-month follow-up higher in IDMI group;
response maintained in
77% of subjects at
6-month follow-up
Brief interventions and motivational interviewing

Dickerson, Hinchy, CBT workbook vs. 29 enrolled Both groups improved at 6
& England, 1990 workbook + a single months
in-depth interview

duration
Hodgins, Currie, & CBT workbook vs. 102 enrolled 74% with motivational
el-Guebaly, 2001 workbook + 85 available at 12 enhancement
motivational months improved (Clinical
enhancement Global Impression)
intervention via vs. 61% with
telephone vs. workbook and 44%
wait-list on wait-list
Hodgins & Holub, Single-session MI with Unclear The MI group gambled

2007 self-help workbook less often and spent
vs. workbook alone. less money at
Single session with 12-month follow-up
12-month follow-up vs. the
workbook-alone
group
Hodgins, Currie, Relapse-prevention 169 enrolled The repeated-mailing

el-Guebaly, & bibliotherapy; 142 available at group improved more
Diskin, 2007 single-mailing vs. 12-month than the
repeated mailings follow-up single-mailing group
over a 12-month (58% male) but not significantly.
period; mailings However, 70% of the
done once for first sample still met
group (n = 85) vs. 7 SOGS criteria for PG
mailings for second at 12-month
group (n = 84), with follow-up
12-month follow-up
Hodgins, Toneatto, Intervention groups 186 enrolled Intervention groups had

Makarchuk, (based on CRAFT): less days gambled but
Skinner, & Self-help workbook behavioral principles
Vincent, 2007 vs. workbook + too complicated for
telephone support family members to
vs. control group; 3- implement
and 6-month
follow-up
Table 57.1

duration
Carlbring & Smit, Web-based CBT with 66 enrolled Nearly 75% of treatment
2008 telephone support 60 with subjects reported
and online posttreatment data moderate to large
workbook materials improvements
vs. wait-list control; maintained at
6-, 18-, and 36-month follow-up
36-month follow-up
Hodgins, Currie, MI + mailed self-help 314 enrolled Brief MI resulted in
Currie, & Fick, workbook vs. 6-week 267 completed the decreased gambling
2009 wait-list control or 12-month at follow-up;
workbook-only follow-up workbook-only group
control; 6-, 9-, and (55.4% female) just as improved as
12-month follow-up MI group
completed
Diskin & Hodgins, Single in-person MI vs. 81 enrolled MI group reported

2009 control interview; 1-, 69 completed significant reductions
3-, 6-, and 12-month in gambling severity
12-month follow-up follow-up and maintained at 12
(43.2% female) months
postintervention
Petry, Weinstock, 4 conditions: Brief 117 enrolled All treatment conditions

Morasco, & advice vs. MET vs. 114 completed provided significant
Ledgerwood, MET + CBT vs. week 6 evaluation; symptom improve-
2009 no-treatment 113 completed ment although MET
control; 9-month 9-month follow-up had the most signifi-
follow-up (15.4% female) cant effect relative to
the control group
Oei, Raylu, & Weekly group vs. 102 enrolled Both group and
Casey, 2010 individual CBT with 86% completed individual CBT
MI vs. a wait-list Group and resulted in significant
control for 6 weeks; individual CBT PG improvements,
6-month follow-up conditions maintained at
6-month follow-up

duration
Carlbring, Jonsson, Group CBT (8 150 enrolled Group CBT and

Josephson, & sessions) vs. MI (4 motivational
Forsberg, 2010 sessions) vs. interviewing both
no-treatment control improved PG,
group; 6- and anxiety, and
12-month follow-up depression symptoms
significantly
∗
CBT = cognitive behavioral therapy, CMBT = cognitive motivational behavior therapy, CT = cognitive
therapy, GCBT = group cognitive behavioral therapy, GCT = group cognitive therapy, ID = imaginal
desensitization, IDMI = imaginal desensitization and motivational interviewing, IR = imaginal relaxation,
MET = motivational enhancement therapy, MI = motivational interviewing, PG = pathological gambling,
SCERP = stimulus control, in vivo exposure, relapse prevention, SOGS = South Oaks Gambling Screen,
TAU = treatment as usual.
Cognitive Therapy
Cognitive treatment focuses specifically on modifying the maladaptive and distorted

cognitions associated with gambling, including overestimating probabilities of win-
ning, illusions of control over the outcome of a gamble, the belief that a win is
due following a series of losses (i.e., the gambler’s fallacy), and memory biases in
favor of remembering wins and discounting losses (Toneatto, 1999). Superstitious
beliefs surrounding gambling behavior, including talismanic superstitions in which
the person believes that carrying certain items (such as a rabbit foot keychain or lucky
coin) or cognitive superstitions (such as the belief that doing things in a certain way
will increase the “odds” of winning), are common and are the focus of cognitive
therapy.
Three controlled studies have examined the effect of cognitive restructuring in PG.
One study (N = 40) used a combination of individual cognitive therapy and relapse
prevention strategies (Sylvain, Ladouceur, & Boisvert, 1997). At 12 months, the
treatment group showed significant reductions in gambling frequency and an increase
in self-perceived control over their gambling behavior. The same cognitive therapy
techniques combined with relapse prevention were compared with a 3-month wait-list
control in a group of 88 pathological gamblers. The treatment group experienced
gambling symptom improvement at 3 months and maintained it at the 12-month
follow-up (Ladouceur et al., 2001).
Group cognitive therapy has also been tested in 71 subjects with PG against a
wait-list control condition (Ladouceur et al., 2003). Groups met for 2 hours weekly
for 10 weeks. After 10 sessions, 88% of those in group CBT no longer met PG criteria,
compared with 20% in the wait-list condition. At the 24-month follow-up, 68% of
the original group’s CBT subjects still did not meet the criteria.
Although both individual and group cognitive therapies have shown promise in
treating PG, rates of treatment discontinuation were high in these studies (up to
Gambling 1373
47%). In addition, the cognitive therapy studies have not yet determined the optimal
number of sessions needed to reduce gambling symptoms and maintain improvement.
Although a small number of trials have evaluated the efficacy of a purely cognitive
approach, the largest number and the most rigorously designed trials have evaluated
a combined CBT model. The rubric of CBT, however, encompasses a wide range of
therapeutic approaches. Overall, while there is variability in the content and outcomes
of CBT, positive effects have generally been found by different research groups
(Gooding & Tarrier, 2009).
Behavioral models conceptualize disordered gambling as learned patterns of rein-
forcement within a functional framework. Continued gambling behavior stems from a
variable pattern of reinforcement with respect to antecedents (e.g., external gambling
cues, positive or negative emotions), behaviors (e.g., chasing of losses, strategizing to
attain money), and consequences (e.g., financial loss) (Hodgins et al., 2011). CBT
treatments focus on altering one or more components of this functional relationship
in order to modify the learned patterns. Behavioral strategies include reducing avoid-
ance, reducing exposure to high-risk situations, behavioral experiments to challenge
distorted thoughts, and developing skills in various areas (e.g., assertiveness, problem
solving, and relaxation).
A randomized study of CBT in slot-machine-playing pathological gamblers assigned
subjects to one of four groups: (a) individual stimulus control and in vivo exposure
with response prevention, (b) group cognitive restructuring, (c) a combination of (a)
and (b), or (d) a wait-list control (Echeburúa, Baez, & Fernández-Montalvo, 1996).
At 12-month follow-up, rates of abstinence or minimal gambling were higher in the
individual treatment subjects (69%) compared with the cognitive restructuring (38%)
and combined treatment (38%) groups. The same investigators also assessed individual
and group relapse prevention for subjects completing a 6-week individual treatment
program. At 12 months, 86% of those receiving individual relapse prevention and 78%
of those in group relapse prevention had not relapsed, compared with 52% of those
who received no follow-up treatment (Echeburúa, Fernández-Montalvo, & Baez,
2001).
Milton, Crino, Hunt, and Prosser (2002) compared CBT with CBT combined with
interventions designed to improve treatment compliance (the interventions included
positive reinforcement, identifying barriers to change, and applying problem-solving
skills) in 40 subjects receiving eight sessions of manualized individual therapy. Only
35% of the CBT-alone group completed treatment compared with 65% of the CBT
plus interventions group. At 9-month follow-up, there was no difference in outcomes
between treatments, although both produced clinically significant change (Milton
et al., 2002).
Melville, Davis, Matzenbacher, and Clayborne (2004) reported two studies that
used a system targeting three topics (understanding randomness, problem solving,
and relapse prevention) to improve outcome. In the first study, 13 subjects were
assigned to 8 weeks of (a) group CBT, (b) group CBT with the topic-enhanced
treatment, or (c) a wait-list. In the second study, 19 subjects were assigned to a

topic-enhanced group or a wait-list group for 8 weeks. For those subjects who were
in the topic-targeting CBT group, significant improvement was maintained both
posttreatment and at 6-month follow-up (Melville et al., 2004).
Another study examined an eight-session manualized form of CBT, randomizing
231 subjects to weekly sessions with an individual counselor, therapy in the form of
a workbook, or referral to Gamblers Anonymous (Petry et al., 2006). Although all
groups reduced their gambling, subjects assigned to individual therapy or to the self-
help workbook reduced gambling behaviors more than those referred to Gamblers
Anonymous (Petry et al., 2006).
In a study examining cognitive motivational behavior therapy (CMBT), a method
that combines gambling-specific CBT with motivational interviewing techniques to
aid in resolving treatment ambivalence and improve retention rates, nine subjects
received manualized treatment and were compared with a control group of 12
who received treatment as usual (TAU). All nine subjects (100%) in the CMBT
group completed treatment versus only eight (66.7%) in the TAU group. Significant
improvements were observed at 12-month follow-up of the CMBT group (Wulfert,
Blanchard, & Freidenberg, 2006).
Cue-Exposure
Cue-exposure, based on classical conditioning, is a well-validated form of CBT used

in the treatment of fear-based problems (Foa & Kozak, 1986) and has the goal
of extinguishing the feared or learned response. The learned response (fear, panic)
is extinguished through repeated exposure to a conditioned stimulus (dogs) in the
absence of the feared consequence (not all dogs bite, I am safe). There is preliminary
evidence, in the use of cue-exposure therapy with addictions, that urges or cravings can
be elicited using in vivo and imaginal exposure techniques (Carter & Tiffany, 1999).
Cue reactivity to relevant stimuli (drug/alcohol) appears to be an important factor
in addiction that can contribute to relapse (Cooney, Litt, Morse, Bauer, & Gaupp,
1997). Cue-exposure studies conducted with PG (Echeburúa, Baez, & Fernández-
Montalvo, 1996; Kushner et al., 2007; McConaghy, Blaszczynski, & Frankova, 1991;
Symes & Nicki, 1997) have reported positive findings to date, yet with only a few
randomized controlled trials.
The first randomized study compared imaginal desensitization (i.e., subjects
were taught relaxation and then instructed to imagine experiencing and resist-
ing triggers to gambling) with traditional aversion therapy (McConaghy, Arm-
strong, Blaszczynski, & Allcock, 1983). Both therapies had positive effects, but the
imaginal desensitization group was more successful in reducing gambling urges and
behavior.
In a second study, 20 inpatient subjects were randomized to receive either imaginal
desensitization or imaginal relaxation in 14 sessions over a 1-week period. Both
groups improved posttreatment, but the therapeutic gains were not maintained
by either group at 12-month follow-up (McConaghy, Armstrong, Blaszczynski, &
Allcock, 1988). In a larger study, 120 subjects were randomly assigned to aversion
Gambling 1375
therapy, imaginal desensitization, in vivo desensitization, or imaginal relaxation.

Subjects assigned to imaginal desensitization reported better outcomes one month
and up to 9 years later (McConaghy et al., 1991).
Using imaginal desensitization and combining cue-exposure with negative mood
induction, Grant et al. (2009) examined 68 pathological gamblers assigned to six
sessions of treatment or Gamblers Anonymous. The negative mood induction involves
focusing on the negative consequences of the problem behavior while the urge to
engage in gambling is active. Idiosyncratic scripts were developed for each gambler,
including gambling-related cues, with the intention of activating each gambler’s
urge via imagination (repeatedly listening to a recording of the script). The scripts
emphasized internal events including thoughts and emotions experienced before,
during, and after a gambling episode (e.g., euphoria before and during gambling
and dysphoria and agitation after gambling). In the study, the pleasurable aspects of
the script (i.e., anticipation of gambling and initial excitement) were then followed
by the negative consequences of gambling unique to each gambler (negative mood
induction). Grant et al. (2011) found that 64% of participants receiving imaginal
exposure plus the negative mood induction as part of a six-session CBT program were
able to maintain abstinence for one month, as opposed to only 17% of those randomly
assigned to Gamblers Anonymous. For the CBT with imaginal exposure plus negative
mood induction group, among those participants who responded to therapy after six
sessions, 77% maintained their response for 6 months (Grant, Donahue, Odlaug, &
Kim, 2011).
Brief Interventions and Motivational Interviewing
Brief treatments are not necessarily conceptualized as treatment by individuals who

access them (Hodgins et al., 2011) and therefore may be more appealing to gamblers
who report significant ambivalence about stopping their behavior. Brief treatments are
designed to use less professional resources or time than face-to-face interventions and
may include single-session interventions, workbooks, or bibliotherapy. Motivational
interviewing (MI), an approach that is often used in brief interventions, is empathic
and uses the strengths of the client to enhance self-efficacy regarding changes in
behavior.
In an early study of brief interventions, Dickerson, Hinchy, and England (1990)
randomly assigned 29 subjects either to a workbook or to a workbook plus a single
in-depth interview. The workbook included CBT and motivational-enhancement
techniques. Both groups reported significant reductions in gambling at 6-month
follow-up.
Hodgins, Currie, and el-Guebaly (2001) assigned 102 gamblers to a CBT
workbook, a workbook plus a telephone motivational-enhancement intervention, or a
wait-list. Rates of abstinence at 6-month follow-up did not differ between the groups,
although the frequency of gambling and amount of money lost gambling were lower
in the motivational intervention group. Compared with the workbook alone, the
motivational intervention and workbook together reduced gambling throughout a
2-year follow-up period; notably, 77% of the entire follow-up sample were rated as
improved at the 2-year assessment (Hodgins, Currie, el-Guebaly, & Peden, 2004).
Another study conducted by Diskin and Hodgins (2009) compared a single-session
motivational interviewing module plus a self-help workbook with the workbook and
speaking with an interviewer about gambling for 30 minutes. Half of the sample was
randomized to each intervention. At 12-month follow-up, those who received the
motivational interviewing plus the workbook gambled less and spent less money than
the workbook-alone group (Diskin & Hodgins, 2009).
Motivational interviewing has also been compared in individual versus group
settings. Oei, Raylu, and Casey (2010) randomized 102 gamblers to receive 6 weeks
of individual or group CBT with motivational interviewing. At posttreatment and 6-
month follow-up, those completing the individual CBT program had better sustained
outcomes in regard to gambling severity and DSM-IV criteria compared to the group
CBT and wait-list control groups (although group CBT produced significant results
versus the wait-list control group as well) (Oei et al., 2010).
A study using a short-term group CBT (GCBT) model for 14 subjects (78.6% male)
found that 85.7% of the treatment group experienced significant improvements in
DSM-IV PG criteria at posttreatment compared to 42.9% of a wait-list control group
(Myrseth, Litlerè, Støylen, & Pallesen, 2009). The other dependent variable, money
spent gambling over the past week, however, failed to indicate any significant group
differences, with 28.6% of both the GCBT and wait-list control groups experiencing
improvement.
A study using a relapse-prevention bibliotherapy randomized 169 subjects who had
recently quit gambling to receive either a summary booklet that detailed all available
relapse prevention information (single mailing group) (n = 85) or to the same
booklet plus seven additional informational booklets mailed over the next 12 months
(repeated mailing group) (n = 84) (Hodgins, Currie, el-Guebaly, & Diskin, 2007).
At the 12-month assessment, 24% of the repeated mailing group reported using the
strategies regularly to prevent relapse compared with 13% of the single mailing group.
Only 44% of the overall sample, however, reported having not gambled over the 3
months prior to the 12-month assessment.
Two self-directed motivational interventions were compared with a 6-week wait-list
control and a workbook-only control in 314 pathological gamblers. Brief motivational
treatment involved a motivational interview by telephone and a mailed self-help
workbook. Brief motivational booster treatment involved a motivational interview by
telephone, a workbook, and six booster telephone calls over a 9-month period. Both
the brief and the brief booster treatment participants reported less gambling at 6
weeks than those assigned to the control groups. Brief and brief booster treatment
participants gambled significantly less often over the first 6 months of the follow-up
than workbook-only participants. Participants in the brief booster treatment group,
however, showed no greater improvement than brief treatment participants (Hodgins,
Currie, Currie, & Fick, 2009).
A similar combination of motivation interviewing and CBT was adapted to a
Web-based format in Sweden (Carlbring & Smit, 2008) in which a therapist provides
telephone support for individuals using online recovery materials. A wait-list control
was compared with an 8-week Internet-based CBT program with minimal therapist
Gambling 1377
contact via e-mail and weekly telephone calls of less than 15 minutes. The average time
spent on each participant, including phone conversations, e-mail, and administration,
was 4 hours. The Internet-based intervention resulted in favorable changes in PG,
anxiety, depression, and quality of life. Follow-ups in the treatment group at 6, 18,
and 36 months indicated that treatment effects were sustained.
A total of 150 primarily self-recruited patients with current gambling problems
or PG were randomized to four individual sessions of motivational interviewing,
eight sessions of CBT group therapy, or a no-treatment wait-list control. Treatment
showed superiority in some areas over the no-treatment control in the short term,
but no differences were found between motivational interviewing and group CBT
at any point in time. Instead, both interventions produced significant within-group
decreases on most outcome measures up to the 12-month follow-up (Carlbring,
Jonsson, Josephson, & Forsberg, 2010).
A randomized controlled study found that a 10-minute session of behavioral advice,
one session of motivational enhancement therapy, or one session of motivational
enhancement therapy plus three sessions of CBT were all equally effective in reducing
gambling among a sample of 117 college students with either problem or pathological
gambling (Petry, Weinstock, Morasco, & Ledgerwood, 2009). Two small trials have
shown that the addition of motivational interviewing to CBT reduces treatment
attrition and improves outcomes (Diskin & Hodgins, 2009; Wulfert et al., 2006).
Dropout rates from psychosocial treatment are high, so interventions that lead patients
to complete treatment are potentially very valuable.
Family Therapy
Advances in family therapy interventions for treating substance abuse problems

have been adapted for gambling disorders. Families of pathological gamblers often
feel intense dissatisfaction and a lack of trust over the deception often present in
PG (Mazzoleni, Gorenstein, Fuentes, & Tavares, 2009). Gamblers Anonymous for
families, also known as GAM-ANON and modeled after AL-ANON for substance
addiction, was established as a program for the families and friends of compulsive
gamblers to understand and cope with these feelings and the interpersonal damage
caused by problem gambling (Vander Bilt & Franklin, 2003). In a small study assessing
the impact of family involvement (N = 43) in GAM-ANON in relation to gambling
relapse for a spouse/significant other involved in Gamblers Anonymous, Zion, Tracy,
and Abell (1991) found no association between GAM-ANON involvement and
client relapse. Likewise, Johnson and Nora (1992) found nonsignificant differences
in patients whose spouses participated in Gamblers Anonymous treatment with them.
Given the high concordance of gambling to marital and familial discourse, however,
the significant negative impact of PG on family members should not be ignored
(Shaw, Forbush, Schlinder, Rosenman, & Black, 2007).
A self-help workbook of the Community Reinforcement and Family Therapy
(CRAFT) model, adapted for gambling, has been evaluated in two randomized con-
trolled trials (Hodgins, Toneatto, Makarchuk, Skinner, & Vincent, 2007; Makarchuk,
Hodgins, & Peden, 2002). In CRAFT, family members are trained to use behavioral
principles to reinforce nongambling behavior in individuals who are not addressing

their gambling problem. Although positive effects for family members and their gam-
bling relatives were found in both trials, the studies found that behavioral principles
were too complex for family members to implement without the support of a therapist
(Hodgins et al., 2007).
A coping skills training program developed for alcohol problems has also been
evaluated for gambling. The program consists of 10 weekly individual sessions to
teach more effective coping skills. A small (N = 23) randomized controlled trial
comparing the coping skills program to a delayed treatment condition showed
that partners of gamblers improved their ability to manage feelings of depression and
anxiety. Partner gambling during that period decreased in both conditions but did not
differ between them, nor did partner help-seeking differ (Rychtarik & McGillicuddy,
2006).
Conclusions
These studies show that CBT is beneficial for gambling disorders, but many questions
remain.
Which form of CBT is best, and for whom? There have been no comparison studies
of the different manualized forms of CBT, and so one cannot make recommendations
at this time regarding which approach is most effective. Also, no manualized CBT
treatment has been examined in a confirmatory study by another independent
investigator. The heterogeneity of gambling treatment samples may also complicate
identification of effective treatments.
What is the optimal duration of therapy? Given the success and low cost of brief
interventions, should everyone undergo a brief intervention first and only if they fail
that move on to more intensive therapy?
What specific components should be included in the CBT program? Which com-
ponents are most effective? Do certain people respond differently to different CBT
components? No study has examined whether certain individuals with gambling dis-
orders would benefit differentially from specific CBT treatments. The matching of
different treatment approaches to different subtypes of gambling disorders, based on
neurobiology or genetics, may improve treatment outcomes.
What role does comorbidity play? Although naturalistic follow-up research on
gamblers demonstrates that drug use disorders are associated with lower likeli-
hood of gambling abstinence (Hodgins & el-Guebaly, 2000), some research shows
that gamblers with or without mental health problems respond equally well to
CBT (Champine & Petry, 2010). Other research suggests that comorbidity with
nicotine dependence may result in greater rates of relapse following treatment (Grant
et al., 2011), and that perhaps gamblers who have comorbid schizophrenia may
require more sessions of therapy (i.e., 20 sessions) (Echeburúa, Gómez, & Freixa,
2011).
Should the goal of treatment be abstinence? Offering flexibility (i.e., abstinence,
decreased gambling, more control) to individuals may increase treatment-seeking and
decrease treatment dropout. In a recent study, 89 individuals undergoing 14 sessions
Gambling 1379
of CBT were offered treatment with controlled gambling as the goal (Ladouceur,
Lachance, & Fournier, 2009). The majority (66%) of participants changed their
goal to abstinence during the 12 weeks of treatment. Outcomes, however, did
not differ between those who maintained a goal of controlled gambling compared
to those whose goal was abstinence. The goal of controlled gambling did not
result in a lower rate of dropout compared with studies of abstinence-oriented
treatment.
Although multiple forms of CBT have demonstrated benefits for gambling disor-
ders, the limitations associated with these data preclude making specific treatment
recommendations, on an individual level, with a substantial degree of confidence.
Despite the progress in the development of effective treatments for gambling
disorders, more research is needed to address the remaining questions. Simulta-
neously, there is a growing availability of gambling avenues. Internet gambling,
for example, is providing around-the-clock home access to multiple types of gam-
bling activities for an increasing number of people around the world (Hodgins
et al., 2011). Thus, although significant progress has been made, this evolution
warrants more sophisticated research into gambling disorders and their clinical
treatment.
References
Abroms, L. C., Windsor, R., & Simons-Morton, B. (2008). Getting young adults to quit
smoking: A formative evaluation of the X-Pack program. Nicotine & Tobacco Research,
10, 27–33. doi:10.1080/14622200701767852
Afifi, T. O., Cox, B. J., Martens, P. J., Sareen, J., & Enns, M. W. (2010). The relationship
between problem gambling and mental and physical health correlates among a nationally
representative sample of Canadian women. Canadian Journal of Public Health, 101,
171–175.
American Gaming Association. (2012). Gaming revenue, 10-year trends. Retrieved from http://
www.americangaming.org/industry-resources/research/fact-sheets/gaming-revenue-10-
year-trends
Bakken, I. J., Götestam, K. G., Gråwe, R. W., Wenzel, H. G., & Øren, A. (2009). Gambling
behavior and gambling problems in Norway 2007. Scandinavian Journal of Psychology,
50, 333–339. doi:10.1111/j.1467-9450.2009.00713.x
Balodis, I. M., Kober, H., Worhunsky, P. D., Stevens, M. C., Pearlson, G. D., & Potenza, M.
N. (2012). Diminished frontostriatal activity during processing of monetary rewards and
losses in pathological gambling. Biological Psychiatry. Advance online publication. PMID:
22336565
Barnes, G. M., Welte, J. W., Hoffman, J. H., & Tidwell, M. C. (2011). The co-occurrence
of gambling with substance use and conduct disorder among youth in the United States.
American Journal on Addictions, 20, 166–173. doi:10.1111/j.1521-0391.2010.00116.x
Bergh, C., & Kühlhorn, E. (1994). Social, psychological, and physical consequences of patho-
logical gambling in Sweden. Journal of Gambling Studies, 10, 275–285. doi:10.1007/
BF02104968
Blaszczynski, A., & McConaghy, N. (1989). Anxiety and/or depression in the pathogenesis of
addictive gambling. International Journal of the Addictions, 24, 337–350.
Breyer, J. L., Botzet A. M., Winters, K. C., Stinchfield, R. D., August, G., & Realmuto, G.
(2009). Young adult gambling behaviors and their relationship with the persistence of
ADHD. Journal of Gambling Studies, 25, 227–238. doi:10.1007/s10899-009-9126-z
Caillon, J., Grall-Bronnec, M., Bouju, G., Lagadec, M., & Vénisse, J. L. (2012). Pathological
gambling in adolescence. Archives of Pediatrics, 19, 173–179.
Carlbring, P., Jonsson, J., Josephson, H., & Forsberg, L. (2010). Motivational interviewing
versus cognitive behavioral group therapy in the treatment of problem and pathological
gambling: A randomized controlled trial. Cognitive Behaviour Therapy, 39, 92–103.
doi:10.1080/16506070903190245
Carlbring, P., & Smit, F. (2008). Randomized trial of Internet-delivered self-help with
telephone support for pathological gamblers. Journal of Consulting and Clinical Psychology,
76, 1090–94. doi:10.1037/a0013603
Carter, B. L., & Tiffany, S. T. (1999). Meta-analysis of cue-reactivity in addiction research.
Addiction, 94, 327–340. doi:10.1046/j.1360-0443.1999.9433273.x
Cavedini, P., Riboldi, G., Keller, R., D’Annucci, A., & Bellodi, L. (2002). Frontal lobe
dysfunction in pathological gambling patients. Biological Psychiatry, 51, 334–341.
doi:10.1016/S0006-3223(01)01227-6
Chalmers, H., & Willoughby, T. (2006). Do predictors of gambling involvement dif-
fer across male and female adolescents? Journal of Gambling Studies, 22, 373–392.
doi:10.1007/s10899-006-9024-6
Champine, R. B., & Petry, N. M. (2010). Pathological gamblers respond equally well to
cognitive-behavioral therapy regardless of other mental health treatment status. American
Journal on Addictions, 19, 550–556. doi:10.1111/j.1521-0391.2010.00085.x
Chase, H. W., & Clark, L. (2010). Gambling severity predicts midbrain response to near-miss
outcomes. Journal of Neuroscience, 30, 6180–6187. doi:10.1523/JNEUROSCI.5758-
09.2010
Chaumeton, N. R., Ramowski, S. K., & Nystrom, R. J. (2011). Correlates of gambling among
eighth-grade boys and girls. Journal of School Health, 81, 374–385. doi:10.1111/j.1746-
1561.2011.00605.x
Chou, K. L., & Afifi, T. O. (2011). Disordered (pathologic or problem) gambling and
Axis I psychiatric disorders: Results from the National Epidemiologic Survey on Alco-
hol and Related Conditions. American Journal of Epidemiology, 173, 1289–1297.
doi:10.1093/aje/kwr017
Clark, L. (2010). Decision-making during gambling: An integration of cognitive and psy-
chobiological approaches. Philosophical Transactions of the Royal Society of London: Series
B, Biological Sciences, 365, 319–330. doi:10.1098/rstb.2009.0147
Clark, L. (2012). Epidemiology and phenomenology of pathological gambling. In J. E. Grant
& M. N. Potenza (Eds.), The Oxford handbook of impulse control disorders (pp. 94–116).
Oxford, England: Oxford University Press.
Clark, L., Bechara, A., Damasio, H., Aitken, M. R., Sahakian, B. J., & Robbins, T. W.
(2008). Differential effects of insular and ventromedial prefrontal cortex lesions on risky
decision-making. Brain, 131, 1311–1322.
Cooney, L., Litt, M. D., Morse, P. A., Bauer, L. O., & Gaupp, L. (1997). Alcohol cue
reactivity, negative-mood reactivity, and relapse in treated alcoholic men. Journal of
Abnormal Psychology, 106, 243–250. doi:10.1037/0021-843X.106.2.243
Crisp, B. R., Thomas, S. A., Jackson, A. C., Smith, S., Borrell, J., Ho, W. Y., … Thomason,
N. (2004). Not the same: a comparison of female and male clients seeking treatment
from problem gambling counseling services. Journal of Gambling Studies, 20, 283–299.
doi:10.1023/B:JOGS.0000040280.64348.d1
Gambling 1381
Cunningham, J. A. (2005). Little use of treatment among problem gamblers. Psychiatric

Services, 56, 1024–1025. doi:10.1176/appi.ps.56.8.1024-a
Cunningham-Williams, R. M., Cottler, L. B., Compton, W. M., & Spitznagel, E. L. (1998).
Taking chances: Problem gamblers and mental health disorders—Results from the St.
Louis Epidemiologic Catchment Area Study. American Journal of Public Health, 88,
1093–1096. doi:10.2105/AJPH.88.7.1093
Derevensky, J. L., & Gupta, R. (2000). Prevalence estimates of adolescent gambling: A
comparison of the SOGS-RA, DSM-IV-J, and the GA 20 questions. Journal of Gambling
Research, 16, 227–251. doi:10.1023/A:1009485031719
Desai, R. A., Desai, M. M., & Potenza, M. N. (2007). Gambling, health and age: Data from
the National Epidemiologic Survey on Alcohol and Related Conditions. Psychology of
Addictive Behaviors, 21, 431–440. doi:10.1037/0893-164X.21.4.431
Dickerson, M., Hinchy, J., & England, S. L. (1990). Minimal treatments and problem gamblers:
A preliminary investigation. Journal of Gambling Studies, 6, 87–102. doi:10.1007/
BF01015751
Diskin, K. M., & Hodgins, D. C. (2009). A randomized controlled trial of a single session
motivational intervention for concerned gamblers. Behaviour Research and Therapy, 47 ,
382–388.
Echeburúa, E., Baez, C., & Fernández-Montalvo, J. (1996). Comparative effectiveness of
three therapeutic modalities in psychological treatment of pathological gambling: Long
term outcome. Behavioural and Cognitive Psychotherapy, 24, 51–72. doi:10.1017/
S1352465800016830
Echeburúa, E., Fernández-Montalvo, J., & Baez, C. (2001). Predictors of therapeutic failure
in slot-machine pathological gamblers following behavioural treatment. Behavioural and
Echeburúa, E., Gómez, M., & Freixa, M. (2011). Cognitive-behavioural treatment of patho-
logical gambling in individuals with chronic schizophrenia: A pilot study. Behaviour
Echeburúa, E., González-Ortega, I., de Corral, P., & Polo-López, R. (2011). Clinical gender
differences among adult pathological gamblers seeking treatment. Journal of Gambling
Studies, 27 , 215–227. doi:10.1007/s10899-010-9205-1
Edens, E. L., & Rosenheck, R. A. (2011). Rates and correlates of pathological gambling among
VA mental health service users. Journal of Gambling Studies. Advance online publication.
Erickson, L., Molina, C. A., Ladd, G. T., Pietrzak, R. H., & Petry, N. M. (2005). Problem
and pathological gambling are associated with poorer mental and physical health in older
adults. International Journal of Geriatric Psychiatry, 20, 754–759. doi:10.1002/gps.1357
Feigelman, W., Wallisch, L. S., & Lesieur, H. R. (1998). Problem gamblers, problem substance
users, and dual-problem individuals: An epidemiological study. American Journal of Public
Health, 88, 467–470. doi:10.2105/AJPH.88.3.467
Forbush, K. T., Shaw, M., Graeber, M. A., Hovick, L., Meyer, V. J., Moser, D. J., Bayless,
J., … Black, D. W. (2008). Neuropsychological characteristics and personality traits in
pathological gambling. CNS Spectrums, 13, 306–315.
Gainsbury, S. (2011). Seeking help online: A new approach for youth-specific gambling
interventions. In J. Derevensky, D. Shek, & J. Merrick (Eds.), Youth gambling: The
hidden addiction (pp. 187–200). Berlin, Germany: De Gruyter.
Germain, C., Vahanian, A., Basquin, A., Richoux-Benhaim, C., Embouazza, H., & Lejoyeux,
M. (2011). Brief report: Coronary heart disease: An unknown association to pathological
gambling. Frontiers in Psychiatry, 2, 11.
Gooding, P., & Tarrier, N. (2009). A systematic review and meta-analysis of cognitive-
behavioural interventions to reduce problem gambling: Hedging our bets? Behaviour
Goudriaan, A. E., Oosterlaan, J., de Beurs, E., & Van den Brink, W. (2004). Pathological gam-
bling: A comprehensive review of biobehavioral findings. Neuroscience & Biobehaviroal
Review, 28, 123–141.
Grall-Bronnec, M., Wainstein, L., Augy, J., Bouju, G., Feuillet, F., Vénisse, J. L., & Sébille-
Rivain, V. (2011). Attention deficit hyperactivity disorder among pathological and at-
risk gamblers seeking treatment: A hidden disorder. European Addiction Research, 17 ,
231–240.
Grant, J. E. (2008). Impulse control disorders: A clinician’s guide to understanding and treating
behavioral addictions. New York, NY: W. W. Norton.
Grant, J. E., Donahue, C. B., Odlaug, B. L., & Kim, S. W. (2011). A 6-month follow-up of
imaginal desensitization plus motivational interviewing in the treatment of pathological
gambling. Annals of Clinical Psychiatry, 23, 3–10.
Grant, J. E., Donahue, C. B., Odlaug, B. L., Kim, S. W., Miller, M. J., & Petry, N.
M. (2009). Imaginal desensitisation plus motivational interviewing for pathological
gambling: Randomised controlled trial. British Journal of Psychiatry, 195, 266–267.
doi:10.1192/bjp.bp.108.062414
Grant, J. E., & Kim, S. W. (2001). Demographic and clinical characteristics of 131 adult
pathological gamblers. Journal of Clinical Psychiatry, 62, 957–962.
Grant, J. E., & Potenza, M. N. (2007). Commentary: Illegal behavior and pathological
gambling. Journal of the American Academy of Psychiatry and the Law, 35, 302–305.
Grant, J. E., Schreiber, L. R. N., Odlaug, B. L., & Kim, S. W. (2010). Pathological gambling and
bankruptcy. Comprehensive Psychiatry, 51, 115–120. doi:10.1053/comp.2002.29857
Gupta, R., & Derevensky, J. L. (1998). Adolescent gambling behavior: A prevalence study and
examination of the correlates associated with problem gambling. Journal of Gambling
Studies, 14, 319–345. doi:10.1023/A:1023068925328
Gupta, R., Derevensky, J. L., & Ellenbogen, S. (2006). Personality characteristics and risk-
taking tendencies among adolescent gamblers. Canadian Journal of Behavioral Science,
38, 201–213. doi:10.1037/cjbs2006008
Hodgins, D. C., Currie, S. R., Currie, G., & Fick, G. H. (2009). Randomized trial of brief
motivational treatments for pathological gamblers: More is not necessarily better. Journal
of Consulting and Clinical Psychology, 77 , 950–960. doi:10.1037/a0016318
Hodgins, D. C., Currie, S., & el-Guebaly, N. (2001). Motivational enhancement and self-help
treatments for problem gambling. Journal of Consulting and Clinical Psychology, 69,
50–57. doi:10.1037/0022-006X.69.1.50
Hodgins, D. C., Currie, S., el-Guebaly, N., & Diskin, K. M. (2007). Does providing extended-
release prevention bibliotherapy to problem gamblers improve outcome? Journal of
Gambling Studies, 23, 41–54.
Hodgins, D. C., Currie, S., el-Guebaly, N., & Peden, N. (2004). Brief motivational treatment
for problem gambling: A 24-month follow-up. Psychology of Addictive Behavior, 18,
293–296. doi:10.1037/0893-164X.18.3.293
Hodgins, D. C., & el-Guebaly, N. (2000). Natural and treatment-assisted recovery from
gambling problems: A comparison of resolved and active gamblers. Addiction, 95,
777–785. doi:10.1046/j.1360-0443.2000.95577713.x
Hodgins, D. C., & Holub, A. (2007). Treatment of problem gambling. In G. Smith, D. C.
Hodgins, & R. J. Williams (Eds.), Research and measurement issues in gambling studies
(pp. 371–397). Burlington, MA: Elsevier.
Gambling 1383
Hodgins, D. C., Stea, J. N., & Grant, J. E. (2011). Gambling disorders. Lancet, 378,
1874–1884.
Hodgins, D. C., Toneatto, T., Makarchuk, K., Skinner, W., & Vincent, S. (2007). Minimal
treatment approaches for concerned significant others of problem gamblers: A randomized
controlled trial. Journal of Gambling Studies, 23, 215–230.
Hodgins, D. C., Wynne, H., & Makarchuk, K. (1999). Pathways to recovery from gambling
problems: Follow-up from a general population survey. Journal of Gambling Studies, 15,
93–104. doi:10.1023/A:1022237807310
Ibáñez, A., Blanco, C., & Sáiz-Ruiz, J. (2002). Neurobiology and genetics of pathological
gambling. Psychiatric Annals, 32, 181–185.
Ingle, P. J., Marotta, J., McMillan, G., & Wisdom, J. P. (2008). Significant others and
gambling treatment outcomes. Journal of Gambling Studies, 24, 381–392.
Johansson, A., Grant, J. E., Kim, S. W., Odlaug, B. L., & Götestam, K. G. (2009). Risk factors
for problematic gambling: A critical literature review. Journal of Gambling Studies, 25,
67–92. doi:10.1007/s10899-008-9088-6
Johnson, E. E., & Nora, R. M. (1992). Does spousal participation in Gamblers Anonymous ben-
efit compulsive gamblers? Psychological Reports, 71, 914. doi:10.2466/pr0.1992.71.3.914
Kushner, M. G., Abrams, K., Donahue, C., Thuras, P., Frost, R., & Kim, S. W. (2007). Urge
to gamble in problem gamblers exposed to a casino environment. Journal of Gambling
Studies, 23, 121–132. doi:10.1007/s10899-006-9050-4
Ladd, G. T., & Petry, N. M. (2002). Gender differences among pathological gamblers seeking
treatment. Experimental and Clinical Psychopharmacology, 10, 302–309.
Ladouceur, R., Boisvert, J. M., & Dumont J. (1994). Cognitive-behavioral treat-
ment for adolescent pathological gamblers. Behavior Modification, 18, 230–242.
doi:10.1177/01454455940182006
Ladouceur, R., Jacques, C., Giroux, I., Ferland, F., & Leblond, J. (2000). Analysis of a casino’s
self-exclusion program. Journal of Gambling Studies, 16, 453–460.
Ladouceur, R., Lachance, S., & Fournier, P. M. (2009). Is control a viable goal in the treatment
of pathological gambling? Behaviour Research and Therapy, 47 , 189–197.
Ladouceur, R., Sylvain, C., Boutin, C., Lachance, S., Doucet, C., Leblond, J., & Jacques, C.
(2001). Cognitive treatment of pathological gambling. Journal of Nervous and Mental
Disease, 189, 774–780.
Ladouceur, R., Sylvain, C., Boutin, C., Lachance, S., Doucet, C., & Leblond, J. (2003). Group
therapy for pathological gamblers: A cognitive approach. Behaviour Research and Therapy,
41, 587–596.
Ladouceur, R., Sylvain, C., & Gosselin, P. (2007). Self-exclusion program: A longitudinal
evaluation study. Journal of Gambling Studies, 23, 85–94. doi:10.1007/s10899-006-
9032–6
Langhinrishsen-Rohling, J., Rohde, P., Seeley, J. R., & Rohling, M. L. (2004). Individual,
family, and peer correlates of adolescent gambling. Journal of Gambling Studies, 20,
23–46. doi:10.1023/B:JOGS.0000016702.69068.53
Ledgerwood, D. M., & Petry, N. M. (2004). Gambling and suicidality in treatment-seeking
pathological gamblers. Journal of Nervous and Mental Disease, 192, 711–714.
Ledgerwood, D. M., Weinstock, J., Morasco, B. J., & Petry, N. M. (2007). Clinical features
and treatment prognosis of pathological gamblers with and without recent gambling-
related illegal behavior. Journal of the American Academy of Psychiatry and the Law, 35,
294–301.
Lesieur, H. R. (1979). The compulsive gambler’s spiral of options and involvement. Psychiatry,
42, 79–87.
Lorains, F. K., Cowlishaw, S., & Thomas, S. A. (2011). Prevalence of comorbid disorders in
problem and pathological gambling: Systematic review and meta-analysis of population
surveys. Addiction, 106, 490–498. doi:10.1111/j.1360-0443.2010.03300.x
Makarchuk, K., Hodgins, D. C., & Peden, N. (2002). Development of a brief intervention
for concerned significant others of problem gamblers. Addictive Disorders and Their
Treatment, 1, 126–134.
Mazzoleni, M. H., Gorenstein, C., Fuentes, D., & Tavares, H. (2009). Wives of pathological
gamblers: Personality traits, depressive symptoms and social adjustment. Revista Brasileira
Psiquiatria, 31, 332–337.
McConaghy, N., Armstrong, M. S., Blaszczynski, A., & Allcock, C. (1983). Controlled
comparison of aversive therapy and imaginal desensitization in compulsive gambling.
British Journal of Psychiatry, 142, 366–372.
McConaghy, N., Armstrong, M. S., Blaszczynski, A., & Allcock, C. (1988). Behavior com-
pletion versus stimulus control in compulsive gambling: Implications for behavioral
assessment. Behavior Modification, 12, 371–384.
McConaghy, N., Blaszczynski, A., & Frankova, A. (1991). Comparison of imaginal desensiti-
zation with other behavioural treatments of pathological gambling: A two- to nine-year
follow-up. British Journal of Psychiatry, 159, 390–393. doi:10.1192/bjp.159.3.390
McGrath, D. S., & Barrett, S. P. (2009). The comorbidity of tobacco smoking and gambling:
A review of the literature. Drug and Alcohol Review, 28, 676–681.
Melville, C. L., Davis, C. S., Matzenbacher, D. L., & Clayborne, J. (2004). Node-link-
mapping-enhanced group treatment for pathological gambling. Addictive Behavior, 29,
73–87.
Milton, S., Crino, R., Hunt, C., & Prosser, E. (2002). The effect of compliance-improving
interventions on the cognitive-behavioural treatment of pathological gambling. Journal
of Gambling Studies, 18, 207–229. doi:10.1023/A:1015580800028
Monaghan, S., & Wood, R. T. (2010). Internet-based interventions for youth dealing with gam-
bling problems. International Journal of Adolescent Medicine and Health, 22, 113–128.
Morasco, B. J., Pietrzak, R. H., Blanco, C., Grant, B. F., Hasin, D., & Petry, N. M. (2006).
Health problems and medical utilization associated with gambling disorders: Results from
the National Epidemiologic Survey on Alcohol and Related Conditions. Psychosomatic
Medicine, 68, 976–984. doi:10.1097/01.psy.0000238466.76172.cd
Myrseth, H., Brunborg, G. S., & Eldem, M. (2010). Differences in cognitive distortions
between pathological and non-pathological gamblers with preferences for chance or skill
games. Journal of Gambling Studies, 26, 561–569. doi:10.1007/s10899-010-9180-6
Myrseth, H., Litlerè, I., Støylen, I. J., & Pallesen, S. (2009). A controlled study of the
effect of cognitive-behavioural group therapy for pathological gamblers. Nordic Journal
of Psychiatry, 63, 22–31. doi:10.1080/08039480802055139
Najavits, L. M. (2003). How to design an effective treatment outcome study. Journal of
Gambling Studies, 19, 317–337. doi:10.1023/A:1024211605799
Nathan, P. E. (2003). The role of natural recovery in alcoholism and pathological gambling.
Journal of Gambling Studies, 19, 279–286. doi:10.1023/A:1024255420820
National Opinion Research Center. (1999). Gambling Impact and Behavior Study:
Report to the National Gambling Impact Study Commission. Chicago, IL:
National Opinion Research Center at the University of Chicago. Retrieved from
http://govinfo.library.unt.edu/ngisc/reports/fullrpt.html
Nelson, S. E., Kleschinsky, J. H., LaBrie, R. A., Kaplan, S., & Shaffer, H. J. (2010). One
decade of self exclusion: Missouri casino self-excluders four to ten years after enrollment.
Journal of Gambling Studies, 26, 129–144. doi:10.1007/s10899-009-9157-5
Gambling 1385
Odlaug, B. L., Chamberlain, S. R., Kim, S. W., Schreiber, L. R., & Grant, J. E. (2010).
A neurocognitive comparison of cognitive flexibility and response inhibition in gamblers
with varying degrees of clinical severity. Psychological Medicine, 41, 2111–2119.
Odlaug, B. L., & Grant, J. E. (2010). Impulse-control disorders in a college sam-
ple: Results from the self-administered Minnesota Impulse Disorders Interview
(MIDI). Primary Care Companion to the Journal of Clinical Psychiatry, 12, e1–e5.
doi:10.4088/PCC.09m00842whi
Odlaug, B. L., Marsh, P. J., Kim, S. W., & Grant, J. E. (2011). Strategic vs. nonstrategic
gambling: Characteristics of pathological gamblers based on gambling preference. Annals
of Clinical Psychiatry, 23, 105–112.
Oei, T. P., Raylu, N., & Casey, L. M. (2010). Effectiveness of group and individual formats
of a combined motivational interviewing and cognitive behavioral treatment program for
problem gambling: A randomized controlled trial. Behavioural & Cognitive Psychotherapy,
38, 233–238.
Pallesen, S., Mitsem, M., Kvale, G., Johnsen, B. H., & Molde, H. (2005). Outcome of
psychological treatments of pathological gambling: A review and meta-analysis. Addiction,
100, 1412–1422. doi:10.1111/j.1360-0443.2005.01204.x
Petry, N. M. (2005). Pathological gambling: Etiology, comorbidity, and treatment. Washington,
DC: American Psychological Association.
Petry, N. M., Ammerman, Y., Bohl, J., Doersch, A., Gay, H., Kadden, R., … Steinberg, K.
(2006). Cognitive-behavioral therapy for pathological gamblers. Journal of Consulting
Petry, N. M., & Armentano, C. (1999). Prevalence, assessment, and treatment of pathological
gambling: A review. Psychiatric Services, 50, 1021–1027.
Petry, N. M., Weinstock, J., Morasco, B. J., & Ledgerwood, D. M. (2009). Brief motiva-
tional interventions for college student problem gamblers. Addiction, 104, 1569–1578.
doi:10.1111/j.1360-0443.2009.02652.x
Potenza, M. N., Maciejewski, P. K., & Mazure, C. M. (2006). A gender-based exami-
nation of past-year recreational gambling. Journal of Gambling Studies, 22, 41–64.
doi:10.1007/s10899-005-9002-4
Potenza, M. N., Steinberg, M. A., McLaughlin, S. D., Rounsaville, B. J., & O’Malley, S. S.
(2000). Illegal behaviors in problem gambling: Analysis of data from a gambling helpline.
Journal of the American Academy of Psychiatry and the Law, 28, 389–403.
Potenza, M. N., Steinberg, M. A., McLaughlin, S. D., Wu, R., Rounsaville, B. J., & O’Malley,
S. S. (2001). Gender-related differences in the characteristics of problem gamblers using
a gambling helpline. American Journal of Psychiatry, 158, 1500–1505.
Potenza, M. N., Steinberg, M. A., Skudlarski, P., Fulbright, R. K., Lacadie, C. M., Wilber,
M. K., … Wexler, B. E. (2003). Gambling urges in pathological gambling: A functional
magnetic resonance imaging study. Archives of General Psychiatry, 60, 828–836.
Potenza, M. N., Wareham, J. D., Steinberg, M. A., Rugle, L., Cavallo, D. A., Krishnan-
Sarin, S., & Desai, R. A. (2011). Correlates of at-risk/problem Internet gambling in
adolescents. Journal of the American Academy of Psychiatry and the Law, 50, 150–159.
doi:10.1016/j.jaac.2010.11.006
Rash, C. J., Weinstock, J., & Petry, N. M. (2011). Drinking patterns of pathological gamblers
before, during, and after gambling treatment. Psychology of Addictive Behaviors, 25,
664–674. doi:10.1037/a0025565
Rychtarik, R. G., & McGillicuddy, N. B. (2006). Preliminary evaluation of a coping skills
training program for those with a pathological-gambling partner. Journal of Gambling
Studies, 22, 165–178. doi:10.1007/s10899-006-9008-6
Shaffer, H. J., & Hall, M. N. (1996). Estimating the prevalence of adolescent gambling
disorders: A quantitative synthesis and guide toward standard gambling nomenclature.
Journal of Gambling Studies, 12, 193–214.
Shaffer, H. J., Hall, M. N., & Vander Bilt, J. (1999). Estimating the prevalence of disordered
gambling behavior in the United States and Canada: A research synthesis. American
Journal of Public Health, 89, 1369–1376. doi:10.2105/AJPH.89.9.1369
Shaw, M. C., Forbush, K. T., Schlinder, J., Rosenman, E., & Black, D. W. (2007). The
effect of pathological gambling on families, marriages, and children. CNS Spectrums, 12,
615–622.
Slutske, W. S. (2006). Natural recovery and treatment-seeking in pathological gambling:
Results of two U.S. national surveys. American Journal of Psychiatry, 163, 297–302.
doi:10.1176/appi.ajp.163.2.297
Slutske, W. S., Meier, M. H., Zhu, G., Statham, D. J., Blaszczynski, A., & Martin, N.
G. (2009). The Australian Twin Study of Gambling (OZ-GAM): Rationale, sample
description, predictors of participation, and a first look at sources of individual differences
in gambling involvement. Twin Research and Human Genetics, 12, 63–78.
Sobell, L. C., Cunningham, J. A., & Sobell, M. B. (1996). Recovery from alcohol problems
with and without treatment: Prevalence in two population surveys. American Journal of
Public Health, 86, 966–972. doi:10.2105/AJPH.86.7.966
Splevins, K., Mireskandari, S., Clayton, K., & Blaszczynski, A. (2010). Prevalence of adolescent
problem gambling, related harms and help-seeking behaviours among an Australian
population. Journal of Gambling Studies, 26, 189–204. doi:10.1007/s10899-009-
9169-1
Ste-Marie, C., Gupta, R., & Derevensky, J. (2006). Anxiety and social stress related to
adolescent gambling behaviour and substance use. Journal of Child and Adolescent
Substance Abuse, 15, 55–74. doi:10.1300/J029v15n04_03
Stevens, M., & Young, M. (2010). Who plays what? Participation profiles in chance versus
skill-based gambling. Journal of Gambling Studies, 26, 89–103. doi:10.1007/s10899-
009-9143-y
Suurvali, H., Cordingley, J., Hodgins, D. C., & Cunningham, J. (2009). Barriers to seeking
help for gambling problems: A review of the empirical literature. Journal of Gambling
Studies, 25, 407–424. doi:10.1007/s10899-009-9129-9
Suurvali, H., Hodgins, D., Toneatto, T., & Cunningham, J. (2008). Treatment seeking
among Ontario problem gamblers: Results of a population survey. Psychiatric Services, 59,
1343–1346. doi:10.1176/appi.ps.59.11.1343
Suurvali, H., Hodgins, D. C., Toneatto, T., & Cunningham, J. A. (2011). Hesitation to
seek gambling-related treatment among Ontario problem gamblers. Journal of Addiction
Medicine. Advance online publication.
Sylvain, C., Ladouceur, R., & Boisvert, J. M. (1997). Cognitive and behavioral treatment of
pathological gambling: A controlled study. Journal of Consulting and Clinical Psychology,
65, 727–732. doi:10.1037/0022-006X.65.5.727
Symes, B. A., & Nicki, R. M. (1997). A preliminary consideration of cue-exposure, response-
prevention treatment for pathological gambling behaviour: Two case studies. Journal of
Gambling Studies, 13, 145–157. doi:10.1023/A:1024951301959
Tavares, H., Martins, S. S., Lobo, D. S., Silveira, C. M., Gentil, V., & Hodgins, D. C. (2003).
Factors at play in faster progression for female pathological gamblers: An exploratory
analysis. Journal of Clinical Psychiatry, 64, 433–438.
Toce-Gerstein, M., Gerstein, D. R., & Volberg, R. A. (2009). The NODS-CLiP: A rapid
screen for adult pathological and problem gambling. Journal of Gambling Studies, 25,
541–555. doi:10.1007/s10899-009-9135-y
Gambling 1387
Toneatto, T. (1999). Cognitive psychopathology of problem gambling. Substance Use &

Misuse, 34, 1593–1604.
Tremblay, N., Boutin, C., & Ladouceur, R. (2008). Improved self-exclusion program:
Preliminary results. Journal of Gambling Studies, 24, 505–518. doi:10.1007/s10899-
008-9110-z
Vander Bilt, J., & Franklin, J. (2003). Gambling in a familial context. In H. J. Shaffer, M. N.
Hall, J. Vander Bilt, & E. M. George (Eds.), Futures at stake: Youth, gambling, & society
(pp. 100–125). Reno, NV: University of Nevada Press.
Walters, S. T., Miller, E., & Chiauzzi, E. (2005). Wired for wellness: E-interventions
for addressing college drinking. Journal of Substance Abuse Treatment, 29, 139–145.
doi:10.1016/j.jsat.2005.05.006
Walters, S. T., Wright, J. A., & Shegog, R. (2005). A review of computer and
Internet-based interventions for smoking behavior. Addictive Behaviors, 31, 264–277.
doi:10.1016/j.addbeh.2005.05.002
Wardle, H., Sproston, K., Orford, J., Erens, B., Griffiths, M., Constantine, R., & Pigott, S.
(2007). British Gambling Prevalence Survey 2007 . London, England: National Center for
Social Research.
Weinstock, J., Burton, S., Rash, C. J., Moran, S., Biller, W., Krudelbach, N., … Morasco,
B. J. (2011). Predictors of engaging in problem gambling treatment: Data from the
West Virginia Problem Gamblers Help Network. Psychology of Addictive Behaviors, 25,
372–379. doi:10.1037/a0023240
Wong, P. W., Chan, W. S., Conwell, Y., Conner, K. R., & Yip, P. S. (2010). A psychological
autopsy study of pathological gamblers who died by suicide. Journal of Affective Disorders,
120, 213–216. doi:10.1016/j.jad.2009.04.001
Wulfert, E., Blanchard, E. B., & Freidenberg, B. M. (2006). Retaining pathological gamblers
in cognitive behavior therapy through motivational enhancement. Behavior Modification,
30, 315–340. doi:10.1177/0145445503262578
Yip, S. W., Desai, R. A., Steinberg, M. A., Rugle, L., Cavallo, D. A., Krishnan-Sarin, S.,
& Potenza, M. N. (2011). Health/functioning characteristics, gambling behaviors, and
gambling-related motivations in adolescents stratified by gambling problem severity:
Findings from a high school survey. American Journal on Addictions, 20, 495–508.
doi:10.1111/j.1521-0391.2011.00180.x
Zion, M. M., Tracy, E., & Abell, N. (1991). Examining the relationship between spousal
involvement in GAM-ANON and relapse behaviors in pathological gamblers. Journal of
Gambling Studies, 7 , 117–131. doi:10.1007/BF01014527

The Wiley Handbook of Cognitive Behavioral Therapy

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

The Wiley Handbook of Cognitive Behavioral Therapy

Uploaded by

Copyright:

Available Formats

PC4-Galliard c001.tex V1 - 07/30/2013 9:59 P.M.

Jonathan S. Abramowitz, University of North Carolina at Chapel Hill,

Matthew R. Capriotti, University of Wisconsin-Milwaukee, United States

Jennifer D. Gottlieb, Boston University, United States

Michael R. McCart, Medical University of South Carolina, United States

Steven A. Safren, Massachusetts General Hospital and Harvard Medical School,

Douglas W. Woods, University of Wisconsin-Milwaukee, United States

My position is not that technique is irrelevant to outcome. Rather I maintain that,

The Wiley Handbook of Cognitive Behavioral Therapy, First Edition.

The Therapeutic Relationship

The Therapeutic Bond

The Therapeutic Alliance

• taking and accepting the role as a helping authority;

Resistances and Impediments to the Working Relationship

• The therapist lacks either interpersonal skills or therapeutic skills.

• environmental stressors that preclude change;

Problem or Pathology Factors

• rigid cognitive style;

Building and Enhancing the Working Relationship

Altering the Working Alliance

Process and Content of Therapy

A. T. Beck’s cognitive therapy (CT) has made a substantial contribution to current

The Wiley Handbook of Cognitive Behavioral Therapy, First Edition.

CT have referred to the cognitive interventions utilized to achieve schematic change

The Nature of Cognitive Restructuring

Defining Schematic Change

of adaptive schematic processing over the maladaptive disorder-related schemas. It

organization or interconnectedness, reduce the accessibility or activation threshold of

Key Components of Cognitive Restructuring

Collaborative empiricism. A. T. Beck and colleagues (A. T. Beck et al., 1979; A. T.

assignments. This strong emphasis on mutual responsibility and joint involvement

Table 2.1 Verbal Intervention Strategies Employed in Cognitive Restructuring

Intervention strategy Description

1. Evidence Obtaining schema-congruent and -incongruent evidence from

Empirical hypothesis-testing can be defined as “planned experiential activities,

Empirical Evidence for Cognitive Restructuring

such as CR, or whether it is also evident in noncognitive treatments such as exposure

Based on an RCT comparing CBT and pharmacotherapy for panic disorder,

CR is a multifaceted therapeutic intervention that seeks symptom reduction by

Exposure refers to the systematic and controlled confrontation of feared objects

Historical Roots of Exposure Therapy

The Wiley Handbook of Cognitive Behavioral Therapy, First Edition.

Contemporary Exposure Methods

Virtual Reality Exposure

Mechanisms Underlying Exposure

Fear reduction is a central feature of any effective exposure treatment, whether in

Mowrer’s Two-Factor Theory

absence of a feared consequence. Although it was previously believed that extinction

Emotional Processing Theory

Exposure Practices within Cognitive

Exposure therapy is often included as a component of broader cognitive behav-

Generating Exposure Practices

Third, it is important that patients’ learning be independent of contexts that will

Guidelines for Conducting Effective Exposure Practices

Predictability and Perceived Control

Frequency of Exposure Practices

Duration of Exposure Practices

Intensity of Exposure Practices

Role of Safety Behaviors

interfere with the acquisition of corrective information in the exposure environment.

Use of Medication During Exposure Therapy

Problem-solving therapy (PST) is a psychosocial intervention, generally considered to

The Wiley Handbook of Cognitive Behavioral Therapy, First Edition.

(e.g., cancer, Alzheimer’s disease, cardiovascular disease, heart failure, diabetes),